Electrical stimulation of fibers in the stratum radiatum causes an excitatory postsynaptic potential in CA1 neurons of the hippocampus. Other excitatory inputs to or direct depolarization of these CA1 neurons during stimulation of the stratum radiatum caused a subsequent increase in the excitatory postsynaptic potential. This enhancement was characterized as a brief potentiation (2 to 3 minutes, similar to posttetanic potentiation) and a long-term potentiation (presumed to be involved in learning and memory). These potentiations are probably induced by an interaction of the postsynaptic cell or other presynaptic terminals with the test presynaptic terminals.
SUMMARY1. The slowly decaying, calcium-dependent after-hyperpolarization (a.h.p.) that follows action potentials in bullfrog ganglion B cells has previously been shown to be generated by a potassium current called IAHP. We have recorded IAHP using a switched, single-electrode hybrid clamp where current-clamp mode was changed to voltage-clamp mode immediately after repolarization of a spike or the last spike of a train.2. Reduction of extracellular calcium reduced the decay time Of IAHP following a single spike. At all levels of extracellular calcium tested (0 5-4 mM), the decay time of IAHP was longer following a train of action potentials than following a single action potential. Thus, the time course of IAHP evoked by action potentials is a function of the calcium load induced by the action potentials. Conversely, agents that reduce the amount of IAHP activated without affecting its rate of decay, probably do not affect calcium influx.3. Muscarine (2 or 10 #/M) inhibits IAHP following an action potential by at most 30 % and has no effect on decay rate Of IAHP. These results suggest that muscarine has little or no effect on either calcium influx or sequestration. Decay of the a.h.p. is accelerated by muscarine but this effect is due to an increased leak conductance.4. Charybdotoxin (CTX) between 4 and 20 nm, prolongs action potential duration in a manner consistent with blockade of the voltage-and calcium-dependent potassium current (Ic) involved in spike repolarization in these cells. This action is consistent with its reported action on analogous channels in other systems. However, CTX also reduces IAHP. Thus, in bullfrog ganglion neurones, two distinct calciumdependent potassium currents exhibit a comparable sensitivity to CTX. This cannot .be due to a decreased influx of calcium because the decay rate Of IAHP following an action potential is unchanged. The action of CTX was observed with both crude and purified preparations of CTX.
High-frequency (tetanic) stimulation of presynaptic nerve tracts in the hippocampal region of the brain can lead to long-term synaptic potentiation (LTP). Pertussis toxin prevented the development of tetanus-induced LTP in the stratum radiatum-CA1 synaptic system of rat hippocampal slices, indicating that a guanosine triphosphate-binding protein (G protein) may be required for the initiation of LTP. This G protein may be located at a site distinct from the postsynaptic neuron (that is, in presynaptic terminals or glial cells) since maximal activation of CA1 neuronal G proteins by intracellular injection of guanosine-5'-O-(3-thiotriphosphate), a nonhydrolyzable analog of guanosine 5'-triphosphate, did not occlude LTP.
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