Muscarinic receptor antagonism in the basolateral amygdala blocks acquisition of cocaine-stimulus association in a model of relapse to cocaine-seeking behavior in rats.

The lateral orbitofrontal cortex (lOFC) and basolateral amygdala (BLA) promote cocaine-seeking behavior in response to drug-associated conditioned stimuli (CS) and share dense reciprocal...

The lateral orbitofrontal cortex (lOFC) and basolateral amygdala (BLA) promote cocaine-seeking behavior in response to drug-associated conditioned stimuli (CS) and share dense reciprocal.

Understanding the Context

Optogenetic induction of LTD resulted in diminished cue-motivated drug-seeking behavior in rats. The manipulation of synaptic activity led to long-term inhibitory effects relevant to relapse..

A role for activation of the PL to initiate behavior may seem paradoxical in the context of a recent finding by Chen et al. (2013) who were able to suppress compulsive cocaine seeking by optogenetically.

Inhibitory optogenetics was used to examine the roles of the prelimbic cortex (PL), the nucleus accumbens core (NAcore) and the PL projections to the NAcore in the reinstatement of.

The present study examined the effect of deep brain stimulation (DBS) in the nucleus accumbens shell on cocaine seeking and neuronal plasticity in rats. Electrical DBS of the accumbens.

Key Insights

Summary: Using optogenetics to stimulate the amygdala, researchers intensify the desire to consume cocaine in rats. Source: University of Michigan. Researchers have identified a portion of.

Rats were then re-exposed to the cocaine-paired context for 15 min to destabilize cocaine memories (memory reactivation) or remained in their home cages (no-reactivation).

We paired optogenetic channelrhodopsin (ChR2) stimulation in either central nucleus of amygdala (CeA) or basolateral amygdala (BLA) of female rats with one particular nose-poke porthole option for.

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