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|Title:||BEHAVIORAL AND ELECTROPHYSIOLOGICAL STUDIES OF CHOLINERGIC MODULATION OF CORTICAL PROCESSING DURING VISUAL ACTIVATION|
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|Authors/Affiliations:||1 Jun Il Kang*; 1 Elvire Vaucher; |
1 École d'optométrie, Université de Montréal, QC, Canada.
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|Content:||Acetylcholine (ACh) is released in the primary visual cortex during visual stimulation and may have a neuromodulatory role in visual processing. Particularly, it is hypothesized that the cholinergic system could enhance the cortical response to stimuli through mechanisms related to long-term potentiation. The present study uses both behavior and electrophysiology to examine this hypothesis in the rat. |
In the first set of experiments an ACh deficit was performed by lesioning the cholinergic system with 192 IgG-saporin (n=8/group) and behavioral performance in a visual water maze task was assessed. In order to further examine the role of Ach in visual processing VEP was recorded during visual stimulation coupled with pharmacological manipulations. The VEP were evoked by sinusoidal gratings during 7 cycles (10 min of stimulation and 20 min of rest, 4h). Five experimental groups were analyzed: saline- i.c. injection (n=4), carbachol (Ach analog: 5mM, CCh) i.c. injection (n=6), scopolamine (a muscarinic receptor antagonist 10mg/kg) i.p. + CCh i.c. injection (n=4), mecamylamine (a nicotinic receptor antagonist, 10uM) i.c. + CCh i.c. injection (n=5), CPP (a NMDA receptor antagonist, 20uM) i.c. + CCh i.c. injection (n=5).
The cholinergic lesion did not affect the visual acuity measured pre- and post-lesion but it did reduce the efficiency to perform in a novel orientation discrimination task post-lesion. CCh coupling with visual stimulation significantly increased VEP amplitude (50%) during at least 3h, compared to the sham group. Pre-treatment with scopolamine, mecamylamine or CPP abolished this long term enhancement.
These experiments suggest that a deficit in ACh levels induced an impairment of visual learning capacities. This effect could be related to the role of ACh in enhancing visual stimuli processing through mechanisms which resembles term potentiation involving nicotinic and muscarinic receptors and NMDA transmission in the visual cortex. Altogether, these results demonstrate the involvement of the basal forebrain cholinergic system in the modulation of post-synaptic visual processing, which could be related to cognitive enhancement.
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