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Emotional behavior is regulated by a host of chemicals, including neurotransmitters and neuromodulators, acting on specific circuits within the brain. One of the primary focuses of the Kash lab is to understand how chronic drugs of abuse and stress alter neuronal function, focusing on these stress and anti-stress systems in brain circuitry important for anxiety-like behavior. In particular, we are interested in defining alterations in synaptic function, modulation and plasticity using a combination of whole-cell patch-clamp physiology, biochemistry and mouse models.

Research Contributions

  • Chronic alcohol exposure leads to an upregulation of NR2B subunit containing NMDA receptors in the Bed Nucleus of the Stria Terminalis (BNST), a region critical for regulation of stress and anxiety related behavior.
  • Chronic alcohol exposure leads to a reduction of the effects of alcohol on glutamatergic transmission in the BNST. This alteration in acute alcohol sensitivity could be related to the behavioral tolerance in alcohol-dependent individuals.
  • Dopamine regulates synaptic transmission and plasticity in the BNST through activation of Corticotropin-releasing factor (CRF) signaling. The BNST receives a novel dopaminergic input from the periacqueductal grey (PAG), suggesting a role for these particular neurons in regulation of BNST function.