A pinboard by
Geith Maal-Bared

I'm interested in journalism. I find myself drawn to the challenge of communicating science with unwatered-down accuracy. I'm an avid consumer (and writer, I suppose) of music; I'm fascinated by the ever-changing nature of popular music and the factors that contribute to the emergence of musical subcultures and movements. I enjoy baking and the indescribable sensory experience of cinnamon buns.


This pinboard explores how BDNF and CRF contribute to drug dependence

This pinboard contains papers looking at the effects of BDNF and CRF signaling in the context of motivation. Specifically, how those proteins alter the reward circuitry and produce a drug-dependent phenotype. The pinboard also contains articles that contradict these findings and suggest a different role for BDNF.


Deletion of α5 nicotine receptor subunits abolishes nicotinic aversive motivational effects in a manner that phenocopies dopamine receptor antagonism.

Abstract: Nicotine addiction is a worldwide epidemic that claims millions of lives each year. Genetic deletion of α5 nicotinic acetylcholine receptor (nAChR) subunits has been associated with increased nicotine intake, however, it remains unclear whether acute nicotine is less aversive or more rewarding, and whether mice lacking the α5 nAChR subunit can experience withdrawal from chronic nicotine. We used place conditioning and conditioned taste avoidance paradigms to examine the effect of α5 subunit-containing nAChR deletion (α5 -/-) on conditioned approach and avoidance behaviour in nondependent and nicotine-dependent and -withdrawn mice, and compared these motivational effects with those elicited after dopamine receptor antagonism. We show that nondependent α5 -/- mice find low, non-motivational doses of nicotine rewarding, and do not show an aversive conditioned response or taste avoidance to higher aversive doses of nicotine. Furthermore, nicotine-dependent α5 -/- mice do not show a conditioned aversive motivational response to withdrawal from chronic nicotine, although they continue to exhibit a somatic withdrawal syndrome. These effects phenocopy those observed after dopamine receptor antagonism, but are not additive, suggesting that α5 nAChR subunits act in the same pathway as dopamine and are critical for the experience of nicotine's aversive, but not rewarding motivational effects in both a nondependent and nicotine-dependent and -withdrawn motivational state. Genetic deletion of α5 nAChR subunits leads to a behavioural phenotype that exactly matches that observed after antagonizing dopamine receptors, thus we suggest that modulation of nicotinic receptors containing α5 subunits may modify dopaminergic signalling, suggesting novel therapeutic treatments for smoking cessation. This article is protected by copyright. All rights reserved.

Pub.: 13 May '17, Pinned: 31 Aug '17