Vaishali P. Bakshi
- Associate Professor, Department of Psychiatry
- (608) 265-6062
Ph.D. University of California, San Diego
Neural Substrates and Stress Regulation of Psychiatric Illness
1. What are neural substrates of schizophrenia-like deficits?
2. How does traumatic stress enact neural plasticity?
I am a behavioral neuroscientist with a specialization in neuropsychopharmacology. My research focuses on delineating the neural substrates of psychiatric disorders by studying animal models for dysfunctional behavioral processes in various mental illnesses including anxiety disorders, depression, and schizophrenia. One area of research concentrates on the neural substrates underlying stress-related disorders such as anxiety and depression. Because exposure to stress is known to play an important role in the development and expression of these illnesses, I study the neural substrates mediating stress-induced behavioral responses in rodents. This research is centered on brain peptide receptors, and involves not only behavioral pharmacology strategies, but also molecular biology and virology approaches to specifically target and knock down particular stress-related proteins in discrete brain regions. By microinfusing selective drugs or viral vectors (for gene transfer) into specific limbic brain regions such as the septum or amygdala, I study the role that corticotropin-releasing homone (CRH) receptors play in regulating stress-like behaviors in rodents. I am specifically interested in the possibility that acute or chronic treatment to block CRH receptors could prevent the deleterious effects of long-term stress.
My other main area of research focuses on understanding the mechanism of action of antipsychotic medications---specifically, through which brain regions and neurotransmitter systems do these drugs produce their beneficial effects? I employ both pharmacological and developmental rodent models for some of the information processing deficits that are commonly observed in schizophrenia patients, and evaluate the ability of candidate antipsychotic medications to ameliorate these deficits. In addition, by mapping out the basic neurobiology underlying these information processing deficits, I seek to identify novel transmitter and peptide systems that may eventually be used as potential targets for antipsychotic drug development. The main focus of this research has been on interactions between glutamate and monoamine systems using site-specific drug microinfusion techniques to study brain regions such as the amygdala, hippocampus, and nucleus accumbens.
Finally, in collaboration with colleagues, I am interested in identifying some of the molecular correlates of these animal models. Specifically, which genes are activated in response to long-term treatment with various psychotomimetic drugs such as phencyclidine, LSD, or amphetamine? What are the effects on gene expression of antipsychotic medications? How does exposure to stress influence gene expression?
Rajbhandari AK, Baldo BA, Bakshi VP (2015). Predator stress-induced CRF release causes enduring sensitization of basolateral amygdala norepinephrine systems that promote PTSD-like startle abnormalities, Journal of Neuroscience, in press.
Baisley SK, Bremer Q, Bakshi VP, Baldo BA (2014). Antipsychotic-like actions of the satiety peptide, amylin, in ventral striatal regions marked by overlapping calcitonin receptor and RAMP-1 gene expression, Journal of Neuroscience, 34(12):4318-4325.
Bakshi VP, Alsene KM, Roseboom PH, Connors EE (2012). Enduring sensorimotor gating abnormalities following predator exposure or corticotropin-releasing factor in rats: A model for PTSD-like information-processing deficits?, Neuropharmacology-special issue on PTSD, 62(2):737-48.
Alsene KM and Bakshi VP (2011). Pharmacological stimulation of locus coeruleus reveals a new antipsychotic-responsive pathway for deficient sensorimotor gating, Neuropsychopharmacology, 36(8): 1656-1667.
- Bakshi, V.P., S. Smith-Roe, S.M. Newman, D.E. Grigoriadis, and N.H Kalin. 2002. Reduction of stress-induced behavior by antagonism of corticotropin_releasing hormone 2 (CRH-2) receptors in lateral septum or CRH-1 receptors in amygdla. J. Neurosci. 22: 2926-2935.
- Bakshi, V.P. and N.H Kalin. 2000. Corticotropin-releasing hormone and animal models of anxiety: Gene-environment interactions. Bio. Psychiatry. 48: 1175-1198.
- Bakshi, V.P. and M.A. Geyer. 1998. Multiple limbic regions mediate the disruption of prepulse inhibition produced in rats by the noncompetitive NMDA antagonist, dizocilpine. J. Neurosci. 18: 8397-8401.
- Bakshi, V.P. and M.A. Geyer. 1997. Phencyclidine-induced deficits in prepulse inhibition of startle are reversed by prazosin, and alpha-1 noraddrenergic antagonist. J. Pharmacol. Exper. Ther. 283: 666-674.