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Transmitters in Motor Systems

K. Krnjević

10.1002/cphy.cp010204

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 Chemical Transmitters
1.1 Definition
1.2 Varieties of Transmitters
1.3 Identification of Transmitters
2 Transmitters in Peripheral Motor Systems
3 Transmitters in Spinal Motor Mechanisms
3.1 Spinal Motoneurons and Their Synaptic Control
4 Transmitters in Supraspinal Motor Systems
4.1 Brain Stem
4.2 Cerebellum
4.3 Basal Ganglia
4.4 Motor Cortex
Figure 1. Figure 1.

The avoiding reaction of Paramecium. A: retreat from stimulus and resumption of forward locomotion. B: sequence of steps corresponding to numbers in A. Step 1, stretch of anterior membrane upon collision with obstacle; step 2, local increase in membrane conductance; step 3, inward receptor current through stimulated membrane; step 4, electrotonic spread of receptor current produces step 5, outward current through rest of membrane (arrows show current flow). Step 6, depolarization of cell membrane (receptor potential) produces step 7, increase in calcium conductance; step 8, inward Ca2+ current; step 9, rise in intracellular Ca2+ concentration; step 10, cilia reverse beat; and step 11, cell swims backward. Step 12, Ca2+ is pumped out; step 13, intracellular concentration of Ca2+ drops, cilia resume normal orientation; and step 14, cell swims forward.

From Eckert 119. Copyright 1972 by the American Association for the Advancement of Science
Figure 2. Figure 2.

Scheme illustrating synthesis, storage, and release of ACh in a model cholinergic nerve terminal. Choline acetyltransferase is represented by filled dots inside terminal, acetylcholinesterase by open triangles both inside terminal and on surface of postsynaptic cell, and receptors on latter by open squares. Ch, choline.

From MacIntosh and Collier 323
Figure 3. Figure 3.

Acetylcholine action at muscle end plate. A: end‐plate potential in Mg‐paralyzed rat diaphragm. B: ACh‐evoked potential; ACh was released by 1‐ms pulse of current (35 nA) through ACh‐containing micropipette. Thus when released near end plate, ACh can closely reproduce effect of natural transmission. C, D: ACh potentials and end‐plate potentials evoked in frog sartorius muscle have similar reversal potentials. C: nerve‐activated end‐plate potentials are superimposed on long depolarizing pulses of increasing intensity. D: ACh potentials superimposed on long depolarizing pulses.

A, B from Krnjević and Miledi 270; C,D from Katz and Miledi 244
Figure 4. Figure 4.

Diagram demonstrating technique for measuring γ‐aminobutyric acid (GABA) content inside Deiters' neurons and in their immediate surroundings in thin sections of frozen tissue.

From Okada and Shimada 371
Figure 5. Figure 5.

Unlike end‐plate potentials, monosynaptic excitatory postsynaptic potentials (EPSPs) in spinal motoneurons are seldom easily reversed and do not show quantal properties. A: monosynaptic group Ia EPSP in cat motoneurons diminishes with progressive depolarization (increasing depolarizing currents are indicated), but there is no true reversal by even the largest currents. Calibration pulses indicate 2 mV and time marks indicate ms. B‐D: charge fluctuations recorded in cat spinal motoneuron during stimulation of single Ia‐fiber. B shows fluctuations caused by unitary EPSP as well as background noise; C shows fluctuations caused by noise alone; D indicates charge variations due to EPSP alone (computed). Note all‐or‐none character indicating no quantal components.

A from Shapovalov and Kurchavyi 441. B‐D from Edwards et al. 121
Figure 6. Figure 6.

Depression of monosynaptic excitatory postsynaptic potentials (EPSP) in spinal cord of cats by extracellular Mn2+. Intracellular recording from sacral motoneuron, and EPSP evoked by stimulating posterior biceps‐semitendinosus nerve at intensity 1.25 × threshold for evoking detectable response from dorsal root fibers. Traces show, from above down, afferent volley monitored from dorsal roots near point of entry into spinal cord, EPSP at high‐gain AC amplification (see calibration bar in B), resting potential, and EPSP at lower gain DC amplification (see calibration bar in A), and time signal. In each instance two or more traces are superimposed during stimulation at 2/s. A, B: control EPSPs on fast and slow time base, respectively. C, D: EPSPs evoked by same intensity of stimulation after 2 min of Mn2+ release (from extracellular micropipettes). Note hyperpolarizing shift of DC trace. E, F: substantial recovery of EPSP between 7 and 8 min after end of release of Mn2+. Arrows in A, C., and E indicate small potential, apparently reflecting presynaptic fiber or terminal activity.

From Krnjević et al. 266
Figure 7. Figure 7.

Effect of glutamate on spinal motoneurons in isolated frog spinal cord. A, B: depolarizing effect evoked by brief application of glutamate. Iontophoretic current pulse is monitored in traces labeled 1 (110 nA for A, 130 nA for B). Superimposed constant current pulses, repeated at regular intervals, indicate marked reduction in input resistance of cell A, but little or no change in that of cell B. C: plot of peak amplitude of glutamate response against membrane potential. Note highly nonlinear relation and absence of reversal.

From Shapovalov et al. 440
Figure 8. Figure 8.

Some effects of substance P on spinal neurons. A: depolarizing action of glutamate (GLU) or substance P (SP) on frog motoneurons; note much longer effect of substance P. Responses obtained by sucrose‐gap technique from ventral root of isolated frog cord. B: after treatment with tetrodotoxin to prevent action potentials in adjacent cells and indirect excitation of motoneurons. C: selective block of ACh action on Renshaw cell, excited alternatively with glutamate, aspartate, or ACh (dots below traces indicate ACh applications).

A, B from Nicoll 361; C from Krnjević and Lekić 267. Reproduced by permission of the Natl. Res. Counc. Can. from the Can. J. Physiol. Pharmacol. 55: 958–961, 1977
Figure 9. Figure 9.

Depolarizing action of acetylcholine on spinal neurons in cats. A: superimposed traces show slow and prolonged depolarizing effect of increasing iontophoretic doses of acetylcholine, each applied for 20 s. B: current‐voltage plot obtained from interneuron in control state (filled circles) and during applications of ACh (250 nA) and glutamaté (200 nA). Note that ACh causes resistance to increase, and depolarizing action has negative reversal potential. By contrast, depolarizing action of glutamaté causes resistance to fall, and extrapolated reversal potential appears to be much more positive than resting potential.

From Zieglgänsberger and Reiter 531, © 1974, with permission of Pergamon Press, Ltd
Figure 10. Figure 10.

Effects of glycine on membrane potentials and conductance of cat spinal motoneuron. A1–A4, progressive block of antidromic action potential by increasing amounts of glycine (iontophoretic current of 31 nA in A2 and 90 nA in A3). A1 and A4 are initial and final control potentials. Iontophoretic current monitored by additional trace. Note also hyperpolarization in A3. Glycine also markedly depresses postsynaptic potentials (PSPs): compare excitatory PSPs in B1 and B2, the latter obtained while applying glycine (155 nA), similarly compare inhibitory PSPs in C1 and C2 (control and during glycine release of 69 nA). Finally, traces D1 and D2 show reduction in membrane resistance (as well as block of antidromic invasion) during application of glycine (189 nA), again monitored by extra trace.

From Aprison and Werman 11. With permission from M. H. Aprison and R. Werman. In: Neurosciences Research, edited by S. Ehrenpreis and O. C. Solnitsky. New York: Academic, 1968, vol. 1, p. 143–174. Copyright by Academic Press Inc. (London) Ltd
Figure 11. Figure 11.

Intracellular potentials recorded in two spinal motoneurons in cat demonstrate action of strychnine. A, B: control IPSP and EPSP evoked in gastrocnemius motoneuron by stimulating peroneal and gastrocnemius nerves, respectively. C, D: same PSPs after release of strychnine by diffusion from extracellular electrode for 3 min. Note marked reduction of IPSP, but little change in EPSP. E, F: hyperpolarizing responses evoked in another motoneuron by 30 nA glycine and 60 nA γ‐aminobutyric acid (GABA). Much briefer IPSPs are superimposed on DC trace. G, H: same responses during extracellular iontophoresis of strychnine. Note selective block of glycine response.

From Curtis 71
Figure 12. Figure 12.

A: electron‐microscopic autoradiograph from rat spinal cord slice incubated with [3H]‐glycine. Note strong radioactivity over presumed glycinergic bouton (×30,000). B: concentrations of glycine and γ‐aminobutyric acid (GABA) in four areas of cat spinal cord; distribution of glutamine included for comparison.

A from Hökfelt and Ljungdahl 192; B from Aprison and Werman 11. With permission from M. H. Aprison and R. Werman. In: Neurosciences Research, edited by S. Ehrenpreis and O. C. Solnitsky. New York: Academic, 1968, vol. 1, p. 143–174. Copyright by Academic Press Inc. (London) Ltd
Figure 13. Figure 13.

Evidence indicating involvement of γ‐aminobutyric acid (GABA) in spinal presynaptic inhibition. A: dorsal root reflex (DDR) and dorsal root potential (DRP) recorded in unanesthetized spinal cat practically eliminated by intravenous bicuculline. Note only partial recovery 1 h later. B: photomicrograph of dorsal horn from rat lumbosacral spinal cord. Arrows point to site of intense glutamic acid decarboxylase activity in marginal layer and in substantia gelatinosa. × 70.

A from Levy 311, B from McLaughlin et al. 339
Figure 14. Figure 14.

Diagram of connections between motoneurons (M), Renshaw cells (R), and interneuron mediating Ia inhibition (IN). Cholinergic terminals represented by filled triangles, glycinergic terminals by filled circles (strychnine sensitive) or half‐filled circles (strychnine resistant).

From Belcher et al. 23
Figure 15. Figure 15.

A–F: effect of L‐dopa on dorsal root potentials evoked from flexor‐reflex afferents. Upper traces show dorsal root potentials recorded from most caudal dorsal root in L6. Lower traces recorded from L7 dorsal root entry zone. A–C are initial control traces. In A, sural nerve was stimulated with intensity of about 10 × threshold. In B and C, anterior biceps‐semimembranous nerves were stimulated at 2.1 and 27 × threshold intensity. D–F: corresponding records obtained after injection of dopa. Note depression of early dorsal root potential and appearance of late component evoked by high‐threshold stimulation. G: diagram of postulated neuronal pathways involved in depolarization of Ia‐afferent terminals by activity in flexor reflex afferents (such as sensory pathways activated in A–F above). In spinal cat, activity in pathway through A normally prevents dorsal root potential evoked in Ia‐afferent through pathway B. By suppressing pathway through A, dopa would permit long‐latency depolarization of Ia‐terminals through pathway B. Filled circles represent postsynaptic inhibitory neuron.

From Anden et al. 8
Figure 16. Figure 16.

Inhibitory actions of norepinephrine (NA) in cat spinal cord. A: repetitive firing of spinal interneuron excited by single shock to peroneal nerve. B: ventral horn interneuron also firing repetitively in response to stimulation of gastrocnemius nerve. Iontophoretic applications of norepinephrine (14 nA in A, 25 nA in B) depress synaptic response. C: spontaneous firing of another ventral horn interneuron markedly reduced by short application of norepinephrine (50 nA); calibration shows frequency of firing in spikes per second.

A from Engberg and Ryall 130; B, C from Jordan et al. 232. Reproduced by permission of the Natl. Res. Counc. Can. from the Can. J. Physiol. Pharmacol. 55: 399–412, 1977
Figure 17. Figure 17.

Effects of possible transmitters and antagonists on synaptic responses in red nucleus of cat. A, B: intracellular records show that aspartic acid, applied iontophoretically, reduces amplitude of EPSPs evoked from cortex (A) or interpositus nucleus (B). Diminished amplitude of resistance‐measuring pulses in B also indicates marked increase in membrane conductance. C: iontophoretic application of bicuculline methochloride (120 nA for 100 s) abolished positive field potential (compare inset trace), reflecting inhibition evoked in red nucleus by cortical stimulation. Lack of effect of strychnine also indicates GABAergic nature of this inhibition.

A, B from Altmann et al. 2; C from Altmann et al. 1
Figure 18. Figure 18.

Action of serotonin (5‐HT), dopamine (DA), and norepinephrine (NA) on spontaneous firing of reticulospinal neuron, identified by antidromic activation from cervical spinal cord in decerebrated cat. Note short refractory period when 2 pulses were applied (A–C) and good following at high frequency of stimulation (110/s) and constant latency in D. Note also strong firing evoked by serotonin and norepinephrine.

From Hösli et al. 202
Figure 19. Figure 19.

Identification of γ‐aminobutyric acid as inhibitory transmitter responsible for IPSPs evoked in Deiters' neurons of cat by cerebellar stimulation. A–C: examples of experimental data. In A, reversal potential for IPSP (evoked at arrow) demonstrated by applying depolarizing or hyperpolarizing current, indicated in nA. B: similar series during iontophoretic administration of GABA (270 nA). C: control runs performed extracellularly. D: graph of voltage current data showing fall in resistance during IPSP (filled circles) and GABA application (triangles), and common reversal level at horizontal arrow.

From Obata et al. 369
Figure 20. Figure 20.

Gamma aminobutyric acid (GABA) and inhibition of frog cerebellar Purkinje cells. A: iontophoretic application of GABA causes hyperpolarization (upper trace) and marked reduction in resistance as shown by diminution of resistance‐testing pulses (below). Calibrations indicate 5 s and 20 mV (top) and 80 ms and 50 mV (bottom). B: synaptic inhibitory action evoked by local stimulation of parallel fibers blocked by topical application of picrotoxin (5 × 10–5 M). At left, controls show inhibitory pause in extracellularly recorded unit firing (above) and corresponding poststimulus time histogram (below). Traces at right illustrate disappearance of inhibition during application of picrotoxin.

From Woodward et al. 510
Figure 21. Figure 21.

Glutamate decarboxylase (GAD) reaction product indicates presumed GABAergic synaptic terminal (arrow) in molecular layer of rodent cerebellar cortex. Two adjacent terminals (t) not labeled. ×43,000.

From Wood et al. 509
Figure 22. Figure 22.

Climbing fiber‐evoked EPSPs in Purkinje cell of cat cerebellum are easily reversed by depolarization. Both sets of records obtained from same cell, those at right with slower sweeps and lower amplification.

From Eccles et al. 118
Figure 23. Figure 23.

Properties of EPSPs and effects of dopamine recorded in caudate neurons. A–F: EPSP, evoked from median forebrain bundle, was enhanced by hyperpolarization (A–C) and then depressed or reversed by depolarization (D–F); lower trace of each pair is an extracellular control. G: action potential evoked by nigral stimulus recorded on high‐gain AC and low‐gain DC traces (above and below); lowest trace is an extracellular control. H: depolarizing response evoked by extracellular dopamine (DA) release (14 nA for 10 ms). Repeated applications of same dopamine pulse evoked progressively greater responses (compare I and J at same gain, and K at much lower gain). L: control recorded while applying pulse of Na+ instead of dopamine.

From Kitai et al. 256
Figure 24. Figure 24.

Inhibition of nigral unit in cat by caudate stimulation. A, B: ongoing firing of unit in substantia nigra maintained by slow release of glutamate; single shock stimulation in caudate was 1.5 × threshold in A and 2 × threshold in B. C: strong inhibitory effect of γ‐aminobutyric acid on glutamate‐evoked discharge of same unit. D–E: poststimulus time histograms of firing of nigral unit inhibited by caudate stimulation, before and after injection of 2.5 mg/kg picrotoxin.

A–C from Feltz 136. Reproduced by permission of the Natl. Res. Counc. Can. from the Can. J. Physiol. Pharmacol. 49: 1113–1115, 1971. D–E from Precht and Yoshida 402
Figure 25. Figure 25.

Schematic diagram of basal ganglia showing main connections between various nuclei as well as probable function. Cx, cerebral cortex; Cd, caudate; Thal, thalamus; Pal i. and Pal e., internal and external segments of globus pallidus; ST, subthalamic nucleus; SN, substantia nigra; Py, pyramidal tract; Put, putamen; M, midbrain.

From Yoshida and Obata 524
Figure 26. Figure 26.

Excitatory action of glutamate and ACh on caudate neuron in cat: above, DC trace showing quick depolarization caused by glutamate and slow depolarization caused by ACh (resting potential −38 mV). Discharge frequency indicated on same time base by histogram below.

From Bernardi et al. 29
Figure 27. Figure 27.

Electrical stimulation of guinea pig cortical slices causes selective enhancement of release of endogenous putative transmitter amino acids: glutamate (GLU), aspartate (ASP), and γ‐aminobutyric acid (GABA); in contrast to alanine (ALA), threonine, serine, and glutamine (TSGn), and also α‐aminoisobutyric (aib). Selective release clearly seen in control graph above is totally abolished in absence of calcium or in presence of high concentration of magnesium (compare two graphs below). Endogenous amino acids labeled by superfusion with radioactive glucose; exogenous ones by super‐fusion with radioactive amino acids. Increase in release during electrical stimulation (ordinates) expressed as multiple of spontaneous release

From Potashner 401, © 1978, with permission of Pergamon Press, Ltd
Figure 28. Figure 28.

A: excitation of cortical neuron in cat by acetylcholine shows typical slow time course of depolarization and firing. B: changes in resistance of motor cortex neuron evoked by ACh with and without simultaneous electrical excitation (heavy bar indicates period of ACh release). Open triangles, mean values of resistance increase from 21 cells (with standard errors) in absence of other stimulation; open circles, corresponding data from 24 cells made to fire throughout period of ACh application by intracellular injection of depolarizing current; note longer persisting increase in resistance. Filled circles, control data from 15 cells made to discharge by depolarizing current but without application of ACh.

A from Krnjević et al. 284; B from Woody et al. 513
Figure 29. Figure 29.

Effects of muscarinic agents on rate constants of [3H]acetylcholine release evoked by 25 mM K+ in 3 different cerebral tissues. Note enhancement of release by atropine and depression by physostygmine.

From Szerb 478


Figure 1.

The avoiding reaction of Paramecium. A: retreat from stimulus and resumption of forward locomotion. B: sequence of steps corresponding to numbers in A. Step 1, stretch of anterior membrane upon collision with obstacle; step 2, local increase in membrane conductance; step 3, inward receptor current through stimulated membrane; step 4, electrotonic spread of receptor current produces step 5, outward current through rest of membrane (arrows show current flow). Step 6, depolarization of cell membrane (receptor potential) produces step 7, increase in calcium conductance; step 8, inward Ca2+ current; step 9, rise in intracellular Ca2+ concentration; step 10, cilia reverse beat; and step 11, cell swims backward. Step 12, Ca2+ is pumped out; step 13, intracellular concentration of Ca2+ drops, cilia resume normal orientation; and step 14, cell swims forward.

From Eckert 119. Copyright 1972 by the American Association for the Advancement of Science


Figure 2.

Scheme illustrating synthesis, storage, and release of ACh in a model cholinergic nerve terminal. Choline acetyltransferase is represented by filled dots inside terminal, acetylcholinesterase by open triangles both inside terminal and on surface of postsynaptic cell, and receptors on latter by open squares. Ch, choline.

From MacIntosh and Collier 323


Figure 3.

Acetylcholine action at muscle end plate. A: end‐plate potential in Mg‐paralyzed rat diaphragm. B: ACh‐evoked potential; ACh was released by 1‐ms pulse of current (35 nA) through ACh‐containing micropipette. Thus when released near end plate, ACh can closely reproduce effect of natural transmission. C, D: ACh potentials and end‐plate potentials evoked in frog sartorius muscle have similar reversal potentials. C: nerve‐activated end‐plate potentials are superimposed on long depolarizing pulses of increasing intensity. D: ACh potentials superimposed on long depolarizing pulses.

A, B from Krnjević and Miledi 270; C,D from Katz and Miledi 244


Figure 4.

Diagram demonstrating technique for measuring γ‐aminobutyric acid (GABA) content inside Deiters' neurons and in their immediate surroundings in thin sections of frozen tissue.

From Okada and Shimada 371


Figure 5.

Unlike end‐plate potentials, monosynaptic excitatory postsynaptic potentials (EPSPs) in spinal motoneurons are seldom easily reversed and do not show quantal properties. A: monosynaptic group Ia EPSP in cat motoneurons diminishes with progressive depolarization (increasing depolarizing currents are indicated), but there is no true reversal by even the largest currents. Calibration pulses indicate 2 mV and time marks indicate ms. B‐D: charge fluctuations recorded in cat spinal motoneuron during stimulation of single Ia‐fiber. B shows fluctuations caused by unitary EPSP as well as background noise; C shows fluctuations caused by noise alone; D indicates charge variations due to EPSP alone (computed). Note all‐or‐none character indicating no quantal components.

A from Shapovalov and Kurchavyi 441. B‐D from Edwards et al. 121


Figure 6.

Depression of monosynaptic excitatory postsynaptic potentials (EPSP) in spinal cord of cats by extracellular Mn2+. Intracellular recording from sacral motoneuron, and EPSP evoked by stimulating posterior biceps‐semitendinosus nerve at intensity 1.25 × threshold for evoking detectable response from dorsal root fibers. Traces show, from above down, afferent volley monitored from dorsal roots near point of entry into spinal cord, EPSP at high‐gain AC amplification (see calibration bar in B), resting potential, and EPSP at lower gain DC amplification (see calibration bar in A), and time signal. In each instance two or more traces are superimposed during stimulation at 2/s. A, B: control EPSPs on fast and slow time base, respectively. C, D: EPSPs evoked by same intensity of stimulation after 2 min of Mn2+ release (from extracellular micropipettes). Note hyperpolarizing shift of DC trace. E, F: substantial recovery of EPSP between 7 and 8 min after end of release of Mn2+. Arrows in A, C., and E indicate small potential, apparently reflecting presynaptic fiber or terminal activity.

From Krnjević et al. 266


Figure 7.

Effect of glutamate on spinal motoneurons in isolated frog spinal cord. A, B: depolarizing effect evoked by brief application of glutamate. Iontophoretic current pulse is monitored in traces labeled 1 (110 nA for A, 130 nA for B). Superimposed constant current pulses, repeated at regular intervals, indicate marked reduction in input resistance of cell A, but little or no change in that of cell B. C: plot of peak amplitude of glutamate response against membrane potential. Note highly nonlinear relation and absence of reversal.

From Shapovalov et al. 440


Figure 8.

Some effects of substance P on spinal neurons. A: depolarizing action of glutamate (GLU) or substance P (SP) on frog motoneurons; note much longer effect of substance P. Responses obtained by sucrose‐gap technique from ventral root of isolated frog cord. B: after treatment with tetrodotoxin to prevent action potentials in adjacent cells and indirect excitation of motoneurons. C: selective block of ACh action on Renshaw cell, excited alternatively with glutamate, aspartate, or ACh (dots below traces indicate ACh applications).

A, B from Nicoll 361; C from Krnjević and Lekić 267. Reproduced by permission of the Natl. Res. Counc. Can. from the Can. J. Physiol. Pharmacol. 55: 958–961, 1977


Figure 9.

Depolarizing action of acetylcholine on spinal neurons in cats. A: superimposed traces show slow and prolonged depolarizing effect of increasing iontophoretic doses of acetylcholine, each applied for 20 s. B: current‐voltage plot obtained from interneuron in control state (filled circles) and during applications of ACh (250 nA) and glutamaté (200 nA). Note that ACh causes resistance to increase, and depolarizing action has negative reversal potential. By contrast, depolarizing action of glutamaté causes resistance to fall, and extrapolated reversal potential appears to be much more positive than resting potential.

From Zieglgänsberger and Reiter 531, © 1974, with permission of Pergamon Press, Ltd


Figure 10.

Effects of glycine on membrane potentials and conductance of cat spinal motoneuron. A1–A4, progressive block of antidromic action potential by increasing amounts of glycine (iontophoretic current of 31 nA in A2 and 90 nA in A3). A1 and A4 are initial and final control potentials. Iontophoretic current monitored by additional trace. Note also hyperpolarization in A3. Glycine also markedly depresses postsynaptic potentials (PSPs): compare excitatory PSPs in B1 and B2, the latter obtained while applying glycine (155 nA), similarly compare inhibitory PSPs in C1 and C2 (control and during glycine release of 69 nA). Finally, traces D1 and D2 show reduction in membrane resistance (as well as block of antidromic invasion) during application of glycine (189 nA), again monitored by extra trace.

From Aprison and Werman 11. With permission from M. H. Aprison and R. Werman. In: Neurosciences Research, edited by S. Ehrenpreis and O. C. Solnitsky. New York: Academic, 1968, vol. 1, p. 143–174. Copyright by Academic Press Inc. (London) Ltd


Figure 11.

Intracellular potentials recorded in two spinal motoneurons in cat demonstrate action of strychnine. A, B: control IPSP and EPSP evoked in gastrocnemius motoneuron by stimulating peroneal and gastrocnemius nerves, respectively. C, D: same PSPs after release of strychnine by diffusion from extracellular electrode for 3 min. Note marked reduction of IPSP, but little change in EPSP. E, F: hyperpolarizing responses evoked in another motoneuron by 30 nA glycine and 60 nA γ‐aminobutyric acid (GABA). Much briefer IPSPs are superimposed on DC trace. G, H: same responses during extracellular iontophoresis of strychnine. Note selective block of glycine response.

From Curtis 71


Figure 12.

A: electron‐microscopic autoradiograph from rat spinal cord slice incubated with [3H]‐glycine. Note strong radioactivity over presumed glycinergic bouton (×30,000). B: concentrations of glycine and γ‐aminobutyric acid (GABA) in four areas of cat spinal cord; distribution of glutamine included for comparison.

A from Hökfelt and Ljungdahl 192; B from Aprison and Werman 11. With permission from M. H. Aprison and R. Werman. In: Neurosciences Research, edited by S. Ehrenpreis and O. C. Solnitsky. New York: Academic, 1968, vol. 1, p. 143–174. Copyright by Academic Press Inc. (London) Ltd


Figure 13.

Evidence indicating involvement of γ‐aminobutyric acid (GABA) in spinal presynaptic inhibition. A: dorsal root reflex (DDR) and dorsal root potential (DRP) recorded in unanesthetized spinal cat practically eliminated by intravenous bicuculline. Note only partial recovery 1 h later. B: photomicrograph of dorsal horn from rat lumbosacral spinal cord. Arrows point to site of intense glutamic acid decarboxylase activity in marginal layer and in substantia gelatinosa. × 70.

A from Levy 311, B from McLaughlin et al. 339


Figure 14.

Diagram of connections between motoneurons (M), Renshaw cells (R), and interneuron mediating Ia inhibition (IN). Cholinergic terminals represented by filled triangles, glycinergic terminals by filled circles (strychnine sensitive) or half‐filled circles (strychnine resistant).

From Belcher et al. 23


Figure 15.

A–F: effect of L‐dopa on dorsal root potentials evoked from flexor‐reflex afferents. Upper traces show dorsal root potentials recorded from most caudal dorsal root in L6. Lower traces recorded from L7 dorsal root entry zone. A–C are initial control traces. In A, sural nerve was stimulated with intensity of about 10 × threshold. In B and C, anterior biceps‐semimembranous nerves were stimulated at 2.1 and 27 × threshold intensity. D–F: corresponding records obtained after injection of dopa. Note depression of early dorsal root potential and appearance of late component evoked by high‐threshold stimulation. G: diagram of postulated neuronal pathways involved in depolarization of Ia‐afferent terminals by activity in flexor reflex afferents (such as sensory pathways activated in A–F above). In spinal cat, activity in pathway through A normally prevents dorsal root potential evoked in Ia‐afferent through pathway B. By suppressing pathway through A, dopa would permit long‐latency depolarization of Ia‐terminals through pathway B. Filled circles represent postsynaptic inhibitory neuron.

From Anden et al. 8


Figure 16.

Inhibitory actions of norepinephrine (NA) in cat spinal cord. A: repetitive firing of spinal interneuron excited by single shock to peroneal nerve. B: ventral horn interneuron also firing repetitively in response to stimulation of gastrocnemius nerve. Iontophoretic applications of norepinephrine (14 nA in A, 25 nA in B) depress synaptic response. C: spontaneous firing of another ventral horn interneuron markedly reduced by short application of norepinephrine (50 nA); calibration shows frequency of firing in spikes per second.

A from Engberg and Ryall 130; B, C from Jordan et al. 232. Reproduced by permission of the Natl. Res. Counc. Can. from the Can. J. Physiol. Pharmacol. 55: 399–412, 1977


Figure 17.

Effects of possible transmitters and antagonists on synaptic responses in red nucleus of cat. A, B: intracellular records show that aspartic acid, applied iontophoretically, reduces amplitude of EPSPs evoked from cortex (A) or interpositus nucleus (B). Diminished amplitude of resistance‐measuring pulses in B also indicates marked increase in membrane conductance. C: iontophoretic application of bicuculline methochloride (120 nA for 100 s) abolished positive field potential (compare inset trace), reflecting inhibition evoked in red nucleus by cortical stimulation. Lack of effect of strychnine also indicates GABAergic nature of this inhibition.

A, B from Altmann et al. 2; C from Altmann et al. 1


Figure 18.

Action of serotonin (5‐HT), dopamine (DA), and norepinephrine (NA) on spontaneous firing of reticulospinal neuron, identified by antidromic activation from cervical spinal cord in decerebrated cat. Note short refractory period when 2 pulses were applied (A–C) and good following at high frequency of stimulation (110/s) and constant latency in D. Note also strong firing evoked by serotonin and norepinephrine.

From Hösli et al. 202


Figure 19.

Identification of γ‐aminobutyric acid as inhibitory transmitter responsible for IPSPs evoked in Deiters' neurons of cat by cerebellar stimulation. A–C: examples of experimental data. In A, reversal potential for IPSP (evoked at arrow) demonstrated by applying depolarizing or hyperpolarizing current, indicated in nA. B: similar series during iontophoretic administration of GABA (270 nA). C: control runs performed extracellularly. D: graph of voltage current data showing fall in resistance during IPSP (filled circles) and GABA application (triangles), and common reversal level at horizontal arrow.

From Obata et al. 369


Figure 20.

Gamma aminobutyric acid (GABA) and inhibition of frog cerebellar Purkinje cells. A: iontophoretic application of GABA causes hyperpolarization (upper trace) and marked reduction in resistance as shown by diminution of resistance‐testing pulses (below). Calibrations indicate 5 s and 20 mV (top) and 80 ms and 50 mV (bottom). B: synaptic inhibitory action evoked by local stimulation of parallel fibers blocked by topical application of picrotoxin (5 × 10–5 M). At left, controls show inhibitory pause in extracellularly recorded unit firing (above) and corresponding poststimulus time histogram (below). Traces at right illustrate disappearance of inhibition during application of picrotoxin.

From Woodward et al. 510


Figure 21.

Glutamate decarboxylase (GAD) reaction product indicates presumed GABAergic synaptic terminal (arrow) in molecular layer of rodent cerebellar cortex. Two adjacent terminals (t) not labeled. ×43,000.

From Wood et al. 509


Figure 22.

Climbing fiber‐evoked EPSPs in Purkinje cell of cat cerebellum are easily reversed by depolarization. Both sets of records obtained from same cell, those at right with slower sweeps and lower amplification.

From Eccles et al. 118


Figure 23.

Properties of EPSPs and effects of dopamine recorded in caudate neurons. A–F: EPSP, evoked from median forebrain bundle, was enhanced by hyperpolarization (A–C) and then depressed or reversed by depolarization (D–F); lower trace of each pair is an extracellular control. G: action potential evoked by nigral stimulus recorded on high‐gain AC and low‐gain DC traces (above and below); lowest trace is an extracellular control. H: depolarizing response evoked by extracellular dopamine (DA) release (14 nA for 10 ms). Repeated applications of same dopamine pulse evoked progressively greater responses (compare I and J at same gain, and K at much lower gain). L: control recorded while applying pulse of Na+ instead of dopamine.

From Kitai et al. 256


Figure 24.

Inhibition of nigral unit in cat by caudate stimulation. A, B: ongoing firing of unit in substantia nigra maintained by slow release of glutamate; single shock stimulation in caudate was 1.5 × threshold in A and 2 × threshold in B. C: strong inhibitory effect of γ‐aminobutyric acid on glutamate‐evoked discharge of same unit. D–E: poststimulus time histograms of firing of nigral unit inhibited by caudate stimulation, before and after injection of 2.5 mg/kg picrotoxin.

A–C from Feltz 136. Reproduced by permission of the Natl. Res. Counc. Can. from the Can. J. Physiol. Pharmacol. 49: 1113–1115, 1971. D–E from Precht and Yoshida 402


Figure 25.

Schematic diagram of basal ganglia showing main connections between various nuclei as well as probable function. Cx, cerebral cortex; Cd, caudate; Thal, thalamus; Pal i. and Pal e., internal and external segments of globus pallidus; ST, subthalamic nucleus; SN, substantia nigra; Py, pyramidal tract; Put, putamen; M, midbrain.

From Yoshida and Obata 524


Figure 26.

Excitatory action of glutamate and ACh on caudate neuron in cat: above, DC trace showing quick depolarization caused by glutamate and slow depolarization caused by ACh (resting potential −38 mV). Discharge frequency indicated on same time base by histogram below.

From Bernardi et al. 29


Figure 27.

Electrical stimulation of guinea pig cortical slices causes selective enhancement of release of endogenous putative transmitter amino acids: glutamate (GLU), aspartate (ASP), and γ‐aminobutyric acid (GABA); in contrast to alanine (ALA), threonine, serine, and glutamine (TSGn), and also α‐aminoisobutyric (aib). Selective release clearly seen in control graph above is totally abolished in absence of calcium or in presence of high concentration of magnesium (compare two graphs below). Endogenous amino acids labeled by superfusion with radioactive glucose; exogenous ones by super‐fusion with radioactive amino acids. Increase in release during electrical stimulation (ordinates) expressed as multiple of spontaneous release

From Potashner 401, © 1978, with permission of Pergamon Press, Ltd


Figure 28.

A: excitation of cortical neuron in cat by acetylcholine shows typical slow time course of depolarization and firing. B: changes in resistance of motor cortex neuron evoked by ACh with and without simultaneous electrical excitation (heavy bar indicates period of ACh release). Open triangles, mean values of resistance increase from 21 cells (with standard errors) in absence of other stimulation; open circles, corresponding data from 24 cells made to fire throughout period of ACh application by intracellular injection of depolarizing current; note longer persisting increase in resistance. Filled circles, control data from 15 cells made to discharge by depolarizing current but without application of ACh.

A from Krnjević et al. 284; B from Woody et al. 513


Figure 29.

Effects of muscarinic agents on rate constants of [3H]acetylcholine release evoked by 25 mM K+ in 3 different cerebral tissues. Note enhancement of release by atropine and depression by physostygmine.

From Szerb 478
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Article Title: Transmitters in Motor Systems
 

How to Cite

K. Krnjević. Transmitters in Motor Systems. Compr Physiol 2011, Supplement 2: Handbook of Physiology, The Nervous System, Motor Control: 107-154. First published in print 1981. doi: 10.1002/cphy.cp010204