No abstract

Despite the fact that binge alcohol drinking (intake resulting in blood alcohol concentrations (BACs) X80 mg% within a 2-h period) is the most prevalent form of alcohol-use disorders (AUD), a large knowledge gap exists regarding how this form of AUD influences neural circuits mediating alcohol reinforcement. The present study employed integrative approaches to examine the functional relevance of binge drinking-induced changes in glutamate receptors, their associated scaffolding proteins and certain signaling molecules within the central nucleus of the amygdala (CeA). A 30-day history of binge alcohol drinking (for example, 4-5 g kg) elevated CeA levels of mGluR1, GluN2B, Homer2a/b and phospholipase C (PLC) b3, without significantly altering protein expression within the adjacent basolateral amygdala. An intra-CeA infusion of mGluR1, mGluR5 and PLC inhibitors all dose-dependently reduced binge intake, without influencing sucrose drinking. The effects of co-infusing mGluR1 and PLC inhibitors were additive, whereas those of coinhibiting mGluR5 and PLC were not, indicating that the efficacy of mGluR1 blockade to lower binge intake involves a pathway independent of PLC activation. The efficacy of mGluR1, mGluR5 and PLC inhibitors to reduce binge intake depended upon intact Homer2 expression as revealed through neuropharmacological studies of Homer2 null mutant mice. Collectively, these data indicate binge alcohol-induced increases in Group1 mGluR signaling within the CeA as a neuroadaptation maintaining excessive alcohol intake, which may contribute to the propensity to binge drink.

PURPOSE. This study was designed to map the sub-basal nerve plexus (SBNP) in the cornea of orthokeratology (OK) lens wearers.METHODS. Laser scanning confocal microscopy (LSCM) was performed in vivo on three subjects: a non-lens wearer and two OK lens wearers. Scans were performed on the right eye while the left eye fixated a moving target. A total of 575, 430, and 676 contiguous images of the SBNP were taken from the non-lens wearing and the OK lens wearing subjects, respectively, and used to construct maps of the central to midperipheral SBNP.RESULTS. In the non-lens wearing eye, nerves radiated towards a whorl-like complex centered nasally and inferiorly in an overall pattern consistent with previously reported studies. In the OK lens wearing eyes, this whorl pattern was absent, replaced by a tortuous network of nerve fibers centrally, and thicker curvilinear fibers mid-peripherally, particularly in the nasal, inferior, and temporal regions.CONCLUSIONS. This study maps the corneal SBNP in OK lens wearers and provides compelling evidence that OK lens wear alters the normal SBNP distribution observed in healthy, nonlens wearing eyes. (Invest Ophthalmol Vis Sci.

Eyes with higher amounts of corneal toricity give rise to increased amounts of treatment zone decentration in overnight orthokeratology.

OK induces non-uniform corneal changes to the central and paracentral regions. This non-uniformity may influence peripheral refraction profiles reported with OK that have been suggested to be influential in myopia control.

Central corneal sensitivity is reduced after a single overnight wear of OK lenses, as measured using the COBO aesthesiometer. This suggests that the mechanical force exerted by contact lenses may influence corneal sensitivity.

Alterations in corneal nerve morphology occur rapidly with commencement of OK lens wear and appear to underpin functional sensitivity loss. Nerve fiber orientation can provide a useful index for changes in corneal nerve morphology.

This study confirms previous suggestions that the rigidity of the COBO nylon filament is affected by ambient room humidity levels, with implications on the stimulus force delivered by the instrument. A conversion table is provided for converting filament lengths to pressure for a range of relative humidity levels.