Suppression of "fast" IPSP, superposed on "slow", as a possible cause of priming in murine hippocampus

Synaptic plasticity in the hippocampus during afferent activation reproducing the pattern of the theta rhythm (theta plasticity)

“…These studies showed firstly that the time course of the increase in the duration of FP and EPSP area in "priming" completely agree with the time course of the slow IPSPb in responses to the conditioning stimulus (Fig. 2, A, S1), and secondly that there are significant correlations between the strength of the effect (the increase in the area of the EPSP due to the test signal) and (a) the size of the IPSPa produced in response to the test stimulus, and (b) the size of the conditioning IPSPb [7]. Not only "forward," but also "reverse" rapid inhibition is decreased on "priming" [6].…”

“…This effect was termed "priming" [43]. Evoked responses in the hippocampus consist of EPSP followed by a two-component inhibitory postsynaptic potential (IPSP) (see, for example, [7]). The rapid component of IPSP (IPSPa) is superimposed on the falling edge of the EPSP and shortens its duration, while the slow component (IPSPb) has almost no effect on the duration of EPSP.…”

“…We advanced an alternative hypothesis to explain the "priming" effect [7], which is described next (see Fig. 2).…”

“…As a result, the rapid and slow components of the IPSP due to the test stimulus decrease, which weakens EPSP shunting, thus increasing EPSE The NMDA-dependent component of EPSP is particularly increased, because its latency is close to the latency of IPSPa and is significantly dependent on the value of the membrane potential, which decreases on neuron hyperpolarization. Part of the effect might be mediated by other mechanisms: 1) hyperpolarization of the postsynaptic membrane due to IPSPb, leading to a reduction and, possibly, inversion of the chloride-dependent IPSPa (the equilibrium potential for chloride ions is about 70 mV); 2) an increase in the potassium ion concentration close to the membrane because of generation of potassium-dependent IPSPb, which could inhibit potassium/chloride exchange and thus decrease the intracellular density of chloride ions close to the membrane, affecting the generation of chloride-dependent IPSPa; 3) desensitization of GABA receptors [7,73].…”