Thomas Kash

Tom Kash

Assistant Professor

Department of Pharmacology

Ph.D., Neuroscience
Cornell University

Biosketch [.pdf]
Kash Lab Website

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Research Interests

  • Synaptic Transmission and Plasticity
  • Identification of neuronal substrates that underlie alcohol and drug abuse induced behaviors
  • Determining the impact of stress on neuronal circuitry important for emotional behavior

Research Synopsis

Emotional behavior is regulated by a host of chemicals, including neurotransmitters and neuromodulators, acting on specific circuits within the brain.  There is strong evidence for the existence of both endogenous stress and anti-stress systems.  Chronic exposure to drugs of abuse and stress are hypothesized to modulate the relative balance of activity of these systems within key circuitry in the brain leading to dysregulated emotional behavior.  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.

Publications

pubmed

Click above for PubMed publications.

  • Kash, T.L., Nobis, W.P., Matthews, R.T., and Winder, D.G. (2008) Dopamine enhances fast excitatory synaptic transmission in the extended amygdala by a CRF-R1-dependent process. J Neurosci 28: 13856-13865. Abstract
  • Healey, J.C., Winder, D.G., and Kash, T.L. (2008) Chronic ethanol exposure leads to divergent control of dopaminergic synapses in distinct target regions. Alcohol 42: 179-190. Abstract
  • Kash, T.L., Matthews, R.T., and Winder, D.G. (2008) Alcohol inhibits NR2B-containing NMDA receptors in the ventral bed nucleus of the stria terminalis. Neuropsychopharmacology 33: 1379-1390. Abstract
  • Kash, T.L., and Winder, .DG. (2006) Neuropeptide Y and corticotropin-releasing factor bi-directionally modulate inhibitory synaptic transmission in the bed nucleus of the stria terminalis. Neuropharmacology 51: 1013-1022. Abstract
  • Keramidas, A., Kash, T.L., and Harrison, N.L. (2006) The pre-M1 segment of the alpha1 subunit is a transduction element in the activation of the GABAA receptor. J Physiol 575: 11-22. Abstract

 

Contact Information


Office Location:
5023 Thurston Bowles

Mailing Address:
CB # 7178
UNC School of Medicine
Chapel Hill, NC 27599-7178

Office Phone: 919-966-7116
Lab Phone:

tkash[at]email.unc.edu

Kash Lab Website

 

 

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