[The activation of GABA-B receptors, the decrease in intracellular Ca++ concentration and the inhibition of protein kinases--the possible mechanisms of prolonged posttetanic modification in the efficiency of inhibitory transmission in the neocortex].

I G Sil'kis

PubMed · 7754689

[The activation of GABA-B receptors, the decrease in intracellular Ca++ concentration and the inhibition of protein kinases--the possible mechanisms of prolonged posttetanic modification in the efficiency of inhibitory transmission in the neocortex].

Abstract

We suggest hypothetical mechanisms of posttetanic potentiation of inhibitory synaptic transmission (LTPi). Our previous results allow us to suppose that modifiable synapses are located on dendritic spines where metabotropic GABAb receptors (GABAbR) have been found. We assume that GABAbR may be involved in LTPi. Their activation leads to inactivation of protein kinases C and A (PKC and PKA) due to intracellular Ca++ decrease and inhibition of cAMP. This hypothesis is confirmed by the experiments in which LTP-like phenomena for early and late cortical IPSPs were shown to be the result of inactivation of PKA and PKC. We assume that metabolites of arachidonic acid 5- and 12-HPETE can be considered as retrograde messengers for LTPi. New hypothetical mechanisms underlying posttetanic homosynaptic long-term depression of excitatory synaptic transmission (LTDe) is also proposed. According to this hypothesis the target cell must be excited monosynaptically and inhibited disynaptically by the same tetanized afferents. LTDe may be induced only in those pathways which activate postsynaptic GABAb receptors. Both hypotheses are confirmed by experimental data and allow to explain some surprising experimental results.

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Animals Calcium Cerebral Cortex Efficiency Long-Term Potentiation Neural Inhibition Protein Kinase Inhibitors Receptors, GABA-B Synaptic Transmission English Abstract Journal Article Review

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I G Sil'kis. [The activation of GABA-B receptors, the decrease in intracellular Ca++ concentration and the inhibition of protein kinases--the possible mechanisms of prolonged posttetanic modification in the efficiency of inhibitory transmission in the neocortex].. https://pubmed.ncbi.nlm.nih.gov/7754689/

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