GABA(B) RECEPTOR ACTIVATION, INTRACELLULA R CA-KINASES - POSSIBLE MECHANISMS OF LONG-TERM POSTTETANIC MODIFICATION OF THE EFFICACY OF INHIBITORY TRANSMISSION IN NEOCORTEX(+ DECREASE, INHIBITION OF PROTEIN)

We suggest hypothetical mechanisms of post tetanic potentiation of inh ibitory synaptic transmission (LTPi). Our previous results allow us to suppose that modifiable synapses are located on dendritic spines wher e metabotropic GABAb receptors (GABAbR) have been found. We assume tha t GABAbR may be involved in LTPi. Their activation leads to inactivati on of protein kinases C and A (PKC and PKA) due to intracellular Ca+decreas and inhibition of cAMP. This hypothesis is confirmed by the ex periments in which LTP-like phenomena for early and late cortical IPSP s were shown to be the result of inactivation of PKA and PKC. We assum e that metabolites of arachidonic acid 5- and 12-HPETE can be consider ed as retrograde messengers for LTPi. New hypothetical mechanisms unde rlying posttetanic homosynaptic long-term depression of excitatory syn aptic transmission (LTDe) is also proposed. According to this hypothes is the target cell must be excited monosynaptically and inhibited disy naptically by the same tetanized afferents. LTDe may be induced only i n those pathways which activate postsynaptic GABAb receptors. Both hyp otheses are confirmed by experimental, data and allow to explain some surprising experimental results.