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Biol1F25 November 4th.docx

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Brock University
John Mitterer

Biol1F25 November 4 , 2013 Molecular and Cellular Mechanisms of Cocaine Addiction Last Lecture: Chronic administration of cocaine up regulates CREB and increases dynorphon release from NAcL impairs reward pathways. Produces decreased sensitivity to rewarding effects of subsequent drug exposure (tolerance) Role of FosB: Transcription factor in NAc c-Fos induced in NAc by acute cocaine use, but proteins are unstable and levels return to normal within 8-12 hours Chronic cocaine induced a novel FoB protein: FosB in NAc – very stable FosB induced in Nac by many drugs of abuse and non-drug rewards Experimental evidence for role of FosB: Over-expressed FosB in NAc in mice Produced increased cocaine self administration Because of stability of FosB – may drive behavioural changes for weeks and months SUSTAINED MOLECULAR SWITCH - Initiates and maintains state of addiction? Mechanisms of permanent plastic changes in brain: Changes in FosB not long-lived enough to account for life-long addictions What underlies the stable changes in brain? Hypothesis: Structural changes in neurons of reward pathway are responsible. Structural changes in reward pathways of brain: Chronic cocaine use: increases # of dendrites of NAc neurons – persist for months BUT- no current direct evidence that increased # of dendrites underlie long-lived behavioural changes Analogous to learning and memory field – difficult to associate cellular changes with behavioural changes. Amphetamine or cocaine limits the ability of later experience to promote structural plasticity in the neocortex and nucleus accumbens (Nac) Data from 1960’s showed that experience produces more extensive branches of dendrites. Increased length of dendrites + increased density of spines: Advantageous to nervous system Changes in den
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