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Andrew M. Farrar

Research Fellow

The basal ganglia are a highly-interconnected network of sub-cortical brain structures that are essential for the execution of voluntary motor behavior. In addition to motor output, the basal ganglia are also involved in cognitive processes, including learning and memory, decision making, and motivation. The transmission of neural information throughout the basal ganglia is governed by complex neurochemical interactions, ultimately giving rise to behavioral output. My research utilizes behavioral, in vivo neurochemical, and genetic approaches to understand how function of the basal ganglia contributes to complex behavioral functions. Additionally, by employing genetically-modified animal models of disease (e.g., mouse models of Huntington's disease), we can study how dysfunction of basal ganglia circuitry contributes to behavioral disturbances that closely resemble disease symptoms in humans.

Current Research
Ongoing efforts are aimed at characterizing cognitive, behavioral and neurochemical phenotypic differences between rat strains, coupled with next-generation sequencing methods, to ultimately determine the genetic basis of individual differences in behavior and susceptibility to neurological disease at a mechanistic level.

Academic Background

  • PhD, University of Connecticut, 2009
  • Postdoctoral training, Rutgers Center for Molecular and Behavioral Neuroscience
Curtin PCP, Farrar AM, Oakeshott S, Sutphen J, Berger J, Mazzella M, Cox K, He D, Alosio W, Park LC, Howland D and Brunner D (2016) Cognitive Training at a Young Age Attenuates Deficits in the zQ175 Mouse Model of HD. Front. Behav. Neurosci. 9:361.
Farrar AM, Murphy CA, Paterson NE, Oakeshott S, He D, Alosio W, McConnell K, Menalled LB, Ramboz S, Park LC, Howland D, Brunner D. (2014) Cognitive deficits in transgenic and knock-in HTT mice parallel those in Huntington's disease. J Huntingtons Dis. 2014;3(2):145-58.
Farrar AM, Callahan JW, Abercrombie ED. (2011) Reduced striatal acetylcholine efflux in the R6/2 mouse model of Huntington's disease: an examination of the role of altered inhibitory and excitatory mechanisms. Exp Neurol. 2011 Dec;232(2):119-25.
Farrar AM, Segovia KN, Randall PA, Nunes EJ, Collins LE, Stopper CM, Port RG, Hockemeyer J, Müller CE, Correa M, Salamone JD. (2010) Nucleus accumbens and effort-related functions: behavioral and neural markers of the interactions between adenosine A2A and dopamine D2 receptors. Neuroscience. 2010 Apr 14;166(4):1056-67.
 
Contact Info

Department of Psychological and Brain Sciences
N273 Life Science Laboratory
240 Thatcher Road
Amherst, MA 01003-9292

afarrar@psych.umass.edu