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The Nathan S. Kline Institute for Psychiatric Research

Analytical Psychopharmacology

Balapal Lab

Lab Name
Postdoctoral Research Scientist
Postdoctoral Research Scientist

The central focus of Dr. Raj Balapal’s laboratory is to understand the function of endocannabinoid systems and epigenetics in synaptic plasticity and learning and memory disorders. While the main focus of the lab is on fetal alcohol spectrum disorder (FASD), our studies span many different drug (marijuana and synthetic cannabinoids or Spice) induced synaptic disorders.


Research in the Balapal lab is focused on the function of lipid-derived messengers, with particular emphasis on the endogenous cannabinoids anandamide and 2-arachidonoylglycerol. Current research efforts converge on three areas: endocannabinoids signaling; physiological roles of the endogenous cannabinoid system during early brain development; understanding the role of endogenous cannabinoid system in synaptic plasticity and learning and memory disorders.

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Hippocampal slices and primary neural cell cultures and state-of-the-art double patch-clamp and slices electrophysiology is used to understand the physiological role of endocannabinoids; liquid chromatography/mass-spectrometry is used to investigate the formation and deactivation of anandamide and 2-arachidonoylglycerol in brain cells. Western blot and molecular biology approaches are employed to characterize the molecular mechanisms underlying these processes. The potential pharmacological agents that interfere with various aspects of endogenous cannabinoid function, and their therapeutic potential is explored in vitro and in vivo for many learning and memory disorders. 

Dr. Balapal also investigates marijuana, synthetic cannabinoids and endocannabinoid compounds that stimulate the CB1 cannabinoid receptor and regulate signal transduction pathways in the brain hippocampus. The lab studies the endocannabinoids and their CB1 receptor signaling in the regulation of synaptic plasticity and learning and memory disorders.

In addition, the lab investigates epigenetic modifications such as histone associated DNA methylation and histone protein acetylation and methylation of many target genes including CB1 receptor gene and their transcriptional regulation in many cognitive disorders. 

Current Research

Dr. Balapal’s current investigation is focused on the function of endocannabinoids such as anandamide and its CB1 receptor mediated signaling in the development of fetal alcohol spectrum disorder (FASD). FASD is one of the major causes of intellectual disability in western nations. The goal is to explore how early ethanol exposure induces persistent expression of CB1R to adulthood and to examine epigenetic modifications at the CB1R promoter in brain structures. The lab also explores how persistent expression of CB1R disrupts development of the synaptic circuit events. Furthermore, the research group evaluates how early ethanol induced neurobehavioral deficits can be attributed to persistent CB1R activity.

Recent Publications
  • Subbanna S, Nagre NN, Umapathy NS, Pace BS, Basavarajappa BS (2017) Postnatal Ethanol Epigenetically Up-regulates CB1R Expression and Induces Neurobehavioral Abnormalities in Adult Mice. Intl J Neuropsychopharmacology (In Press).
  • Shivakumar Subbanna, Nagaraja N. Nagre, Madhu Shivakumar and Basavarajappa BS (2016) A single day of 5-Azacytidine exposure during development induces Neurodegeneration in Neonatal Mice and Long-lasting Synaptic, Learning and Memory Deficits in Adult Mice, Physiology and Behavior, 167:16-27. PMID: 27594097.
  • Yuan A, Sershen H, Veeranna, Basavarajappa BS, Kumar A, Hashim A, Berg M, Lee JH, Sato Y, Rao MV, Mohan PS, Dyakin V, Julien JP, Lee VM, Nixon RA (2015) Functions of neurofilaments in synapses. Mol Psychiatry, 20:915. PMID: 26201270.
  • Shivakumar Subbanna S, Psychoyos D, Xie S and Basavarajappa BS (2015) Postnatal Ethanol Exposure Alters Levels of 2-Arachidonylglycerol-Metabolizing Enzymes and Pharmacological Inhibition of MAGL Does Not Cause Neurodegeneration in Neonatal Mice. J of Neurochemistry 134:276-87.PMID:25857698.
  • Yuan A, Sershen H, Veeranna, Basavarajappa BS, Kumar A, Hashim A, Berg M, Lee J-H, Sato Y, Rao MV, Mohan PS, Dyakin V, Julien JP,  Lee EM-Y and Nixon RA (2015) Neurofilament subunits are integral components of synapses and modulate neurotransmission and behavior in vivo. Molecular Psychiatry, 20: 986-94. PMID:25869803.
  • Nagre NN, Subbanna S, Shivakumar M, Umapathy NS, Psychoyos D, Basavarajappa BS (2015) CB1-Receptor Knockout Neonatal Mice are Protected Against Ethanol-induced Impairments of DNMT1, DNMT3A and DNA Methylation. J. Neurochemistry 132:429-42. PMID: 25487288.
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  • Basavarajappa BS, Subbanna S (2014). CB1 Receptor-Mediated Signaling Underlies the Hippocampal Synaptic, Learning and Memory Deficits Following Treatment with JWH-081, a New Component of Spice/K2 Preparations. Hippocampus 24: 178-88. PMID: 24123667. PMCID: PMC3959795.
  • Subbanna S, Nagre NN, Shivakumar M, Umapathy NS, Psychoyos D, Basavarajappa BS (2014) Ethanol induced acetylation of histone at G9a exon1 and G9a-mediated histone H3 dimethylation leads to neurodegeneration in neonatal mice. Neuroscience, 258:422-432. PMID:24300108. PMCID: PMC: 3954640.
  • Basavarajappa BS, Nagaraja NN, Xie S, Subbanna S (2014). Elevation of Endogenous Anandamide Impairs LTP, Learning and Memory through CB1 Receptor Signaling in Mice. Hippocampus 24: 808-18. PMID:24648181. PMCID: PMC4077345.
  • Kaur G, Sharma A, Xu W, Gerum S, Alldred M, Subbanna S, Basavarajappa BS, Pawlik M, Ohno M, Ginsberg S, Wilson D, Guilfoyle D, Levy E (2014) Glutamatergic transmission aberration: a major cause of behavioral deficits in a murine model of Down's syndrome. J Neuoscience 34: 5099-106.PMID: 24719089. PMCID:PMC: 3983795.
  • Subbanna, S. & Basavarajappa, BS (2014). Pre-administration of G9a/GLP inhibitor during Synaptogenesis Prevents Postnatal Ethanol-induced LTP Deficits and Neurobehavioral Abnormalities in Adult Mice. Experimental Neurology 261 34-43. PMID: 25017367. PMCID: not yet available.