Topic: cocaine exposure

The laterodorsal tegmentum (LDT) is a brainstem nucleus that sends direct projections to the nucleus accumbens (NAc), a key brain region involved in reward and motivation. We have previously shown that LDT-NAc inputs are crucial for reward value, triggering preference and shifting value of natural rewards. However, if and how these specific projections mediate the rewarding properties of drugs of abuse remains elusive. Importantly, ex-vivo studies showed that cocaine exposure triggers neuroplasticity changes in the LDT and in the NAc, suggesting that LDT-NAc circuitry may be an important targe

Cocaine use disorder (CUD) is a chronic neuropsychiatric condition characterized by a compulsion to use cocaine, resulting from enduring cellular and molecular adaptations. Among substance use disorders (SUDs), CUD is notable for its rising prevalence and the lack of approved pharmacotherapies. The nucleus accumbens (NAc), integral to the brain's reward circuitry, plays a crucial role in the initiation and continuation of maladaptive behaviors intrinsic to CUD. Leveraging advancements in neuroproteomics, we undertook an in-depth proteomic analysis of the NAc in a mouse model that spans membran

Dysregulation of dopamine transporters (DAT) within the dopaminergic system is an important biomarker of cocaine exposure. Depending on cocaine amount in-taken, one-time exposure in rats could lead to most (>95% of total) of DAT translocating to plasma membrane of the dopaminergic neurons compared to normal DAT distribution (~5.7% on the plasma membrane). Without further cocaine exposure, the time course of striatal DAT distribution, in terms of intracellular and plasma membrane fractions of DAT, represents a recovery process of the dopaminergic system. In our lab’s studies, we demonstrated

Repetitive cocaine exposure induces the generation of silent synapses in the nucleus accumbens, characterized by the presence of NMDA receptors and absence of AMPA receptors, hindering fast synaptic transmission (Huang et al, 2009). While typically abundant during early postnatal development, cocaine triggers the de novo generation of silent synapses in the adult brain, thereby establishing new synaptic connections within an already refined circuit (Huang et al, 2009; Huang et al, 2015). During withdrawal, some silent synapses undergo unsilencing by incorporating AMPARs, which crucially contri