Purchase this article with an account.
Anita A. Disney, Michael J. Hawken; Modulating visual gain: cholinergic mechanisms in macaque V1. Journal of Vision 2012;12(9):1399. doi: 10.1167/12.9.1399.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Cholinergic neuromodulation has been suggested to underlie arousal and attention in mammals. Acetylcholine (ACh) is released in cortex by volume transmission and so specificity in its effects must largely be conferred by selective expression of ACh receptors (AChRs). To dissect the local circuit action of ACh, we have used both quantitative anatomy and in vivo physiology and pharmacology during visual stimulation in macaque primary visual cortex (V1). We have shown that nicotinic AChRs are found presynaptically at thalamocortical synapses arriving at spiny neurons in layer 4c of V1 and that nicotine acts in this layer to enhance the gain of visual neurons. Similar evidence for nicotinic enhancement of thalamocortical transmission has been found in the primary cortices of other species and across sensory systems. In separate experiments we have shown that, amongst intrinsic V1 neurons, a higher proportion of GABAergic - in particular parvalbumin-immunoreactive - neurons express muscarinic AChRs than do excitatory neurons. We have also shown that ACh strongly suppresses visual responses outside layer 4c of macaque V1 and that this suppression can be blocked using a GABAa receptor antagonist. Suppression by ACh has been demonstrated in other cortical model systems but is often found to be mediated by reduced glutamate release rather than enhanced release of GABA. Recent anatomical data on AChR expression in the extrastriate visual cortex of the macaque and in V1 of rats, ferrets, and humans, suggest that there may be variation in the targeting of muscarinic mechanisms across neocortical model systems.
Meeting abstract presented at VSS 2012
This PDF is available to Subscribers Only