Impaired synaptic plasticity in the visual cortex of mice lacking ?7-nicotinic receptor subunit

The primary visual cortex (V1) is the first step in visual information processing and its function may be modulated by acetylcholine through nicotinic receptors (nAChRs). Since our previous work demonstrated that visual acuity and cortical spatial resolution limit were significantly reduced in ?7 knock-out (KO) mice in the absence of retinal alterations, we decided to characterize the contribution of homomeric ?7 nicotinic receptors (?7nAChRs) to visual information processing at the cortical level. We evaluated long-term forms of synaptic plasticity in occipital slices containing V1 from ?7 KO mice and in wild-type (WT) slices perfused with nAChRs selective blocking agents. In ?7 KO mice slices, electrophysiological recordings demonstrated the absence of long-term potentiation (LTP) and long-term depression (LTD) in layer II/III after the stimulation of different intracortical pathways (layer IV or II/III). Furthermore, the acute and selective blockade of ?7nAChRs in slices from WT mice with either ?-bungarotoxin or methyllycaconitine did not alter the expression of LTP and LTD. Conversely, the perfusion with the unspecific nAChRs antagonist mecamylamine impaired LTP and LTD. Our results suggest the presence of impaired synaptic plasticity in the V1 of ?7 KO mice and indicate a different contribution of nAChRs to visual cortex function.