Activation by GABAb, reduction of the intracellular concentration of Ca++, and inhibition of protein kinases are possible mechanisms of the long-term posttetanic modification of the efficiency of inhibitory transmission in the new cortex.

A hypothetical mechanism is proposed for the induction of long-term posttetanic potentiation of the efficiency of inhibitory synaptic transmission (LTPi). The data we have previously obtained have made it possible to hypothesize that modifiable inhibitory synapses are situated on the dendritic spines on which there are metabotropic GABAb receptors. It is hypothesized that modification of inhibitory transmission is determined precisely by these receptors, the activation of which leads to inactivation of protein kinases C and A (PKC and PKA) as a result of a decrease in the intracellular concentration of Ca++ and the inhibition of cAMP. The hypothesis is confirmed by experiments in which it was demonstrated that an effect similar to LTPi took place as a result of the inactivation of PKC and PKA. It is hypothesized that eicanoid [sic] acids may be retrograde messengers during LTPi. A new hypothetical mechanism underlying long-term depression of excitatory transmission (LTDe) is proposed, according to which tetanized afferent fibers must simultaneously monosynaptically excite and disynaptically inhibit one and the same postsynaptic cell. LTDe may be induced only in those pathways which activate [are activated by--unclear from Russian text--Trans.] GABAb receptors. The proposed hypothesis make it possible to explain the results of certain experiments.