Local disinhibition of neocortical neuronal circuits causes augmentation of glutamatergic and GABAergic synaptic transmission in the rat neostriatum in vitro

Intra- and extracellular recordings were performed to investigate the influence of local disinhibition of neocortical circuits on corticostriatal synaptic transmission. In rat brain slices with preserved corticostriatal connections, electrical stimulation of the neocortex elicited composed postsynaptic responses in neostriatal neurons consisting of glutamatergic excitatory postsynaptic potentials (EPSPs) and weakly expressed GABA(A) receptor-mediated inhibitory postsynaptic potentials (IPSPs). Following local application of the GABA(A) receptor antagonist bicuculline to the neocortex, neocortical neurons responded to intracortical stimulation with transient paroxysmal depolarizations. Simultaneously, the amplitude of neocortically evoked EPSPs recorded from neostriatal neurons was found to be enhanced without changes in duration. Similarly, the amplitude of IPSPs increased following disinhibition of neocortical circuits. In addition and in contrast to EPSPs, the duration of the IPSPs was found to be markedly prolonged. The results demonstrate that local disinhibition of neocortical neuronal circuits potentiates both excitatory and inhibitory synaptic transmission in striatal neurons. However, compared to AMPA receptor-mediated excitation, GABA(A) receptor-mediated inhibition becomes more efficient due to a marked prolongation of IPSPs. The pronounced augmentation of inhibition can be attributed to a strong activation of inhibitory interneurons within the striatum. (C) 1999 Academic Press.