Post-Tetanic and Depolarization-Induced Suppression of Inhibition in Hippocampal Cell Cultures: Are Similar Mechanisms Involved?

Abstract

Several forms of short-term synaptic plasticity of GABA-ergic synaptic transmission selectively expressed only in a fraction of synaptic connections have been described earlier. In particular, this is the phenomenon termed "depolarization-induced suppression of inhibition" (DSI), a transient suppression of GABA-ergic synaptic transmission evoked by postsynaptic spike firing or brief depolarization of the membrane of postsynaptic neurons. On the other hand, the same tetanic stimulation (30 sec -1 , 4 sec) of the presynaptic neuron also revealed the heterogeneity of GABA-ergic synaptic connections: about 45% of the connections were facilitated, while 55% were depressed. In this work, we show that post-tetanic depression is predominantly expressed in neuronal pairs susceptible to DSI, and that both phenomena have a similar time course. Considering our own results and the retrograde involvement of endocannabinoids in DSI, we hypothesize that post-tetanic depression is also due to the release of endocannabinoids acting, in the latter case, on their autoreceptors.

Addictive neurons

“…By relatively brief depolarization may be enabled whether or not retrograde signaling is present between the post− and presynaptic neurons. The release of endocannabinoids in postsynaptic cells may occur with several paradigms, perhaps not necessarily only with depolarization in vitro [54] . The depolarizing paradigms also differ and some represent the close physiological conditions than the others [11,55] .…”

Depolarization-initiated endogenous cannabinoid release and underlying retrograde neurotransmission in interneurons of amygdala

“…The short-term synaptic plasticity in the form of depolarization-induced suppression of either excitation or inhibition (DSE and DSI) has been reported in several regions of the brain (Alger et al 1996;Kano et al 2009;Ivanova and Storozhuk 2011). We have discovered DSE in the lateral amygdala (LA), specifically at cortical inputs into the pyramidal neurons (Kodirov et al 2010).…”