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BIOL 1F25 – Nov 4.docx

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Brock University
Alan Castle

BIOL 1F25 – Nov 4, 2013 When cocaine is present in the brain a) There is more dopamine present in the hippocampus b) There is more dopamine transported into the VTA neurons c) There is more dopamine signaling at the NAc neurons d) There is more dopamine transported into the NAc neurons e) All of the above Glutamate synapses a) Occur in the hippocampus b) Occur in the nucleus accumbens (NAc) c) Exhibit LTP in he hippocampus d) Exhibit LTP in the NAc e) All of the above Can cocaine induce disease? Could cocaine cause Parkinson-like disease?  Chronic drug abuse might spur Parkinson’s like syndrome in your people  Dopamine overload (long-term cocaine): damage cells  Dade County, Florida – one of the highest death toll from cocaine. Addicts have build up (3x) of same protein found in Parkinson’s brain (and other forms of dementia)  a-Synuclein (synaptic protein)  Aggregated forms of this protein are toxic to cells  Found in higher levels in dopamine cells of VTA in cocaine users Molecular and Cellular Mechanisms of Cocaine addiction  Last lecture: Chronic administration of cocaine up regulates CREB and increases dynorphin release from NAc: Impairs reward  Produces decreased sensitivity to rewarding effects of subsequent drug exposure (tolerance) Role of ΔFosB: 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 induces a novel Fos protein: ΔFosB in Nac – very stable  ΔFosB induced in NAc by many drugs of abuse and non-drug rewards Experimental evidence for role of ΔFocB:  Over-expressed ΔFosB in NAc in mice  Produced increased cocaine self-administration  Because of stability of ΔFosB – may drive behavioural changes for weeks and months  SUSTAINED MOLECULAR SWITCH - Indicates and maintains state of addiction? Mechanisms of permanent plastic changes in brain:  Changes in ΔFosB 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 pathway 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 1960s showed that experience produces more extensive branching of dendrites  Increased length of dendrites + increased density of spines: Advantageous to
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