Properties of depolarization-induced suppression of inhibitory transmission in cultured rat hippocampal neurons

Abstract

Properties of depolarization-induced suppression of inhibitory transmission ("DSI") in cultured rat hippocampal neurons were examined, by recording inhibitory postsynaptic currents (IPSCs) evoked by single presynaptic neurons. In about 40% of the inhibitory synapses, transient suppression of IPSCs was induced by applying a depolarizing pulse (to 0 mV, > 2 s) to the postsynaptic neuron, which was identified to be gamma-aminobutyric acid dependent (GABAergic) in some pairs, and to be glutamatergic in some other pairs. This depolarization-induced suppression of IPSCs, "DSI", was Ca2+ dependent, and was associated with an increase in the paired-pulse ratio. Phorbol esters had an occluding effect on DSI when applied to the bath solution, but not to the pipette solution used for the postsynaptic neuron. Application of the opioid receptor antagonist naloxone had no effect on DSI. The present study demonstrates that a pair of cultured hippocampal neurons can exhibit DSI similar to that previously reported to occur in hippocampal slices; this suggests that a dissociated cell culture system can provide a useful model system for the study of DSI. Furthermore, it was found that inhibitory neurons, in addition to excitatory ones, can induce DSI, and that a process sensitive to phorbol esters, but not activation of opioid receptors, is involved in DSI.

Presence of depolarization-induced suppression of inhibition in a fraction of GABAergic synaptic connections in rat neocortical cultures

“…The increase of PPR was statistically significant (p < 0.05; Wilcoxon signed rank test). Thus, our results are in agreement with previously observed changes of PPR during DSI in hippocampal cell cultures [14]. In hippocampal cultures, changes of the quantal content affected PPR [14,22], while changes of membrane potential in the postsynaptic neuron or partial block of GABA A receptor did not [13,14,22].…”

“…1, C) suggests that actually DSI duration is shorter: about 70 sec. Therefore, the duration of DSI in our experiments is comparable to that of DSI in hippocampal cell cultures [14]. Usually, but not always, pronounced changes of pair-pulse ratio (PPR) were observed during DSI (Fig.…”

“…To quantify the suppression of synaptic currents evoked by the depolarization of the postsynaptic neuron, the mean amplitude of five consecutive IPSCs following the depolarization was expressed as a fraction of five IPSCs before the depolarization. As suggested previously [14], connections were considered as "DSI" positive when more than 15% suppression was observed. Using this experimental protocol, we studied 26 neuronal pairs.…”

“…This phenomenon termed "depolarization-induced suppression of inhibition" (DSI), was observed in hippocampal CA1 pyramidal cells [15,16] as well as in Purkinje neurons in cerebellum [11]. Interestingly, DSI in hippocampal cell cultures was observed not only in glutamatergic, but also in GABAergic neurons [14]. Although DSI is triggered by a postsynaptic increase of calcium ion levels, its expression is presynaptic ([1] see also [24] for a review).…”

Endocannabinoid‐mediated short‐term synaptic plasticity: depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE)

“…(2) The frequency, but not the amplitude of miniature inhibitory postsynaptic currents (mIPSCs) decreases during cerebellar DSI (Llano et al, 1991;Glitsch et al, 1996;Figure 2c). (3) During DSI, the percentage of synaptic failures increases (Vincent et al, 1992;Alger et al, 1996;Diana & Marty, 2003), and so does the paired pulse ratio during DSI and DSE (Ohno-Shosaku et al, 1998;Ohno-Shosaku et al, 2002b;Yoshida et al, 2002;Diana & Marty, 2003;Trettel & Levine, 2003; but see Alger et al, 1996;Varma et al, 2002).…”