Abstract
Reciprocal inhibition and slow calcium decay in perigeniculate interneurons explain changes of spontaneous firing of thalamic cells caused by cortical inactivation.
Highlights
In our experiments (Waleszczyk et al 2005) we found that the cessation of cortical input decreased spontaneous activity of most of the lateral geniculate nucleus (LGN) cells while at the same time it increased spontaneous activity of the majority of perigeniculate nucleus (PGN) interneurons
The simplest explanation for the decrease of thalamo-cortical relay (TC) cell activity after inactivation of cortical areas is the removal of cortical feedback to LGN
At all higher retinal input frequencies the elimination of cortical input evoked significant firing rate changes for PGN and TC cells (P < 0.01)
Summary
The thalamo-cortical loop and the role of cortical feedback in thalamic signal processing have been subject of extensive experimental studies and theoretical considerations over the last few decades (Kalil and Chase 1970; Baker and Malpeli 1977; Ahlsen et al 1985; Deschenes and Hu 1990; Lindström and Wróbel 1990; Funke and Eysel 1992; Destexhe et al 1998; Wörgötter et al 1998, 2002; Bal et al 2000; Einevoll and Plesser 2002). The simplest view of the cortical feedback is excitation of TC neurons, so its suppression should lead to decrease of firing of lateral geniculate nucleus (LGN) neurons This view is consistent with the observed decrease of firing rate of cat’s LGN cells caused by the suppression of cortical feedback (by cooling Wörgötter et al 1998; Waleszczyk et al 2005; TMS, Labra et al 2006; or pharmacological application; Wörgötter et al 1998). Cessation of cortical input should decrease the activity of, targeted in parallel, thalamic interneurons, both of feed-forward (intrageniculate)
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