Impaired synaptic plasticity in the visual cortex of mice lacking α7-nicotinic receptor subunit

- We report a synaptic impairment in layer II/III of the visual cortex of mice lacking α7-nicotinic receptor (α7 KO mice).
- Synaptic impairment identified in α7 KO mice involves different long-term forms of plasticity, such as LTP and LTD.
- LTP and LTD impairment in α7 KO mice is not input specific.
- Acute blockade of α7 nAChR does not mimic the synaptic alterations found in α7 KO mice.

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 α7 knock-out (KO) mice in the absence of retinal alterations, we decided to characterize the contribution of homomeric α7 nicotinic receptors (α7nAChRs) to visual information processing at the cortical level. We evaluated long-term forms of synaptic plasticity in occipital slices containing V1 from α7 KO mice and in wild-type (WT) slices perfused with nAChRs selective blocking agents. In α7 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 α7nAChRs in slices from WT mice with either α-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 α7 KO mice and indicate a different contribution of nAChRs to visual cortex function.