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Junctional Transmission I. Postsynaptic Mechanisms

Akira Takeuchi

10.1002/cphy.cp010109

Source: Supplement 1: Handbook of Physiology, The Nervous System, Cellular Biology of Neurons

Originally published: 1977

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Types of Synapses
2 Postsynaptic Responses at Excitatory Synapses
2.1 Excitatory Postsynaptic Potential and End‐plate Potential
2.2 Equivalent Electrical Circuit
2.3 Synaptic Current and End‐plate Current
2.4 Conductance of the Synaptic Membrane During the Transmitter Action
2.5 Generation of the Action Potential
2.6 Equilibrium Potential or Reversal Potential
2.7 Ionic Mechanism of the Excitatory Synapses
2.8 Specificity of Ion Pathways
2.9 Elementary Conductance Changes Induced by Acetylcholine Molecules
2.10 Time Course of the Transmitter Action
2.11 Action of Transmitter Substances
3 Postsynaptic Responses at Inhibitory Synapses
3.1 Inhibitory Postsynaptic Potential
3.2 Mode of Action of the Inhibitory Postsynaptic Potential
3.3 Ionic Mechanism of the Postsynaptic Inhibition
3.4 Ion Specificity in the Inhibitory Postsynaptic Membrane
4 Presynaptic Inhibition
5 Amount of Transmitter Released and the Postsynaptic Responses
6 Electrical Transmission Versus Chemical Transmision
6.1 Synaptic Delay
6.2 Direction of the Transmission
6.3 Relative Size of the Presynaptic and Postsynaptic Fibers
6.4 Inhibition
Figure 1. Figure 1.

Effects of curare on the potentials produced by nerve stimulation, recorded with a fine extracellular electrode at the end‐plate region of an isolated single nerve‐muscle fiber preparation. A: before application of curare. B‐D: during progressive curarization, showing the diminution of the initial end‐plate potential and the progressive lengthening of the latent period. E: end‐plate potential without spike potential (i.e., transmission blocked).

From Kuffler 154
Figure 2. Figure 2.

End‐plate potential recorded with an intracellular microelectrode. The position of the microelectrode was changed in successive 0.5‐mm steps. The numbers give the distance from the end‐plate focus (in mm × 0.97). S, stimulus artifact; time in ms. Note that the amplitude and the time course decline with distance from the end plate.

From Fatt & Katz 76
Figure 3. Figure 3.

A: schematic illustration of the lines of current flow during the action of transmitter at the end plate. N, nerve ending; M, muscle fiber. The current flows from the extrasynaptic membrane into the end‐plate membrane through the synaptic cleft, i.e., the synaptic cleft is a part of the path of the synaptic current. B: equivalent circuit of the end plate and the muscle fiber membrane. During the action of transmitter the switch is closed. Direction and strength of the current are indicated by arrows. C: simplified equivalent circuit. Es and Gs, equivalent potential and membrane conductance of the synaptic membrane, respectively; Er and Gr equivalent potential and membrane conductance of the extrasynaptic membrane respectively; C, membrane capacitance.
Figure 4. Figure 4.

Experimental arrangements and electrical circuits for the constant current and the voltage‐clamp methods. A: constant current method. Microelectrode (1) records the membrane potential, and a current is injected by electrode (2) through a high resistance. B: voltage‐clamp method. The membrane potential recorded with electrode (1) is amplified by feedback amplifier (A) and the negative phase of its output is fed back to the membrane through the electrode (2). The membrane potential is controlled by a command potential (V). C: equivalent circuit of the constant current method. Subscript s, synaptic membrane; subscript r, extrasynaptic membrane. D: equivalent circuit of the voltage‐clamp method. Inside and outside of the membrane are connected with a battery (V). In the voltage‐clamp method, the external circuit is closed, whereas in the constant current method the external circuit is open.
Figure 5. Figure 5.

End‐plate potential (EPP) and end‐plate current (EPC) of a curarized frog end plate. A: EPP recorded intracellularly. B: EPC recorded from the same end plate. Lower beam shows the clamped membrane potential. Voltage scale, 5 mV; current scale, 1 × 10−7 A; temperature, 17°C. C: superimposed tracings of EPP and EPC. Circles indicate potential change calculated from EPC. Time in milliseconds.

From Takeuchi & Takeuchi 225
Figure 6. Figure 6.

Left: end‐plate currents (EPC) at various membrane potentials. Upper traces, clamped membrane potentials; lower traces, feedback currents containing EPC. In A a square pulse was applied to the feedback system to depolarize the end‐plate membrane. In B the EPC was obtained when the membrane was clamped at the resting potential (85 mV). In C‐E the membrane potential was hyperpolarized to various values. The EPC is superimposed on the current, which maintains the membrane potential at various levels. Current scale, 1 × 10−7 A; voltage scale, 10 mV; time in milliseconds. Right: relationship between the membrane potential and the EPC recorded from a curarized end plate. ○ were obtained in 3 × 10−6 g/ml d‐tubocurarine and • in 4 × 10−6 g/ml d‐tubocurarine. Both lines cross the voltage axis at about −18 mV.

From Takeuchi & Takeuchi 226
Figure 7. Figure 7.

Muscle action potential at the end‐plate region elicited by nerve stimulation. The shape of the action potential and the spike latency gradually changed as the microelectrode was moved along the muscle fiber. Inset: the time of the spike peak is plotted against the distance. It shows that the spike starts from positions 5 and 6 and propagates in both directions with a velocity of 1.4 m/s.

From Fatt & Katz 76
Figure 8. Figure 8.

The effect of transmitter at various moments of the muscle action potential. A microelectrode was inserted at the end plate, and the potential changes were recorded intracellularly. M, muscle action potential evoked by direct stimulation; N, action potential induced by nerve stimulation; MN, nerve stimulation was timed to liberate transmitter at various phases of the muscle action potential. Arrows indicate the beginning of N responses.

From del Castillo & Katz 41
Figure 9. Figure 9.

A: synaptic potential and the iontopho‐retically evoked ACh potential in the parasympathetic ganglion neuron of the frog heart; (a), synaptic potential alone; (b), responses from another cell to both iontophoretic ACh and to synaptic stimulation. Dotted lines, zero potential. Reversal potential is −12 mV in (a) and −2 mV in (b). B: reversal potential for synaptic transmitter and applied ACh Idata from (b)]; e.p.s.p., excitatory postsynaptic potential. Note that the reversal potential for neural transmitter is the same as that for ACh.

From Dennis et al. 45
Figure 10. Figure 10.

Equivalent electrical circuit for the synaptic membrane.
Figure 11. Figure 11.

Relationship between the reversal potential of end‐plate current (mean ± SD) and [K]o and [Na]o. Lines are drawn according to Eq. 3, with ΔGCl = 0 and ΔGNa/ΔGK = 1.29; e.p.c., end‐plate current.

From Takeuchi & Takeuchi 226
Figure 12. Figure 12.

End‐plate noise. Intracellular recording from a frog end plate. Upper traces were recorded on a low‐gain direct‐coupled channel (10‐mV scale). Lower traces were recorded on a high‐gain condenser‐coupled channel (0.4‐mV scale). Top row is control without ACh and bottom row during iontophoretic application of ACh. Note that the base‐line noise is much larger in the bottom row. The increased distance between the upper trace and the high condenser‐coupled trace in the bottom row is due to the depolarization of the membrane. Two spontaneous miniature EPP's are shown.

From Katz & Miledi 128
Figure 13. Figure 13.

Power spectra of ACh noise (○) and carbachol (Carb.) noise (•); ACh and carbachol were applied from a double‐barreled electrode to the same spot, and the noise was recorded with an extracellular microelectrode. Temperature, 24°C. Half‐maximal points at arrows (see Eq. 6 in text) are 180 and 410 Hz for ACh and carbachol, respectively.

From Katz & Miledi 128
Figure 14. Figure 14.

Effect of anticholinesterase on the end‐plate potential (EPP) and end‐plate current (EPC). The EPP is shown on the upper row and the EPC on the lower row of each record. A, left: recorded from a curarized end plate. A, right: after adding eserine, 10−5 g/ml. B, left: recorded from an end plate blocked in Nadeficient solution. B, right: after adding eserine, 10−5 g/ml. Voltage scale, 2 mV; current scale, 1 × 10−7 A; time in ms.

From Takeuchi & Takeuchi 225
Figure 15. Figure 15.

Externally recorded miniature end‐plate potentials. A: without anticholinesterase. B: after adding prostigmine, 10−6 g/ml. Note the remarkable prolongation of the falling phase and the variety of the time courses. Temperature, 20°C. C: effect of curare, a, prostigmine 10−6 g/ml in low NaCl solution (9/10 replaced by sucrose). Between a and b curare was applied iontophoretically (amplitude, as well as duration, was reduced during the curare action); c, after recovery. Temperature, 22.5°C.

From Katz & Miledi 130
Figure 16. Figure 16.

End‐plate current measured under voltage‐clamp conditions. Upper traces show membrane potential and lower traces give the corresponding end‐plate current (EPC). Membrane potential was changed from −120 mV (bottom trace) to +38 mV (top trace). Holding current to displace the membrane potential has been subtracted in each case. Note the difference in time course of the EPC at the different holding potentials.

From Magleby & Stevens 178
Figure 17. Figure 17.

Action of ACh on the surface of the muscle fiber. The nerve terminal and the tip of the microelectrode were visually identified by using Nomarski optics. ACh was applied iontophoretically from a micropipette (P) at a series of spots along a line (A and B) labeled on the photomicrograph. The ACh sensitivity was expressed as the ratio of the ACh potential size and the injection current (mV/nC). Note that the sensitivity is critically localized at the end‐plate region. The ACh sensitivity dropped by 34% by moving the pipette only 3 μm from the edge of the nerve terminal (a to b).

From Peper & McMahan 212
Figure 18. Figure 18.

Action of ACh on the parasympathetic ganglion neuron of the frog heart. Synaptic spots were visually identified by using Nomarski optics. ACh was applied iontophoretically, and sample responses from a synaptic spot and randomly chosen spots on the same cell are shown at right. ACh sensitivity (mV/nC) and the time to peak of the response (in ms) are shown at the right of each record. Note that the sensitivity of the synapse was about 18 times greater than that of the upper spot.

From Harris et al. 109
Figure 19. Figure 19.

Effect of denervation on the distribution of chemosensitivity in the frog muscle. ACh sensitivities (mV/nC in log scale) in a muscle fiber 66 days after complete denervation (○) and at normal end plate in the control muscle (•) are plotted against the distance along the muscle fiber. ACh sensitivity was measured by iontophoretic application of ACh. Inset: sample records of ACh potentials of denervated fiber at the distances indicated. Note that in the denervated muscle the ACh sensitivity spreads over the whole length of the muscle, but the sensitivity at the endplate region is almost the same as that in the control muscle.

From Miledi 188
Figure 20. Figure 20.

Chemosensitivity of the parasympathetic ganglion neuron of the frog heart after denervation. ACh was applied iontophoretically to randomly chosen spots on a cell denervated for 21 days. Fast‐rising and sensitive responses were obtained from each spot. Numbers attached to the right of each record are sensitivity (top, in mV/nC) and time to peak of the response (bottom, in ms).

From Kuffler et al. 159
Figure 21. Figure 21.

Desensitization of the ACh response in the frog end plate. Each depolarizing response is the ACh potential produced by short pulse of iontophoretic injection. Injection current is monitored on the lower trace of each record. Conditioning dose of ACh was applied for the period indicated by arrows.

From Katz & Thesleff 134
Figure 22. Figure 22.

The IPSP (A) and EPSP (B) set up in a biceps‐semitendinosus motoneuron of the cat. Note that the IPSP is hyperpolarizing and the time course of the IPSP is almost identical with that of the EPSP.

From Coombs et al. 33
Figure 23. Figure 23.

The IPSP (A) and EPSP (B) recorded from a crayfish muscle. Lower traces, intracellular recording; upper traces, extracellular responses recorded from a single junction with a micro‐electrode. Note that the time course of the IPSP is different from that of the EPSP. Short spikes preceding the extracellular IPSP and EPSP are the nerve terminal spike potentials.

From Takeuchi & Takeuchi 230
Figure 24. Figure 24.

Reversal potential for the IPSP and the GABA potential recorded from a crayfish muscle. N, IPSP produced by a repetitive inhibitory stimulation, 30/s; GABA, GABA potential produced by iontophoretic application to the same muscle. Injection current is monitored on the uppermost trace. Distance between each trace represents the difference in the holding membrane potentials. Bottom trace was obtained at the resting potential (‐70 mV), and the reversal occurred at about −66 mV.

From Takeuchi & Takeuchi 230
Figure 25. Figure 25.

Simplified equivalent circuit for the excitatory and inhibitory responses. Subscript r, nonsynaptic membrane; subscripts i and e, inhibitory and excitatory synaptic membranes, respectively.
Figure 26. Figure 26.

Presynaptic inhibition on the quantal release of the transmitter at the crayfish neuromuscular junction. The EPSP was recorded extracellularly with a microelectrode placed at a single junction. Upper graph, histogram of the size distribution of the extracellular EPSP at stimulation rate of 5/s. Lower graph, histogram in which the inhibitory impulses precede the excitatory ones by 2 ms. Dashed line is calculated theoretical (Poisson) distribution. Unit quantum size was 40 μV. Quantum content (m) decreased from 2.4 to 0.56 by the inhibitory stimulation. Small arrows, multiples of quantum size; large arrow, average size of spontaneous miniature potentials. Excitatory junctional potential (e.j.p.) and inhibitory junctional potential (i.j.p.) correspond to EPSP and IPSP, respectively.

From Dudel & Kuffler 57
Figure 27. Figure 27.

Impulse transmission at the electrical synapse of the crayfish giant motor synapse. Potential changes were recorded with microelectrodes inserted into the pre‐ and postsynaptic fibers. In each case presynaptic fiber potential was recorded on the upper trace. In a, the electrotonic potential of the presynaptic fiber spike exceeded the threshold of the postsynaptic fiber, at the point indicated by arrow, and evoked a spike, a1 and a2 were recorded from the same synapse at different amplifications. In b, only the subthreshold response is seen. Note the short latency of the postsynaptic response.

From Furshpan & Potter 83
Figure 28. Figure 28.

Synaptic transmission at the squid giant synapse. A: simultaneous intracellular recording from presynaptic (lower trace) and postsynaptic (upper trace) fibers. B: upper trace, potential changes recorded from just outside the presynaptic fiber; and lower trace, intracellular EPSP. Note that in the postsynaptic record no potential changes that correspond with the presynaptic spike are observed.

From Takeuchi & Takeuchi 228


Figure 1.

Effects of curare on the potentials produced by nerve stimulation, recorded with a fine extracellular electrode at the end‐plate region of an isolated single nerve‐muscle fiber preparation. A: before application of curare. B‐D: during progressive curarization, showing the diminution of the initial end‐plate potential and the progressive lengthening of the latent period. E: end‐plate potential without spike potential (i.e., transmission blocked).

From Kuffler 154


Figure 2.

End‐plate potential recorded with an intracellular microelectrode. The position of the microelectrode was changed in successive 0.5‐mm steps. The numbers give the distance from the end‐plate focus (in mm × 0.97). S, stimulus artifact; time in ms. Note that the amplitude and the time course decline with distance from the end plate.

From Fatt & Katz 76


Figure 3.

A: schematic illustration of the lines of current flow during the action of transmitter at the end plate. N, nerve ending; M, muscle fiber. The current flows from the extrasynaptic membrane into the end‐plate membrane through the synaptic cleft, i.e., the synaptic cleft is a part of the path of the synaptic current. B: equivalent circuit of the end plate and the muscle fiber membrane. During the action of transmitter the switch is closed. Direction and strength of the current are indicated by arrows. C: simplified equivalent circuit. Es and Gs, equivalent potential and membrane conductance of the synaptic membrane, respectively; Er and Gr equivalent potential and membrane conductance of the extrasynaptic membrane respectively; C, membrane capacitance.



Figure 4.

Experimental arrangements and electrical circuits for the constant current and the voltage‐clamp methods. A: constant current method. Microelectrode (1) records the membrane potential, and a current is injected by electrode (2) through a high resistance. B: voltage‐clamp method. The membrane potential recorded with electrode (1) is amplified by feedback amplifier (A) and the negative phase of its output is fed back to the membrane through the electrode (2). The membrane potential is controlled by a command potential (V). C: equivalent circuit of the constant current method. Subscript s, synaptic membrane; subscript r, extrasynaptic membrane. D: equivalent circuit of the voltage‐clamp method. Inside and outside of the membrane are connected with a battery (V). In the voltage‐clamp method, the external circuit is closed, whereas in the constant current method the external circuit is open.



Figure 5.

End‐plate potential (EPP) and end‐plate current (EPC) of a curarized frog end plate. A: EPP recorded intracellularly. B: EPC recorded from the same end plate. Lower beam shows the clamped membrane potential. Voltage scale, 5 mV; current scale, 1 × 10−7 A; temperature, 17°C. C: superimposed tracings of EPP and EPC. Circles indicate potential change calculated from EPC. Time in milliseconds.

From Takeuchi & Takeuchi 225


Figure 6.

Left: end‐plate currents (EPC) at various membrane potentials. Upper traces, clamped membrane potentials; lower traces, feedback currents containing EPC. In A a square pulse was applied to the feedback system to depolarize the end‐plate membrane. In B the EPC was obtained when the membrane was clamped at the resting potential (85 mV). In C‐E the membrane potential was hyperpolarized to various values. The EPC is superimposed on the current, which maintains the membrane potential at various levels. Current scale, 1 × 10−7 A; voltage scale, 10 mV; time in milliseconds. Right: relationship between the membrane potential and the EPC recorded from a curarized end plate. ○ were obtained in 3 × 10−6 g/ml d‐tubocurarine and • in 4 × 10−6 g/ml d‐tubocurarine. Both lines cross the voltage axis at about −18 mV.

From Takeuchi & Takeuchi 226


Figure 7.

Muscle action potential at the end‐plate region elicited by nerve stimulation. The shape of the action potential and the spike latency gradually changed as the microelectrode was moved along the muscle fiber. Inset: the time of the spike peak is plotted against the distance. It shows that the spike starts from positions 5 and 6 and propagates in both directions with a velocity of 1.4 m/s.

From Fatt & Katz 76


Figure 8.

The effect of transmitter at various moments of the muscle action potential. A microelectrode was inserted at the end plate, and the potential changes were recorded intracellularly. M, muscle action potential evoked by direct stimulation; N, action potential induced by nerve stimulation; MN, nerve stimulation was timed to liberate transmitter at various phases of the muscle action potential. Arrows indicate the beginning of N responses.

From del Castillo & Katz 41


Figure 9.

A: synaptic potential and the iontopho‐retically evoked ACh potential in the parasympathetic ganglion neuron of the frog heart; (a), synaptic potential alone; (b), responses from another cell to both iontophoretic ACh and to synaptic stimulation. Dotted lines, zero potential. Reversal potential is −12 mV in (a) and −2 mV in (b). B: reversal potential for synaptic transmitter and applied ACh Idata from (b)]; e.p.s.p., excitatory postsynaptic potential. Note that the reversal potential for neural transmitter is the same as that for ACh.

From Dennis et al. 45


Figure 10.

Equivalent electrical circuit for the synaptic membrane.



Figure 11.

Relationship between the reversal potential of end‐plate current (mean ± SD) and [K]o and [Na]o. Lines are drawn according to Eq. 3, with ΔGCl = 0 and ΔGNa/ΔGK = 1.29; e.p.c., end‐plate current.

From Takeuchi & Takeuchi 226


Figure 12.

End‐plate noise. Intracellular recording from a frog end plate. Upper traces were recorded on a low‐gain direct‐coupled channel (10‐mV scale). Lower traces were recorded on a high‐gain condenser‐coupled channel (0.4‐mV scale). Top row is control without ACh and bottom row during iontophoretic application of ACh. Note that the base‐line noise is much larger in the bottom row. The increased distance between the upper trace and the high condenser‐coupled trace in the bottom row is due to the depolarization of the membrane. Two spontaneous miniature EPP's are shown.

From Katz & Miledi 128


Figure 13.

Power spectra of ACh noise (○) and carbachol (Carb.) noise (•); ACh and carbachol were applied from a double‐barreled electrode to the same spot, and the noise was recorded with an extracellular microelectrode. Temperature, 24°C. Half‐maximal points at arrows (see Eq. 6 in text) are 180 and 410 Hz for ACh and carbachol, respectively.

From Katz & Miledi 128


Figure 14.

Effect of anticholinesterase on the end‐plate potential (EPP) and end‐plate current (EPC). The EPP is shown on the upper row and the EPC on the lower row of each record. A, left: recorded from a curarized end plate. A, right: after adding eserine, 10−5 g/ml. B, left: recorded from an end plate blocked in Nadeficient solution. B, right: after adding eserine, 10−5 g/ml. Voltage scale, 2 mV; current scale, 1 × 10−7 A; time in ms.

From Takeuchi & Takeuchi 225


Figure 15.

Externally recorded miniature end‐plate potentials. A: without anticholinesterase. B: after adding prostigmine, 10−6 g/ml. Note the remarkable prolongation of the falling phase and the variety of the time courses. Temperature, 20°C. C: effect of curare, a, prostigmine 10−6 g/ml in low NaCl solution (9/10 replaced by sucrose). Between a and b curare was applied iontophoretically (amplitude, as well as duration, was reduced during the curare action); c, after recovery. Temperature, 22.5°C.

From Katz & Miledi 130


Figure 16.

End‐plate current measured under voltage‐clamp conditions. Upper traces show membrane potential and lower traces give the corresponding end‐plate current (EPC). Membrane potential was changed from −120 mV (bottom trace) to +38 mV (top trace). Holding current to displace the membrane potential has been subtracted in each case. Note the difference in time course of the EPC at the different holding potentials.

From Magleby & Stevens 178


Figure 17.

Action of ACh on the surface of the muscle fiber. The nerve terminal and the tip of the microelectrode were visually identified by using Nomarski optics. ACh was applied iontophoretically from a micropipette (P) at a series of spots along a line (A and B) labeled on the photomicrograph. The ACh sensitivity was expressed as the ratio of the ACh potential size and the injection current (mV/nC). Note that the sensitivity is critically localized at the end‐plate region. The ACh sensitivity dropped by 34% by moving the pipette only 3 μm from the edge of the nerve terminal (a to b).

From Peper & McMahan 212


Figure 18.

Action of ACh on the parasympathetic ganglion neuron of the frog heart. Synaptic spots were visually identified by using Nomarski optics. ACh was applied iontophoretically, and sample responses from a synaptic spot and randomly chosen spots on the same cell are shown at right. ACh sensitivity (mV/nC) and the time to peak of the response (in ms) are shown at the right of each record. Note that the sensitivity of the synapse was about 18 times greater than that of the upper spot.

From Harris et al. 109


Figure 19.

Effect of denervation on the distribution of chemosensitivity in the frog muscle. ACh sensitivities (mV/nC in log scale) in a muscle fiber 66 days after complete denervation (○) and at normal end plate in the control muscle (•) are plotted against the distance along the muscle fiber. ACh sensitivity was measured by iontophoretic application of ACh. Inset: sample records of ACh potentials of denervated fiber at the distances indicated. Note that in the denervated muscle the ACh sensitivity spreads over the whole length of the muscle, but the sensitivity at the endplate region is almost the same as that in the control muscle.

From Miledi 188


Figure 20.

Chemosensitivity of the parasympathetic ganglion neuron of the frog heart after denervation. ACh was applied iontophoretically to randomly chosen spots on a cell denervated for 21 days. Fast‐rising and sensitive responses were obtained from each spot. Numbers attached to the right of each record are sensitivity (top, in mV/nC) and time to peak of the response (bottom, in ms).

From Kuffler et al. 159


Figure 21.

Desensitization of the ACh response in the frog end plate. Each depolarizing response is the ACh potential produced by short pulse of iontophoretic injection. Injection current is monitored on the lower trace of each record. Conditioning dose of ACh was applied for the period indicated by arrows.

From Katz & Thesleff 134


Figure 22.

The IPSP (A) and EPSP (B) set up in a biceps‐semitendinosus motoneuron of the cat. Note that the IPSP is hyperpolarizing and the time course of the IPSP is almost identical with that of the EPSP.

From Coombs et al. 33


Figure 23.

The IPSP (A) and EPSP (B) recorded from a crayfish muscle. Lower traces, intracellular recording; upper traces, extracellular responses recorded from a single junction with a micro‐electrode. Note that the time course of the IPSP is different from that of the EPSP. Short spikes preceding the extracellular IPSP and EPSP are the nerve terminal spike potentials.

From Takeuchi & Takeuchi 230


Figure 24.

Reversal potential for the IPSP and the GABA potential recorded from a crayfish muscle. N, IPSP produced by a repetitive inhibitory stimulation, 30/s; GABA, GABA potential produced by iontophoretic application to the same muscle. Injection current is monitored on the uppermost trace. Distance between each trace represents the difference in the holding membrane potentials. Bottom trace was obtained at the resting potential (‐70 mV), and the reversal occurred at about −66 mV.

From Takeuchi & Takeuchi 230


Figure 25.

Simplified equivalent circuit for the excitatory and inhibitory responses. Subscript r, nonsynaptic membrane; subscripts i and e, inhibitory and excitatory synaptic membranes, respectively.



Figure 26.

Presynaptic inhibition on the quantal release of the transmitter at the crayfish neuromuscular junction. The EPSP was recorded extracellularly with a microelectrode placed at a single junction. Upper graph, histogram of the size distribution of the extracellular EPSP at stimulation rate of 5/s. Lower graph, histogram in which the inhibitory impulses precede the excitatory ones by 2 ms. Dashed line is calculated theoretical (Poisson) distribution. Unit quantum size was 40 μV. Quantum content (m) decreased from 2.4 to 0.56 by the inhibitory stimulation. Small arrows, multiples of quantum size; large arrow, average size of spontaneous miniature potentials. Excitatory junctional potential (e.j.p.) and inhibitory junctional potential (i.j.p.) correspond to EPSP and IPSP, respectively.

From Dudel & Kuffler 57


Figure 27.

Impulse transmission at the electrical synapse of the crayfish giant motor synapse. Potential changes were recorded with microelectrodes inserted into the pre‐ and postsynaptic fibers. In each case presynaptic fiber potential was recorded on the upper trace. In a, the electrotonic potential of the presynaptic fiber spike exceeded the threshold of the postsynaptic fiber, at the point indicated by arrow, and evoked a spike, a1 and a2 were recorded from the same synapse at different amplifications. In b, only the subthreshold response is seen. Note the short latency of the postsynaptic response.

From Furshpan & Potter 83


Figure 28.

Synaptic transmission at the squid giant synapse. A: simultaneous intracellular recording from presynaptic (lower trace) and postsynaptic (upper trace) fibers. B: upper trace, potential changes recorded from just outside the presynaptic fiber; and lower trace, intracellular EPSP. Note that in the postsynaptic record no potential changes that correspond with the presynaptic spike are observed.

From Takeuchi & Takeuchi 228
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Article Title: Junctional Transmission I. Postsynaptic Mechanisms
 

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Akira Takeuchi. Junctional Transmission I. Postsynaptic Mechanisms. Compr Physiol 2011, Supplement 1: Handbook of Physiology, The Nervous System, Cellular Biology of Neurons: 295-327. First published in print 1977. doi: 10.1002/cphy.cp010109