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Electrophysiology of the Corpus Striatum and Brain Stem Integrating Systems

S. T. Kitai

10.1002/cphy.cp010220

Source: Supplement 2: Handbook of Physiology, The Nervous System, Motor Control

Originally published: 1981

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Afferents to Neostriatum
1.1 Corticostriatal Afferents
1.2 Thalamostriatal Afferents
1.3 Nigrostriatal Afferents
1.4 Other Afferents to Striatum
1.5 Convergence of Extrinsic Inputs to Striatal Neurons
2 Striatal Efferent Systems
2.1 Striatopallidal System
2.2 Striatonigral System
2.3 Striatal Projection Neurons
3 Pallidal Efferent System
3.1 Pallidothalamic Projection
3.2 Pallidosubthalamic Projection
4 Nigral Efferent System
4.1 Nigrostriatal Projection
4.2 Nigrothalamic Projection
4.3 Nigrotectal Projection
5 Summary
Figure 1. Figure 1.

Samples of cortically evoked potentials. Single electrical pulse of sufficient intensity delivered to cortical surface (PMS, posterior middle suprasylvian gyrus; ASG, anterior sigmoid gyrus) evoked a sequence of potential waves—an initial positive deflection followed by a long‐lasting negative wave. When PMS and ASG were stimulated simultaneously, the potential waves summed without occlusion. Each trace was formed by super‐imposition of 6 sweeps. Traces were triggered by 0.5‐ms stimulus.

From Blake et al. 10
Figure 2. Figure 2.

Averaged spike‐filtered intracellular responses of caudate neurons to electrical stimulation of thalamus, cerebral cortex, and brain stem. A: substantia nigra (SN). B: precruciate cortex (CX). C: ventrolateral thalamic nucleus (VL). D: anterior median thalamic nucleus (AM). E: central median thalamic nucleus (CM). All traces are computed averages of 10 consecutive responses. Onset of stimulation marked by upward arrow in each trace. Most common type of response was a sequence of EPSPs followed by IPSP.

From Buchwald et al. 13
Figure 3. Figure 3.

Synaptic potentials recorded from rat caudate‐putamen monosynaptically excited following electrical stimulation of cerebral cortex (A, B), central median‐parafascicular complex (C, D), and substantia nigra (E, F). Note superimposed graded responses of constant latency with changes in stimulation intensity. B, D, and F were photographed at a faster steep speed than A, C, and E so that response onset could be discerned. Stimulation onset is indicated by arrows. Bottom trace in each set of traces is the extracellular control response. This is the field potential recorded in the immediate vicinity of the recorded neuron in response to the highest level of stimulation used for the intracellular data. It was taken immediately after coming out of the cell. Calibration in A is also for C. Calibration in B is also for D and F.
Figure 4. Figure 4.

Two types (type I and type II) of extracellular records monitored from rat substantia nigra cells. A shows 3 different type I cells. In general, action potentials are wide, often display a distinct initial segment (1st record in A), and have a large positive component. B show 2 type II cells. Type II cells are characterized by a narrower action potential and have no distinct late positivity.

From Guyenet and Aghajanian 48
Figure 5. Figure 5.

Records from rat striatal spiny neurons monosynaptically excited by electrical stimulation of dorsal raphe nucleus (DRN). A and B: stimulation of DRN at 3 different intensities (8, 12, and 18 V) elicits EPSPs of increasing amplitude but constant latency, indicating monosynaptic nature of inputs. Traces in B are same as in A, but are at a faster sweep and higher gain. Stimulation onset is indicated by arrows. Bottom trace in A and dashed line in B show extracellularly recorded control response. C: passage of 4.7 nA of hyperpolarizing current through recording electrode increased amplitude of DRN‐induced EPSP, whereas 4.8 nA of depolarizing current decreased its amplitude. Middle of the 3 superimposed traces is response when no current was being injected. Bottom trace in C is extracellular control. D and E: EPSP‐IPSP sequences are seen in response to DRN stimulation: action potentials are clipped in D. E: when cell is hyperpolarized by continuously injecting 2.0 nA of negative current, spikes are suppressed, EPSP increases in magnitude, and IPSP decreases. Bottom trace in E is extracellular control for D and E. F and G: low‐gain DC traces from this same cell showing single spike (F) or no spike (G) triggered by initial EPSP, followed by suppression of action potentials during IPSP, followed by rebound excitation with many action potentials. Stimulation was 18 V for both traces, which were recorded within 6 s of each other. Bottom trace in G (with lowered beam intensity) is extracellular control for F and G. H and I: convergence of inputs onto single neuron from stimulation of DRN (H) and cerebral cortex (I). Bottom traces in H and I are low‐gain DC traces (20‐mV calibration), upper traces are high‐gain AC traces (4‐mV calibration), and dashed lines are extracellular control responses. J: frequency histogram of EPSP response latencies for caudateputamen neurons following stimulation of DRN. A–E are computer‐averaged traces (n = 8 sweeps), F and G are single sweeps, and H and I are superimposed sweeps. A and B are from single neuron, C is from a 2nd neuron, D–G are from a 3rd neuron, and H and I are from a 4th neuron. Positivity upward.

From VanderMaelen, Bonduki, and Kitai 113
Figure 6. Figure 6.

Intracellular recordings from cat pallidal‐entopeduncular nucleus following stimulation of substantia nigra. A: stimulation of substantia nigra at 15 V induces IPSPs. B: injection of hyperpolarizing current of 10 nA through recording electrode reverses polarity of IPSPs to positive. C: extracellular control record. D: frequency histogram of IPSP response latencies for entopeduncular neurons following stimulation of substantia nigra. Ordinate shows number of IPSPs and abscissa shows latency.

From Yoshida et al. 116
Figure 7. Figure 7.

Intracellular recordings from pallidal neurons in encéphale isolé cats. A–C: EPSP‐IPSP sequence of responses are elicited in ventral lenticular (pallidal) neuron during low‐frequency (6/s) caudate stimulation. A–C are 1st 3 responses evoked by repetitive stimulus train. The IPSP is well developed following first caudate stimulus. Short‐latency evoked EPSPs in B and C fail to elicit spikes probably as consequence of encroachment by IPSPs. Upper trace in A–C is monopolarly recorded cortical surface response. Negativity upward.

From Malliani and Purpura 81
Figure 8. Figure 8.

Extra‐ and intracellular responses of cat nigral neurons evoked by electrical stimulation of caudate nucleus. A: extracellularly recorded spontaneous discharges of nigral neuron. B: inhibition of neuron in A during positive field potential evoked by stimulation of caudate nucleus. C: IPSP, induced by stimulation of caudate nucleus, followed by depolarizing potential in a nigra cell. D: extracellular control record. E: IPSP evoked in nigra cell of C following stimulation of cerebral peduncle. F: extracellular control for E. G and H: Caudate‐evoked IPSPs averaged by signal averager; 16 traces were averaged. Extracellular control record is superimposed by G. H shows net IPSPs obtained by subtracting extracellular response (upper trace of G) from intracellular response (lower trace of G). I: IPSP response latencies for nigral neurons following stimulation of caudate nucleus and cerebral peduncle plotted against distance between stimulating and recording sites. Regression line drawn through points, calculated by least squares method, has a y‐intercept of 0.8 ms when extrapolated to zero distance. This indicates that IPSPs evoked by caudate stimulation are monosynaptic in nature.

From Yoshida and Precht 115
Figure 9. Figure 9.

Antidromic (A and B) and orthodromic (C and D) responses of cat caudate neurons intracellularly recorded. A: all‐or‐none constant‐latency action potential elicited by nigral stimulation. No synaptic potential was seen when action potential failed. B: superimposed records of responses to paired stimuli in test for collision between intracellularly evoked spike (conditioning) and nigral‐evoked spike (test). Upward and downward arrows indicate onset and offset of depolarizing pulse. First small upward arrow indicates point at which nigral stimulation failed to induce an action potential and second small upward arrow indicates nigral stimulation corresponding to longest latency potential. C: EPSPs evoked by nigral stimulation. Variation of stimulus intensity elicits graded amplitude but constant‐latency responses. Bottom traces show low‐gain DC records. D: thalamic‐induced EPSPs recorded from neuron in C. Bottom traces are low‐gain DC; 10‐ms calibration in B applies also to C and D. High‐gain 4 mV and low‐gain 20 mV in D also applies to C. E: frequency histogram of antidromic action potentials evoked by nigral stimulation. Abscissa indicates latency of antidromic spike.

From Kitai et al. 67 in Advances in Neurology, © 1979, Raven Press, NY
Figure 10. Figure 10.

Morphology of striatal projection neurons labeled by intracellular injection of horseradish peroxidase (HRP) and reconstructed from serial sections with aid of drawing tube. Recording microelectrodes were filled with HRP solution. Subsequent to electrophysiological analysis, HRP was electrophoresed into impaled neuron to permit later histological processing and morphological identification and analysis. A: reconstruction of cat caudate projection neuron that responded antidromically and synaptically to substantia nigra stimulation. Arrow indicates axon. B: a reconstruction drawing of rat striatal projection neuron, the axon of which was traced into globus pallidus. Arrows in B indicate fine terminal portion of dendrites. Asterisks indicate points of axon‐collateral origin.

From Kitai et al. 67 in Advances in Neurology, © 1979, Raven Press, NY
Figure 11. Figure 11.

Photomicrographically recorded features of rat striatal projection neurons labeled by intracellularly injected horseradish peroxidase. A: sagittal section of striatal projection neuron with dorsorostrally (top) and ventrocaudally (bottom) directed dendrites arising from an oval soma. B: another projection neuron, in frontal section, with dorsally (top) and ventrally (bottom) directed dendrites and an oval soma. C and D: distal terminations of projection‐neuron dendrites. E: sagittal view of polygonal soma of another projection neuron with radially directed dendrites. Arrow points to ventrocaudally directed axon of cell. F, G, and H: high‐power photomicrographs of cell in E. Note absence of spines on soma and proximal dendrites, but high density of spines on distal dendrites in F and on more distal dendrites in G and H. I: initial segment of axon of cell in B. Arrow indicates point where axon thins abruptly to a diameter that is maintained for remainder of projection. J: right‐angle origin of axon collateral from distinct nodal point (arrow). K: beadlike swellings and side branches observed on axon collaterals. Calibration in A also applies to B and E. Calibration in G also applies to F. H, J, and K.

From Preston, Bishop, and Kitai 96
Figure 12. Figure 12.

Intracellular recordings from thalamic (ventrolateral) neurons in cats anesthetized with sodium pentobarbital following stimulation of corpus striatum (ansa lenticularis) and contralateral brachium conjunctivum. A: convergent monosynaptic excitation of a ventrolateral (VL) neuron by ansa lenticularis (A, C, and D) and brachium conjunctivum (B) stimulation. Spikes in B and C truncated for display purposes. Note minimal latency differences of EPSPs in B and C. Ansa lenticularis‐evoked EPSP is shown in isolation in D. E and F: records obtained from different VL neuron following ansa lenticularis (E) and brachium conjunctivum (F) stimulation. Only the brachium‐evoked EPSP is succeeded by prolonged IPSP, early phase of which exhibits low‐frequency oscillations. G and 77: example of convergent, but reciprocal, synaptic effects observed in VL neuron following ansa lenticularis (G) and brachium conjunctivum (H) stimulation. Responses in each case were elicited at 2 levels of membrane polarization. G: upper record obtained during spontaneous discharges, lower record during phase of increased membrane polarization in which spontaneous discharges were eliminated. In each instance ansa lenticularis stimulation evoked a 4‐ to 6‐ms IPSP. 77: lower record of pair obtained during a spontaneous long‐duration IPSP. Brachium conjunctivum stimulation elicits a 4‐ to 6‐ms‐latency EPSP and spike discharge. The EPSP is revealed in isolation during spontaneous IPSP. I‐L: examples of similar long‐latency EPSP‐IPSP sequences elicited in VL neuron by repetitive stimulation in region of entopeduncular nucleus (I and J, continuous recording) and stimulation of medial thalamic nucleus (K and L, continuous recording). Upper channel records obtained from motor cortex. Note prominent long‐latency surface negative recruiting response evoked by medial thalamic stimulation.

From Desiraju and Purpura 24
Figure 13. Figure 13.

Intracellular records of short‐latency IPSPs from cat ventroanterior and ventrolateral thalamic (VA‐VL) neurons following stimulation of entopeduncular nucleus (ENT; medial pallidal segment). A: ENT‐evoked IPSPs in thalamic neuron. B: extracellular control for A. C–E: IPSPs produced in another cell, recorded at 3 different sweep velocities. F: ENT‐evoked IPSPs recorded in thalamic cell. G: reversed IPSPs obtained by injecting chloride ions electrophoretically through microelectrode in same cell as in F. H: inhibition of extracellularly recorded spike discharges following ENT stimulation. I: latency histogram for IPSPs in 24 neurons. J–L: IPSPs evoked by double‐shock stimulation of ENT nucleus. Shock intervals: 0.5 ms, J; 1.1 ms, K; and 6.5 ms, L. Arrows in H and J–L indicate time of stimulation. Voltage scales are 1 mV for A–G, J–L, and 0.5 mV for H. Recording time constant, 10 ms for A, B, F, G, J–L, and 1 s for C–E.

From Uno and Yoshida 111
Figure 14. Figure 14.

Intracellular recordings from cat ventrolateral and ventromedial thalamic (VL‐VM) neurons following stimulation of contralateral brachium conjunctivum (BC) and substantia nigra (SN). A: monosynaptic EPSPs evoked in VL neuron by stimulation of BC (2nd shock; 1st shock was to SN). B: intracellular recording of VM neuron; BC stimulation did not evoke any response in this cell. C: SN‐evoked IPSPs (1st shock) in cell of B. Second shock indicates BC stimulation, producing no transsynaptic potentials. Lower traces in A and C, juxtacellular field potentials. D: inhibition of extracellularly recorded spike discharges of a VM neuron following SN stimulation. Arrow indicates stimulus artifact. E: IPSPs produced by stimulation of SN (1st shock) and midpoint between SN and recording site (2nd shock). F: same as in E, but IPSPs were reversed to depolarizing potentials by iontophoretic injection of chloride into cell through recording electrode. G: superimposed tracing of E and F. Arrows indicate onset of IPSPs. H: latencies of IPSPs (ordinate) plotted against distance between stimulating and recording sites in 5 cells (abscissa). Voltage scales are 1 mV for A–C, 0.5 mV for D, and 2 mV for E–G. Time scales are 2 ms for A–C and E–G, and 10 ms for D.

From Ueki et al. 110
Figure 15. Figure 15.

Summary of neuronal circuitry in basal ganglia and related structures. Open terminals are excitatory connections, and filled terminals are inhibitory connections. CMP, central median‐parafascicular complex; DR, dorsal raphe nucleus; GP, globus pallidus; 1, lateral; m, medial; Pc, pars compacta; Pr, pars reticulata; SN, substantia nigra; ST, subthalamus; TE, midbrain tectum; VA, ventroanterior nucleus of thalamus; VL, ventrolateral nucleus of thalamus; VM, ventromedial nucleus of thalamus.


Figure 1.

Samples of cortically evoked potentials. Single electrical pulse of sufficient intensity delivered to cortical surface (PMS, posterior middle suprasylvian gyrus; ASG, anterior sigmoid gyrus) evoked a sequence of potential waves—an initial positive deflection followed by a long‐lasting negative wave. When PMS and ASG were stimulated simultaneously, the potential waves summed without occlusion. Each trace was formed by super‐imposition of 6 sweeps. Traces were triggered by 0.5‐ms stimulus.

From Blake et al. 10


Figure 2.

Averaged spike‐filtered intracellular responses of caudate neurons to electrical stimulation of thalamus, cerebral cortex, and brain stem. A: substantia nigra (SN). B: precruciate cortex (CX). C: ventrolateral thalamic nucleus (VL). D: anterior median thalamic nucleus (AM). E: central median thalamic nucleus (CM). All traces are computed averages of 10 consecutive responses. Onset of stimulation marked by upward arrow in each trace. Most common type of response was a sequence of EPSPs followed by IPSP.

From Buchwald et al. 13


Figure 3.

Synaptic potentials recorded from rat caudate‐putamen monosynaptically excited following electrical stimulation of cerebral cortex (A, B), central median‐parafascicular complex (C, D), and substantia nigra (E, F). Note superimposed graded responses of constant latency with changes in stimulation intensity. B, D, and F were photographed at a faster steep speed than A, C, and E so that response onset could be discerned. Stimulation onset is indicated by arrows. Bottom trace in each set of traces is the extracellular control response. This is the field potential recorded in the immediate vicinity of the recorded neuron in response to the highest level of stimulation used for the intracellular data. It was taken immediately after coming out of the cell. Calibration in A is also for C. Calibration in B is also for D and F.



Figure 4.

Two types (type I and type II) of extracellular records monitored from rat substantia nigra cells. A shows 3 different type I cells. In general, action potentials are wide, often display a distinct initial segment (1st record in A), and have a large positive component. B show 2 type II cells. Type II cells are characterized by a narrower action potential and have no distinct late positivity.

From Guyenet and Aghajanian 48


Figure 5.

Records from rat striatal spiny neurons monosynaptically excited by electrical stimulation of dorsal raphe nucleus (DRN). A and B: stimulation of DRN at 3 different intensities (8, 12, and 18 V) elicits EPSPs of increasing amplitude but constant latency, indicating monosynaptic nature of inputs. Traces in B are same as in A, but are at a faster sweep and higher gain. Stimulation onset is indicated by arrows. Bottom trace in A and dashed line in B show extracellularly recorded control response. C: passage of 4.7 nA of hyperpolarizing current through recording electrode increased amplitude of DRN‐induced EPSP, whereas 4.8 nA of depolarizing current decreased its amplitude. Middle of the 3 superimposed traces is response when no current was being injected. Bottom trace in C is extracellular control. D and E: EPSP‐IPSP sequences are seen in response to DRN stimulation: action potentials are clipped in D. E: when cell is hyperpolarized by continuously injecting 2.0 nA of negative current, spikes are suppressed, EPSP increases in magnitude, and IPSP decreases. Bottom trace in E is extracellular control for D and E. F and G: low‐gain DC traces from this same cell showing single spike (F) or no spike (G) triggered by initial EPSP, followed by suppression of action potentials during IPSP, followed by rebound excitation with many action potentials. Stimulation was 18 V for both traces, which were recorded within 6 s of each other. Bottom trace in G (with lowered beam intensity) is extracellular control for F and G. H and I: convergence of inputs onto single neuron from stimulation of DRN (H) and cerebral cortex (I). Bottom traces in H and I are low‐gain DC traces (20‐mV calibration), upper traces are high‐gain AC traces (4‐mV calibration), and dashed lines are extracellular control responses. J: frequency histogram of EPSP response latencies for caudateputamen neurons following stimulation of DRN. A–E are computer‐averaged traces (n = 8 sweeps), F and G are single sweeps, and H and I are superimposed sweeps. A and B are from single neuron, C is from a 2nd neuron, D–G are from a 3rd neuron, and H and I are from a 4th neuron. Positivity upward.

From VanderMaelen, Bonduki, and Kitai 113


Figure 6.

Intracellular recordings from cat pallidal‐entopeduncular nucleus following stimulation of substantia nigra. A: stimulation of substantia nigra at 15 V induces IPSPs. B: injection of hyperpolarizing current of 10 nA through recording electrode reverses polarity of IPSPs to positive. C: extracellular control record. D: frequency histogram of IPSP response latencies for entopeduncular neurons following stimulation of substantia nigra. Ordinate shows number of IPSPs and abscissa shows latency.

From Yoshida et al. 116


Figure 7.

Intracellular recordings from pallidal neurons in encéphale isolé cats. A–C: EPSP‐IPSP sequence of responses are elicited in ventral lenticular (pallidal) neuron during low‐frequency (6/s) caudate stimulation. A–C are 1st 3 responses evoked by repetitive stimulus train. The IPSP is well developed following first caudate stimulus. Short‐latency evoked EPSPs in B and C fail to elicit spikes probably as consequence of encroachment by IPSPs. Upper trace in A–C is monopolarly recorded cortical surface response. Negativity upward.

From Malliani and Purpura 81


Figure 8.

Extra‐ and intracellular responses of cat nigral neurons evoked by electrical stimulation of caudate nucleus. A: extracellularly recorded spontaneous discharges of nigral neuron. B: inhibition of neuron in A during positive field potential evoked by stimulation of caudate nucleus. C: IPSP, induced by stimulation of caudate nucleus, followed by depolarizing potential in a nigra cell. D: extracellular control record. E: IPSP evoked in nigra cell of C following stimulation of cerebral peduncle. F: extracellular control for E. G and H: Caudate‐evoked IPSPs averaged by signal averager; 16 traces were averaged. Extracellular control record is superimposed by G. H shows net IPSPs obtained by subtracting extracellular response (upper trace of G) from intracellular response (lower trace of G). I: IPSP response latencies for nigral neurons following stimulation of caudate nucleus and cerebral peduncle plotted against distance between stimulating and recording sites. Regression line drawn through points, calculated by least squares method, has a y‐intercept of 0.8 ms when extrapolated to zero distance. This indicates that IPSPs evoked by caudate stimulation are monosynaptic in nature.

From Yoshida and Precht 115


Figure 9.

Antidromic (A and B) and orthodromic (C and D) responses of cat caudate neurons intracellularly recorded. A: all‐or‐none constant‐latency action potential elicited by nigral stimulation. No synaptic potential was seen when action potential failed. B: superimposed records of responses to paired stimuli in test for collision between intracellularly evoked spike (conditioning) and nigral‐evoked spike (test). Upward and downward arrows indicate onset and offset of depolarizing pulse. First small upward arrow indicates point at which nigral stimulation failed to induce an action potential and second small upward arrow indicates nigral stimulation corresponding to longest latency potential. C: EPSPs evoked by nigral stimulation. Variation of stimulus intensity elicits graded amplitude but constant‐latency responses. Bottom traces show low‐gain DC records. D: thalamic‐induced EPSPs recorded from neuron in C. Bottom traces are low‐gain DC; 10‐ms calibration in B applies also to C and D. High‐gain 4 mV and low‐gain 20 mV in D also applies to C. E: frequency histogram of antidromic action potentials evoked by nigral stimulation. Abscissa indicates latency of antidromic spike.

From Kitai et al. 67 in Advances in Neurology, © 1979, Raven Press, NY


Figure 10.

Morphology of striatal projection neurons labeled by intracellular injection of horseradish peroxidase (HRP) and reconstructed from serial sections with aid of drawing tube. Recording microelectrodes were filled with HRP solution. Subsequent to electrophysiological analysis, HRP was electrophoresed into impaled neuron to permit later histological processing and morphological identification and analysis. A: reconstruction of cat caudate projection neuron that responded antidromically and synaptically to substantia nigra stimulation. Arrow indicates axon. B: a reconstruction drawing of rat striatal projection neuron, the axon of which was traced into globus pallidus. Arrows in B indicate fine terminal portion of dendrites. Asterisks indicate points of axon‐collateral origin.

From Kitai et al. 67 in Advances in Neurology, © 1979, Raven Press, NY


Figure 11.

Photomicrographically recorded features of rat striatal projection neurons labeled by intracellularly injected horseradish peroxidase. A: sagittal section of striatal projection neuron with dorsorostrally (top) and ventrocaudally (bottom) directed dendrites arising from an oval soma. B: another projection neuron, in frontal section, with dorsally (top) and ventrally (bottom) directed dendrites and an oval soma. C and D: distal terminations of projection‐neuron dendrites. E: sagittal view of polygonal soma of another projection neuron with radially directed dendrites. Arrow points to ventrocaudally directed axon of cell. F, G, and H: high‐power photomicrographs of cell in E. Note absence of spines on soma and proximal dendrites, but high density of spines on distal dendrites in F and on more distal dendrites in G and H. I: initial segment of axon of cell in B. Arrow indicates point where axon thins abruptly to a diameter that is maintained for remainder of projection. J: right‐angle origin of axon collateral from distinct nodal point (arrow). K: beadlike swellings and side branches observed on axon collaterals. Calibration in A also applies to B and E. Calibration in G also applies to F. H, J, and K.

From Preston, Bishop, and Kitai 96


Figure 12.

Intracellular recordings from thalamic (ventrolateral) neurons in cats anesthetized with sodium pentobarbital following stimulation of corpus striatum (ansa lenticularis) and contralateral brachium conjunctivum. A: convergent monosynaptic excitation of a ventrolateral (VL) neuron by ansa lenticularis (A, C, and D) and brachium conjunctivum (B) stimulation. Spikes in B and C truncated for display purposes. Note minimal latency differences of EPSPs in B and C. Ansa lenticularis‐evoked EPSP is shown in isolation in D. E and F: records obtained from different VL neuron following ansa lenticularis (E) and brachium conjunctivum (F) stimulation. Only the brachium‐evoked EPSP is succeeded by prolonged IPSP, early phase of which exhibits low‐frequency oscillations. G and 77: example of convergent, but reciprocal, synaptic effects observed in VL neuron following ansa lenticularis (G) and brachium conjunctivum (H) stimulation. Responses in each case were elicited at 2 levels of membrane polarization. G: upper record obtained during spontaneous discharges, lower record during phase of increased membrane polarization in which spontaneous discharges were eliminated. In each instance ansa lenticularis stimulation evoked a 4‐ to 6‐ms IPSP. 77: lower record of pair obtained during a spontaneous long‐duration IPSP. Brachium conjunctivum stimulation elicits a 4‐ to 6‐ms‐latency EPSP and spike discharge. The EPSP is revealed in isolation during spontaneous IPSP. I‐L: examples of similar long‐latency EPSP‐IPSP sequences elicited in VL neuron by repetitive stimulation in region of entopeduncular nucleus (I and J, continuous recording) and stimulation of medial thalamic nucleus (K and L, continuous recording). Upper channel records obtained from motor cortex. Note prominent long‐latency surface negative recruiting response evoked by medial thalamic stimulation.

From Desiraju and Purpura 24


Figure 13.

Intracellular records of short‐latency IPSPs from cat ventroanterior and ventrolateral thalamic (VA‐VL) neurons following stimulation of entopeduncular nucleus (ENT; medial pallidal segment). A: ENT‐evoked IPSPs in thalamic neuron. B: extracellular control for A. C–E: IPSPs produced in another cell, recorded at 3 different sweep velocities. F: ENT‐evoked IPSPs recorded in thalamic cell. G: reversed IPSPs obtained by injecting chloride ions electrophoretically through microelectrode in same cell as in F. H: inhibition of extracellularly recorded spike discharges following ENT stimulation. I: latency histogram for IPSPs in 24 neurons. J–L: IPSPs evoked by double‐shock stimulation of ENT nucleus. Shock intervals: 0.5 ms, J; 1.1 ms, K; and 6.5 ms, L. Arrows in H and J–L indicate time of stimulation. Voltage scales are 1 mV for A–G, J–L, and 0.5 mV for H. Recording time constant, 10 ms for A, B, F, G, J–L, and 1 s for C–E.

From Uno and Yoshida 111


Figure 14.

Intracellular recordings from cat ventrolateral and ventromedial thalamic (VL‐VM) neurons following stimulation of contralateral brachium conjunctivum (BC) and substantia nigra (SN). A: monosynaptic EPSPs evoked in VL neuron by stimulation of BC (2nd shock; 1st shock was to SN). B: intracellular recording of VM neuron; BC stimulation did not evoke any response in this cell. C: SN‐evoked IPSPs (1st shock) in cell of B. Second shock indicates BC stimulation, producing no transsynaptic potentials. Lower traces in A and C, juxtacellular field potentials. D: inhibition of extracellularly recorded spike discharges of a VM neuron following SN stimulation. Arrow indicates stimulus artifact. E: IPSPs produced by stimulation of SN (1st shock) and midpoint between SN and recording site (2nd shock). F: same as in E, but IPSPs were reversed to depolarizing potentials by iontophoretic injection of chloride into cell through recording electrode. G: superimposed tracing of E and F. Arrows indicate onset of IPSPs. H: latencies of IPSPs (ordinate) plotted against distance between stimulating and recording sites in 5 cells (abscissa). Voltage scales are 1 mV for A–C, 0.5 mV for D, and 2 mV for E–G. Time scales are 2 ms for A–C and E–G, and 10 ms for D.

From Ueki et al. 110


Figure 15.

Summary of neuronal circuitry in basal ganglia and related structures. Open terminals are excitatory connections, and filled terminals are inhibitory connections. CMP, central median‐parafascicular complex; DR, dorsal raphe nucleus; GP, globus pallidus; 1, lateral; m, medial; Pc, pars compacta; Pr, pars reticulata; SN, substantia nigra; ST, subthalamus; TE, midbrain tectum; VA, ventroanterior nucleus of thalamus; VL, ventrolateral nucleus of thalamus; VM, ventromedial nucleus of thalamus.

References
 1. Adinolfi, A. M., and G. D. Pappas. The fine structure of the caudate nucleus of the cat. J. Comp. Neurol. 133: 167–184, 1968.
 2. Albe‐Fessard, D., E. Oswaldo‐Cruz, and C. D. Rocha‐Miranda. Activités évoquées dans le noyau caudé du chat en réponse à des types divers d'afferences. I. Étude microphysiologique. Electroencephalogr. Clin. Neurophysiol. 12: 405–420, 1960.
 3. Albe‐Fessard, D., C. D. Rocha‐Miranda, and E. Oswaldo‐Cruz. Activités évoquées dans le noyau caudé du chat en réponse à des types divers d' afferences. II. Étude microphysiologique. Electroencephalogr. Clin. Neurophysiol. 12: 649–661, 1960.
 4. Anden, N. E., A. Dahlstrom, K. Fuxe, K. Larsson, L. Olson, and U. Ungerstedt. Ascending monoamine neurons to the telencephalon and diencephalon. Acta Physiol. Scand. 67: 313–326, 1966.
 5. Anderson, M., and M. Yoshida. Electrophysiological evidence for branching nigral projections to the thalamus and the superior colliculus. Brain Res. 137: 361–364, 1977.
 6. Bak, I. J., W. B. Choi, R. Hassler, K. G. Usnoff, and A. Wagner. A fine structural synaptic organization of the corpus striatum and substantia nigra in rat and cat. Adv. Neurol. 9: 25–41, 1975.
 7. Bedard, P., L. Larochell, A. Parent, and L. Poirier. The nigro‐striatal pathway: a correlative study based on neuroanatomical and neuro‐chemical criteria in the cat and the monkey. Exp. Neurol. 25: 365–377, 1969.
 8. Bernadi, G., M. G. Marciani, C. Morocutti, and P. Stanzione. The action of GABA and dopamine on rat caudate neurons intracellularly recorded. In: Iontophoresis and Transmitter Mechanisms in the Mammalian Central Nervous System. edited by R. W. Ryall and J. S. Kelly. Amsterdam: Elsevier, 1978, pp. 44–46.
 9. Bevan, P., C. M. Bradshaw, and E. Szabadi. Effects of desipramine on neuronal responses to dopamine, noradrenaline, 5‐hydroxytryptamine and acetylcholine in the caudate nucleus of the rat. Br. J. Pharmacol. 54: 285–293, 1975.
 10. Blake, D. J., P. Zarzecki, and G. G. Somjen. Electrophysiological study of cortico‐caudate projections in cats. J. Neurobiol. 7: 143–156, 1976.
 11. Bloom, F. E., E. Costa, and G. C. Salmoiraghi. Anesthesia and the responsiveness of individual neurons of the caudate nucleus of the cat to acetylcholine, norepinephrine and dopamine administered by microelectrophoresis. J. Pharmacol. Exp. Ther. 150: 244–252, 1966.
 12. Bobillier, P., S. Sequin, F. Petitjean, D. Salvert, M. Touret, and M. Jouvet. The raphé nuclei of the cat brain stem: a topographical atlas of their efferent projections as revealed by autoradiography. Brain Res. 113: 449–486, 1976.
 13. Buchwald, N. A., D. D. Price, L. Vernon, and C. D. Hull. Caudate intracellular response to thalamic and cortical inputs. Exp. Neurol. 38: 311–323, 1973.
 14. Bunney, B. S., and G. K. Aghajanian. The precise localization of nigral afferents in the rat as determined by a retrograde tracing technique. Brain Res. 117: 423–435, 1976.
 15. Carpenter, M. B., and P. Peter. Nigrostriatal and nigrothalamic fibers in the rhesus monkey. J. Comp. Neurol. 144: 93–116, 1972.
 16. Conner, J. D. Caudate unit responses to nigral stimuli: evidence for a possible nigro‐neostriatal pathway. Science 160: 899–900, 1968.
 17. Conner, J. D. Caudate nucleus neurons: correlation of the effects of substantia nigra stimulation with iontophoretic dopamine. J. Physiol. London 208: 691–703, 1970.
 18. Cowan, W. M., and T. P. A. Powell. Striopallidal projection in the monkey. J. Neurol. Neurosurg. Psychiatry 29: 426–439, 1966.
 19. Crossman, A. R., R. J. Walker, and G. N. Woodruff. Picrotoxin antagonism of gamma‐aminobutyric acid inhibitory responses and synaptic inhibition in the rat substantia nigra. Br. J. Pharmacol. Chemother. 49: 696–698, 1973.
 20. Deniau, J. M., G. Chevalier, and J. Feger. Electrophysiological study of the nigro‐tectal pathway in the rat. Neurosci. Lett. 10: 215–220, 1978.
 21. Deniau, J. M., J. Feger, and C. LeGuyader. Striatal evoked inhibition of identified nigrothalamic neurons. Brain Res. 104: 152–156, 1976.
 22. Deniau, J. M., C. Hammond, A. Riszk, and J. Feger. Electrophysiological properties of identified output neurons of the rat substantia nigra (pars compacta and pars reticulata): evidences for the existence of branched neurons. Exp. Brain Res. 32: 409–422, 1978.
 23. Deniau, J. M., D. Lackner, and J. Feger. Effect of substantia nigra stimulation on identified neurons in the VL‐VA thalamic complex: comparison between intact and chronically decorticated cats. Brain Res. 145: 27–35, 1978.
 24. Desiraju, T., and D. Purpura. Synaptic convergence of cerebellar and lenticular projections to thalamus. Brain Res. 15: 544–547, 1969.
 25. Divac, I., F. Fonnum, and J. Storm‐Mathisen. High affinity uptake of glutamate in terminals of corticostriatal axons. Nature London 266: 377–378, 1977.
 26. Dormont, S. F., and C. Ohye. Entopeduncular projections to the thalamic ventrolateral nucleus of the cat. Exp. Brain Res. 12: 254–264, 1971.
 27. Dray, A., T. J. Gonye, and N. R. Oakley. Caudate stimulation and substantia nigra activity in the rat. J. Physiol. London 259: 825–849, 1976.
 28. Feger, J., and C. Ohye. The unitary activity of the substantia nigra following stimulation of the striatum in the awake monkey. Brain Res. 89: 155–159, 1975.
 29. Feltz, P. Gamma‐aminobutyric acid and a caudato‐nigral inhibition. Can. J. Physiol. Pharmacol. 49: 1113–1115, 1971.
 30. Feltz, P., and D. Albe‐Fessard. A study of an ascending nigro‐caudate pathway. Electroencephalogr. Clin. Neurophysiol. 33: 179–193, 1972.
 31. Feltz, P., and J. DeChamplain. Enhanced sensitivity of caudate neurons to microiontophoretic injections of dopamine in 6‐hydroxydopamine treated cats. Brain Res. 43: 601–605, 1972.
 32. Feltz, P., and J. S. McKenzie. Properties of caudate unitary responses to repetitive nigral stimulation. Brain Res. 13: 612–616, 1969.
 33. Fox, C. A., A. M. Andrade, I. J. LuQui, and J. A. Rafols. The primate globus pallidus: a Golgi and electron microscopic study. J. Hirnforsch. 15: 75–93, 1974.
 34. Fox, C. A., A. M. Andrade, R. C. Schwyn, and J. A. Rafols. The aspiny neurons and the glia in the primate striatum: a Golgi and electron microscopic study. J. Hirnforsch. 13: 341–362, 1971.
 35. Fricyesi, T. L., and J. Machek. Basal ganglia‐diencephalon synaptic relations in the cat. I. An intracellular study of dorsal thalamic neurons during capsular and basal ganglia stimulation. Brain Res. 20: 201–217, 1970.
 36. Frigyesi, T. L., and J. Machek. Basal ganglia‐diencephalon synaptic relations in the cat. II. Intracellular recordings from dorsal thalamic neurons during low‐frequency stimulation of the caudate‐thalamic projection system and the nigrothalamic pathway. Brain Res. 27: 59–78, 1971.
 37. Frigyesi, T. L., and D. P. Purpura. Electrophysiological analysis of reciprocal caudato‐nigral relations. Brain Res. 6: 440–456, 1967.
 38. Frigyesi, T. L., and A. Rabin. Basal ganglia‐diencephalon synaptic relations. III. An intracellular study of ansa lenticularis, lenticular fasciculus and pallidosubthalamic projection activities. Brain Res. 35: 67–78, 1971.
 39. Frigyesi, T. L., and J. Szabo. Caudate‐evoked synaptic activities in nigral neurons. Exp. Neurol. 49: 123–139, 1975.
 40. Frigyesi, T. L., J. Szabo, and J. J. Grimm. The origin and nature of evoked activities in caudate neurons during nigral stimulation. Int. J. Neurol. 12: 185–209, 1977.
 41. Fuller, D. R. G., C. D. Hull, and N. A. Buchwald. Intracellular responses of caudate output neurons to orthodromic stimulation. Brain Res. 96: 337–341, 1975.
 42. Geyer, M. A., A. Puerta, W. J. Dawsey, S. Knapp, W. P. Bullard, and A. T. Mandell. Histologic and enzymatic studies of the mesolimbic and mesostriatal serotonergic pathways. Brain Res. 106: 241–256, 1976.
 43. Goldman, P. S., and W. J. H. Nauta. An intricately patterned prefronto‐caudate projection in the rhesus monkey. J. Comp. Neurol. 171: 369–386. 1977.
 44. Gonzalez‐Vegas, J. A. Antagonism of dopamine‐mediated inhibition in the nigro‐striatal pathway: a mode of action of some catatonia‐inducing drugs. Brain Res. 80: 219–228, 1974.
 45. Goswell, M. J., and E. M. Sedgwick. An electrophysiological study of a topographical relationship between the caudate nucleus and the substantia nigra of the cat. Brain Res. 23: 112–116, 1970.
 46. Graybiel, A. N. Organization of the nigrotectal connection: an experimental tracer study in the cat. Brain Res. 143: 339–348, 1978.
 47. Grofova, I. The identification of striatal and pallidal neurons projecting to the substantia nigra. An experimental study by means of retrograde axonal transport of horseradish peroxidase. Brain Res. 91: 286–291, 1975.
 48. Guyenet, P. G., and G. K. Aghajanian. Antidromic identification of dopaminergic and other output neurons of the rat substantia nigra. Brain Res. 150: 69–84, 1978.
 49. Hedreen, J. C. Corticostriatal cells identified by the peroxidase method. Neurosci. Lett. 4: 1–7, 1977.
 50. Herz, A., and W. Zieglagansberger. The influence of microelectrophoretically applied biogenic amines, cholinomimetics and procaine on synaptic excitation in the corpus striatum. Int. J. Neuropharmacol. 7: 221–230, 1968.
 51. Hökfelt, T., and U. Ungerstedt. Electron and fluorescence microscopical studies on the nucleus caudatus putamen of the rat after unilateral lesions of ascending nigro‐neostriatal dopamine neurons. Acta Physiol. Scand. 76: 415–426, 1969.
 52. Hong, J. S., H. Y. T. Yang, G. Racaquni, and E. Costa. Projections of substance P containing neurons from neostriatum to substantia nigra. Brain Res. 122: 541–544, 1977.
 53. Hopkins, D. A., and L. W. Niessen. Substantia nigra projections to the reticular formation, superior colliculus and central gray in the rat, cat and monkey. Neurosci. Lett. 2: 253–259, 1976.
 54. Hull, C. D., G. Bernardi, and N. A. Buchwald. Intracellular responses of caudate neurons to brainstem stimulation. Brain Res. 22: 163–179, 1970.
 55. Hull, C. D., G. Bernardi, D. D. Price, and N. A. Buchwald. Intracellular responses of caudate neurons to temporally and spatially combined stimuli. Exp. Neurol. 38: 324–336, 1973.
 56. Jacobs, B. L., S. L. Foote, and F. E. Bloom. Differential projections of neurons within the dorsal raphe nucleus of the rat: a horseradish peroxidase (HRP) study. Brain Res. 147: 149–153, 1978.
 57. Jones, E. G., J. D. Coulter, H. Burton, and R. Porter. Cells of origin and terminal distribution of cortico‐striatal fibers arising in the sensory motor cortex of monkeys. J. Comp. Neurol. 173: 53–80, 1977.
 58. Jones, E. G., and R. Y. Leavitt. Retrograde axonal transport and the demonstration of non‐specific projections to the cerebral cortex striatum from thalamic intralaminar nuclei in the rat, cat and monkey. J. Comp. Neurol. 154: 349–378, 1974.
 59. Kanazawa, I., P. C. Emson, and A. C. Cuello. Evidence for the existence of substance P‐containing fibers in striato‐nigral and pallido‐nigral pathways in rat brain. Brain Res. 119: 447–453, 1977.
 60. Kemp, J. M. The termination of strio‐pallidal and strio‐nigral fibres. Brain Res. 17: 125–128, 1970.
 61. Kemp, J. M., and T. P. S. Powell. The structure of the caudate nucleus of the cat. Light and electron microscopy. Philos. Trans. R. Soc. London Ser. B 262: 383–401, 1971.
 62. Kemp, J. M., and T. P. S. Powell. The synaptic organization of the caudate nucleus. Philos. Trans. R. Soc. London Ser. B 262: 403–412, 1971.
 63. Kemp, J. M., and T. P. S. Powell. The site of termination of afferent fibers in the caudate nucleus. Philos. Trans. R. Soc. London Ser. B 262: 413–427, 1971.
 64. Kim, J., R. Hassler, P. Hang, and K. Paik. Effect of frontal cortex ablation on striatal glutamic acid level in rat. Brain Res. 132: 370–374, 1977.
 65. Kitai, S. T., J. D. Kocsis, R. J. Preston, and M. Sugimori. Monosynaptic inputs to caudate neurons identified by intracellular injection of horseradish peroxidase. Brain Res. 109: 601–606, 1976.
 66. Kitai, S. T., J. D. Kocsis, and J. Wood. Origin and characteristics of the cortico‐caudate afferents: an anatomical and electrophysiological study. Brain Res. 118: 137–141, 1976.
 67. Kitai, S. T., R. J. Preston, G. A. Bishop, and J. D. Kocsis. Striatal projection neurons: morphological and electrophysiological studies. In: Advances in Neurology, edited by L. J. Poirier, T. L. Sourkes, and P. J. Bedard. New York: Raven, 1979, vol. 24, p. 45–51.
 68. Kitai, S. T., M. Sugimori, and J. Kocsis. Excitatory nature of dopamine in the nigro‐caudate pathway. Exp. Brain Res. 24: 351–363, 1976.
 69. Kitai, S. T., A. Wagner, W. Precht, and T. Ohno. Nigrocaudate and caudato‐nigral relationship: an electrophysiological study. Brain Res. 85: 44–48, 1975.
 70. Kocsis, J. D., and S. T. Kitai. Dual excitatory inputs to caudate spiny neurons from substantia nigra stimulation. Brain Res. 138: 271–283, 1977.
 71. Kocsis, J. D., R. J. Preston, and S. T. Kitai. An anatomical and electrophysiological study of the caudate projection system. Soc. Neurosci. Abstr. 2: 65, 1976.
 72. Kocsis, J. D., M. Sugimori, and S. T. Kitai. Convergence of excitatory synaptic inputs to caudate spiny neurons. Brain Res. 124: 403–413, 1976.
 73. Kunzle, H. Bilateral projections from precentral motor cortex to the putamen and other parts of the basal ganglia. An autoradiographic study in Macaca fascicularis. Brain Res. 88: 195–209, 1975.
 74. Levine, M. S., C. D. Hull, and N. A. Buchwald. Pallidal and entopeduncular intracellular responses to striatal, cortical, thalamic and sensory inputs. Exp. Neurol. 44: 448–460, 1974.
 75. Liles, S. L. Cortico‐striatal evoked potentials in cats. Electroencephalogr. Clin. Neurophysiol. 35: 277–285, 1973.
 76. Liles, S. L. Single‐unit responses of caudate neurons to stimulation of frontal cortex, substantia nigra and entopeduncular nucleus in cats. J. Neurophysiol. 37: 254–265, 1974.
 77. Liles, S. L. Cortico‐striatal evoked potentials in the monkey (Macaca mulatto). Electroencephalogr. Clin. Neurophysiol. 38: 121–129, 1975.
 78. Ljungdahl, A., T. Hökfelt, and G. Nilsson. Distribution of substance P‐like immunoreactivity in the central nervous system of the rat‐I. Cell bodies and nerve terminals. Neuroscience 3: 861–943, 1978.
 79. Loreno, S. A., and H. C. Gildberg. Regional 5‐hydroxytryptamine following selective midbrain raphé lesions in the rat. Brain Res. 78: 45–56, 1974.
 80. Maler, L., H. D. Fibiger, and P. L. McGeer. Demonstration of the nigrostriatal projection by silver staining after nigral injections of 6‐hydroxydopamine. Exp. Neurol. 40: 505–515, 1973.
 81. Malliani, A., and D. P. Purpura. Intracellular studies of the corpus striatum. II. Patterns of synaptic activities in lenticular and entopeduncular neurons. Brain Res. 6: 341–354, 1967.
 82. Matsurami, K., and B. Cohen. Afferent modulation of unit activity in globus pallidus and caudate nucleus: changes induced by vestibular nucleus and pyramidal tract stimulation. Brain Res. 91: 140–146, 1975.
 83. McLennan, J., and D. H. York. The action of dopamine on neurons of the caudate nucleus. J. Physiol. London 189: 393–402, 1967.
 84. McNair, J., J. Sutin, and T. Tsubokawa. Suppression of cell firing in the substantia nigra by caudate nucleus stimulation. Exp. Neurol. 37: 395–411, 1972.
 85. Mehler, W. R., Further notes on the center median nucleus of luys. In: The Thalamus, edited by D. P. Purpura and M. D. Yahr. New York: Columbia Univ. Press, 1966.
 86. Miller, J. J., T. L. Richardson, H. C. Fibiger, and H. McLennan. Anatomical and electrophysiological identification of a projection from the mesencephalic raphe to the caudate‐putamen in the rat. Brain Res. 97: 133–138, 1975.
 87. Nauta, W. J. H., and W. R. Mehler. Projection of the lentiform nucleus in the monkey. Brain Res. 1: 7–42, 1966.
 88. Norcross, K., and R. Spehlmann. Selective blockade of caudate responses to nigral stimulation by microiontophoretic application of dopamine antagonists. Neurosci. Lett. 6: 323–328, 1977.
 89. Norcross, K., and R. Spehlmann. A quantitative analysis of the excitatory and depressant effects of dopamine on the firing of caudatal neurons: electrophysiological support for the existence of two distinct dopamine‐sensitive receptors. Brain Res. 156: 168–174, 1978.
 90. Ohye, C., C. LeGuyader, and J. Feger. Responses of subthalamic and pallidal neurons to striatal stimulation: an extracellular study on awake monkeys. Brain Res. 111: 241–252, 1976.
 91. Oka, H., and K. Jinnai. Common projection of the motor cortex to the caudate nucleus and the cerebellum. Exp. Brain Res. 31: 31–42, 1978.
 92. Olpe, H. R., and W. P. Koella. The response of striatal cells upon stimulation of the dorsal and median raphe nuclei. Brain Res. 122: 357–360, 1977.
 93. Potegal, M., P. Copuck, S. M. B. V. DeJones, G. Krathamer, and S. Gilman. Vestibular input to the caudate nucleus. Exp. Neurol. 32: 448–465, 1971.
 94. Powell, T. P. S., and W. M. Cowan. A study of thalamostriate relationship in the monkey. Brain Res. 79: 364–390, 1956.
 95. Precht, W., and M. Yoshida. Blockage of caudate‐evoked inhibition of neurons in the substantia nigra by picrotoxin. Brain Res. 32: 229–233, 1971.
 96. Preston, R. J., G. A. Bishop, and S. T. Kitai. Medium spiny neuron projection from the rat striatum: an intracellular horseradish peroxidase study. Brain Res. 183: 253–263, 1980.
 97. Preston, R. J., R. A. McCrea, H. Chang, and S. T. Kitai. Antidromic and synaptic activation of HRP identified substantia nigra and retrorubral neurons in the cat: anatomical and electrophysiological study. Soc. Neurosci. Abstr. 4: 49, 1978.
 98. Purpura, D., and A. Malliani. Intracellular studies of the corpus striatum. I. Synaptic potentials and discharge characteristics of caudate neurons activated by thalamic stimulation. Brain Res. 6: 325–340, 1967.
 99. Ramon y Cajal, S. Le corps strie. Bibliogr. Anat. 3: 58–62, 1895.
 100. Richardson, T. L., J. J. Miller, and H. McLennan. Mechanisms of excitation and inhibition in the nigrostriatal system. Brain Res. 127: 219–234, 1977.
 101. Rinvik, E. Demonstration of nigrothalamic connections in the cat by retrograde axonal transport of horseradish peroxidase. Brain Res. 90: 313–318, 1975.
 102. Rinvik, E., and I. Grofova. Observations on the fine structure of the substantia nigra in the cat. Exp. Brain. Res. 11: 229–248, 1970.
 103. Rinvik, E., I. Grofova, and O. O'Hersen. Demonstration of nigrotectal and nigroreticular projections in the cat by axonal transport of proteins. Brain Res. 112: 388–394, 1976.
 104. Schwyn, R. C., and C. A. Fox. The primate substantia nigra: a Golgi and electron microscopic study. J. Hirnforsch. 15: 95–126, 1974.
 105. Sedgwick, E. M., and T. D. Williams. The response of single units in the caudate nucleus to peripheral stimulation. J. Physiol. London 189: 281–298, 1967.
 106. Spencer, H. J. Antagonism of cortical excitation of striatal neurons by glutamic acid diethylester: evidence for glutamic acid as an excitatory transmitter in the rat striatum. Brain Res. 102: 91–101, 1976.
 107. Szabo, J. Topical distribution of striatal efferents in the monkey. Exp. Neurol. 5: 21–36, 1962.
 108. Szabo, J. Projections from the body of the caudate nucleus in the rhesus monkey. Exp. Neurol. 27: 1–15, 1970.
 109. Tsubokawa, T., and J. Sutin. Pallidal and tegmental inhibition of oscillatory slow waves and unit activity in the subthalamic nucleus. Brain Res. 41: 101–118, 1972.
 110. Ueki, A., M. Uno, M. Anderson, and M. Yoshida. Monosynaptic inhibition of thalamic neurons produced by stimulation of the substantia nigra. Experientia 33: 1480–1481, 1977.
 111. Uno, M., and M. Yoshida. Monosynaptic inhibition of thalamic neurons produced by stimulation of the pallidal nucleus in cats. Brain Res. 99: 377–380, 1975.
 112. VanderMaelen, C. P., A. C. Bonduki, and S. T. Kitai. Electrophysiological analysis of extrinsic inputs to rat caudatoputamen. Soc. Neurosci. Abstr. 4: 50, 1978.
 113. VanderMaelen, C. P., A. C. Bonduki, and S. T. Kitai. Excitation of caudate‐putamen neurons following stimulation of the dorsal raphé nucleus in the rat. Brain Res. 175: 356–361, 1979.
 114. VanderMaelen, C. P., J. D. Kocsis, and S. T. Kitai. Caudate afferents from the retrorubral nucleus and other midbrain areas in the cat. Brain Res. Bull. 3: 639–644, 1978.
 115. Yoshida, M., and W. Precht. Monosynaptic inhibition of neurons of the substantia nigra by caudatonigral fibers. Brain Res. 32: 225–228, 1971.
 116. Yoshida, M., A. Rabin, and M. Anderson. Monosynaptic inhibition of pallidal neurons by axon collaterals of caudatonigral fibers. Exp. Brain Res. 15: 333–347, 1972.

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Article Title: Electrophysiology of the Corpus Striatum and Brain Stem Integrating Systems
 

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S. T. Kitai. Electrophysiology of the Corpus Striatum and Brain Stem Integrating Systems. Compr Physiol 2011, Supplement 2: Handbook of Physiology, The Nervous System, Motor Control: 997-1015. First published in print 1981. doi: 10.1002/cphy.cp010220