Head of Lab
The central focus of Dr. Raj Balapalís 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.
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
Epigenetic abnormalities due to
developmental ethanol exposure:
- Joshi V, Subbanna S, Shivakumar M, Basavarajappa
BS. CB1R regulates CDK5 signaling and epigenetically controls Rac1
expression contributing to neurobehavioral abnormalities in mice
postnatally exposed to ethanol. Neuropsychopharmacology. 2018 Aug 22.
- Subbanna S, Nagre NN,
Shivakumar M, Joshi V, Psychoyos D, Kutlar A, Umapathy NS, Basavarajappa BS. CB1R-Mediated Activation of
Caspase-3 Causes Epigenetic and Neurobehavioral Abnormalities in Postnatal
Ethanol-Exposed Mice. Front Mol Neurosci. 2018
Feb 20;11:45. PubMed PMID: 29515368.
- Subbanna S, Nagre NN,
Shivakumar M, Basavarajappa BS. A single day of
5-azacytidine exposure during development induces neurodegeneration in
neonatal mice and neurobehavioral deficits in adult mice. Physiol Behav. 2016 Dec 1;167:16-27. PubMed PMID: 27594097.
- Basavarajappa BS, Subbanna S. Epigenetic Mechanisms in Developmental
Alcohol-Induced Neurobehavioral Deficits. Brain Sci. 2016 Apr 8;6(2).
PubMed PMID: 27070644.
- Subbanna S, Nagre NN, Umapathy NS, Pace BS, Basavarajappa
BS. Ethanol exposure induces neonatal neurodegeneration by enhancing CB1R
Exon1 histone H4K8 acetylation and up-regulating CB1R function causing
neurobehavioral abnormalities in adult mice. Int J Neuropsychopharmacol.
2014 Oct 31;18(5). PubMed PMID: 25609594.
- Nagre NN, Subbanna S, Shivakumar M, Psychoyos
D, Basavarajappa BS. CB1-receptor knockout
neonatal mice are protected against ethanol-induced impairments of DNMT1,
DNMT3A, and DNA methylation. J Neurochem. 2015
Feb;132(4):429-442. PubMed PMID: 25487288.
Signaling defects due to alcohol
exposure during development:
- Subbanna S, Joshi V, Basavarajappa
BS. Activity-dependent Signaling and Epigenetic Abnormalities in Mice
Exposed to Postnatal Ethanol. Neuroscience. 2018 Jul 20. PubMed PMID:
- Basavarajappa BS, Shivakumar M, Joshi V, Subbanna S. Endocannabinoid
system in neurodegenerative disorders. J Neurochem.
2017 Sep;142(5):624-648. PubMed PMID: 28608560.
- Basavarajappa BS. Fetal Alcohol Spectrum Disorder: Potential Role of
Endocannabinoids Signaling. Brain Sci. 2015 Oct 29;5(4):456-93. PubMed
- Subbanna S, Shivakumar M, Psychoyos
D, Xie S, Basavarajappa BS. Anandamide-CB1
receptor signaling contributes to postnatal ethanol-induced neonatal
neurodegeneration, adult synaptic, and memory deficits. J Neurosci. 2013 Apr 10;33(15):6350-66. [Erratum in: J Neurosci. 2013 Jul 3;33(27):11323.] PubMed PMID: