Neocortical damage alters synaptic responses of neostriatal neurons in vitro

The present experiments were designed to investigate the physiological impact of a partial decortication upon neostriatal synaptic responses using intracellular recording techniques in the in vitro brain slice preparation. In the intact rat, the locally evoked neostriatal synaptic response is primarily mediated by excitatory amino acid receptor activation. Following neocortex damage, the contributions of both N-methyl-D-aspartate and non-N-methyl-D-aspartate receptor activation were significantly diminished, although responses remained robust in amplitude and duration. Components of the locally evoked synaptic response mediated by activation of GABAA receptors were relatively unchanged, while presynaptic inhibition mediated by activation of GABAB receptors was markedly reduced. Furthermore, the normally minimal acetylcholine contribution to the synaptic response was significantly increased after neocortical damage. This enhanced cholinergic role in the generation of the synaptic response appeared to be mediated primarily by activation of nicotinic receptors. Thus, neocortical damage leads to novel physiological relationships between intrinsic neostriatal cholinergic interneurons and the GABAergic projection neurons. One possibility is that cholinergic interneurons have the potential for substituting for the loss of excitation created by the absence of neocortical glutamatergic input.