PubMed · 9247258
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A M Zador, L E Dobrunz. 1997. Dynamic synapses in the cortex.. https://doi.org/10.1016/s0896-6273(00)80341-4
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Excessive glutamatergic activity is implicated in Parkinson's disease (PD) and sodium channel blockade, resulting in inhibition of glutamate release, is a potential therapeutic approach to PD therapy. Beneficial effects of riluzole and lamotrigine have been reported in animal models of PD, but these compounds have relatively low potency as sodium channel inhibitors and also inhibit N and P/Q-type calcium channels. 202W92, a structural analog of lamotrigine, is a potent sodium channel inhibitor, with no effect on N, P/Q-type channels. Here we present the effects of 202W92 on single patch-clamped dopaminergic neurons. 202W92 (> or =10 microM) inhibited spontaneous action potential firing and reduced amplitude and frequency of evoked action potentials. It also inhibited the frequency of 4-aminopyridine (4-AP)- and electrically evoked excitatory postsynaptic currents (EPSCs) and GABAergic inhibitory postsynaptic currents (IPSCs), with >80% inhibition at 10 microM (IC(50) 1.5 microM). EPSC and IPSC amplitudes were partially inhibited. 202W92 did not affect postsynaptic responses to locally applied glutamate and GABA, nor spontaneously occurring mini-IPSCs. These actions of 202W92 are compatible with sodium channel inhibition and depression of transmitter release.
To investigate subcortical contributions to cortical reorganization, the frequency organization of the ventral nucleus of the medial geniculate body (MGv) in six normal adult cats and in eight cats with restricted unilateral cochlear lesions was investigated using multiunit electrophysiological recording techniques. The tonotopic organization of MGv in the lesioned animals, with severe mid-to-high frequency hearing losses, was investigated 40-186 days following the lesioning procedure. Frequency maps were generated from neural responses to pure tone bursts presented separately to each ear under barbiturate anesthesia. Consideration of the frequency organization in normal animals, and of the apparently normal representation of the ipsilateral (unlesioned) cochlea in lesioned animals, allowed for a detailed specification of the extent of changes observed in MGv. In the lesioned animals it was found that, in the region of MGv in which mid-to-high frequencies are normally represented, there was an "expanded representation" of lesion-edge frequencies. Neuron clusters within these regions of enlarged representation that had "new" characteristic frequencies displayed response properties (latency, bandwidth) very similar to those in normal animals. Thresholds of these neurons were not consistent with the argument that the changes merely reflect the residue of prelesion responses, suggesting a dynamic process of reorganization. The tonotopic reorganization observed in MGv is similar to that seen in the primary auditory cortex and is more extensive than the reorganization found in the auditory midbrain, suggesting that the auditory thalamus plays an important role in cortical plasticity.
We investigated GABA receptor subtypes mediating GABA-induced inhibition of red nucleus (RN) neuronal firing recorded extracellularly from anaesthetized rats. GABA response was mimicked by the GABA(A) agonists muscimol and isoguvacine in all cases and was partially blocked by the GABA(A) antagonist bicuculline. The GABA(B) agonist baclofen induced a long-lasting inhibition in 84% of cells. Neurons responding to either GABA(A) or GABA(B) agonists were equally distributed within the RN. The GABA(C) receptor agonist cis-amino-crotonic acid (CACA) did not modify RN neuronal firing; at high doses CACA occasionally induced inhibition abolished by bicuculline and thus mediated by GABA(A) receptors. We conclude that the inhibitory effects of GABA in the RN are mediated by both GABA(A) and GABA(B) receptors, whereas GABA(C) receptors are not involved.