Corticothalamic interactions in the transfer of visual information

Abstract

Thalamic function does not stand apart, as a discrete processing step, from the cortical circuitry. The thalamus receives extensive feedback from the cortex and this influences the firing pattern, synchronization and sensory response mode of relay cells. A crucial question concerns the extent to which the feedback simply controls the state and transmission mode of relay cells and the extent to which the feedback participates in the specific processing of sensory information. Using examples from experiments examining the influence of feedback from the visual cortex to the lateral geniculate nucleus (LGN), we argue that thalamic mechanisms are selectively focused by visually driven feedback to optimize the thalamic contribution to segmentation and global integration. This involves effects on both the temporal and spatial parameters characterizing the responses of LGN cells and includes, for example, motion-driven feedback effects from MT (middle temporal visual area) relayed via layer 6 of V1 (primary visual cortex).

Functional brain imaging of tobacco use and dependence

“…Given that the thalamus (Groenewegen et al, 1999;Herrero et al, 2002;Sommer, 2003) and ventral striatum/Nac (Groenewegen et al, 1999;Herrero et al, 2002) function as relay centers for information and for paralimbic and motor processing in the brain, the net effect of smoking may be to enhance neurotransmission along cortico-basal ganglia-thalamic loops originating in prefrontal and paralimbic cortices. Neurotransmission through these circuits may be stimulated directly by the interconnected (Sherman, 2001;Sillito and Jones, 2002) nAChR-rich thalamus and visual systems, and/or indirectly through effects on MAO inhibition and DA release in the ventral striatum/NAc (as well as through nicotine stimulation of excitatory glutamatergic input to the dopamine system (Mansvelder et al, 2002)). In the thalamus, for example, nicotine has direct agonist action on excitatory thalamocortical projection neurons and local circuit neurons, although nicotine also stimulates GABAergic interneurons, so that the relationship between nicotine stimulation and thalamocortical stimulation may be complex (Clarke, 2004).…”

Glutamate receptor functions in sensory relay in the thalamus

“…Thus, the level of cortical activity could regulate the sleep-related activity of thalamic neurons via mGlu1 receptor activation (Hughes et al 2002). However, it is also highly likely that there is a contribution from corticofugal systems to sensory responses in vivo, and this has been investigated over many years (Tsumoto et al 1978;Murphy & Sillito 1987;Sillito et al 1994) (and see Sherman & Guillery (2002) and Sillito & Jones (2002)). It has been speculated that the in uence of the cortical input may operate via NMDA receptors or mGlu receptors (Koch 1987;Sherman & Guillery 2000), largely because transmission via these receptor types would allow the non-linear ampli cation of excitatory inputs mediated via, for example, AMPA receptors.…”

Some investigations into non-passive listening

“…Two major effects were observed in the thalamus: the spatial tuning of the cells became broader and their output was less synchronised. Sillito and Jones (2002) interpreted the change in synchronisation as affecting the binding (or grouping) together of elements of the visual scene optimising the thalamic contribution to segmentation and global integration. In the bat auditory thalamus the descending influences from the cortex were deemed responsible for systematic shifts in the echo-delay tuning (Yan and Suga, 1996).…”