Pharmacological Mechanisms of Cortical Enhancement Induced by the Repetitive Pairing of Visual/Cholinergic Stimulation.

Repetitive visual training paired with electrical activation of cholinergic projections to the primary visual cortex (V1) induces long-term enhancement of cortical processing in response to the visual training stimulus. To better determine the receptor subtypes mediating this effect the selective pharmacological blockade of V1 nicotinic (nAChR), M1 and M2 muscarinic (mAChR) or GABAergic A (GABAAR) receptors was performed during the training session and visual evoked potentials (VEPs) were recorded before and after training. The training session consisted of the exposure of awake, adult rats to an orientation-specific 0.

Distribution and effects of the muscarinic receptor subtypes in the primary visual cortex.

Muscarinic cholinergic receptors modulate the activity and plasticity of the visual cortex. Muscarinic receptors are divided into five subtypes that are not homogeneously distributed throughout the cortical layers and cells types. This distribution results in complex action of the muscarinic receptors in the integration of visual stimuli.

Boosting visual cortex function and plasticity with acetylcholine to enhance visual perception.

The cholinergic system is a potent neuromodulatory system that plays critical roles in cortical plasticity, attention and learning. In this review, we propose that the cellular effects of acetylcholine (ACh) in the primary visual cortex during the processing of visual inputs might induce perceptual learning; i.e.

Visual training paired with electrical stimulation of the basal forebrain improves orientation-selective visual acuity in the rat.

The cholinergic afferents from the basal forebrain to the primary visual cortex play a key role in visual attention and cortical plasticity. These afferent fibers modulate acute and long-term responses of visual neurons to specific stimuli. The present study evaluates whether this cholinergic modulation of visual neurons results in cortical activity and visual perception changes.

Axonal varicosity density as an index of local neuronal interactions.

Diffuse transmission is an important non-synaptic communication mode in the cerebral neocortex, in which neurotransmitters released from en passant varicosities interact with surrounding cells. In a previous study we have shown that the cholinergic axonal segments which were in the microproximity with dopaminergic fibers possessed a greater density of en passant varicosities compared to more distant segments, suggesting an activity-dependent level of en passant varicosities in the axonal zone of interaction. To further evaluate this plastic relationship, the density of cholinergic varicosities was quantified on fiber segments within the microproximity of activated or non-activated pyramidal cells of the prefrontal cortex (mPFC).

Inhibition of bacterial adhesion on well ordered comb-like polymer surfaces.

The surfaces of comb-like poly(oxyethylene) derivatives with n-alkylsulfonyl side groups were more effective at reducing Pseudomonas aeruginosa adhesion than the surfaces of common materials such as polystyrene, poly(methyl methacrylate), poly(dimethylsiloxane), fluorinated polyacrylate, and glass. When the comb-like poly(oxyethylene) was mixed with polystyrene and poly(methyl methacrylate), the topology and roughness of the surfaces varied according to the mixture compositions. However the surface energies of the mixtures were close to that of the comb-like poly(oxyethylene) in the range of 21-23 mN/m and bacterial adhesion resistances of the mixture surfaces were also comparable to that of the pure comb-like poly(oxyethylene) surface.

Cholinergic pairing with visual activation results in long-term enhancement of visual evoked potentials.

Acetylcholine (ACh) contributes to learning processes by modulating cortical plasticity in terms of intensity of neuronal activity and selectivity properties of cortical neurons. However, it is not known if ACh induces long term effects within the primary visual cortex (V1) that could sustain visual learning mechanisms. In the present study we analyzed visual evoked potentials (VEPs) in V1 of rats during a 4-8 h period after coupling visual stimulation to an intracortical injection of ACh analog carbachol or stimulation of basal forebrain.