The efforts of the laboratory are directed to understand the neurochemical basis of ethanol and cannabinoid-induced ataxia.  The work exclusively involves the study of the role glutamate-nitric oxide- guanylyl cyclase signaling in the ethanol/cannabinoid-induced cerebellar ataxia.  Using stereotaxic techniques for direct drug microinfusion in CD-1 mice, the lab is also investigating the  modulation of ethanol and Δ⁹-THC (main psychoactive substance in the cannabis plant)-induced cerebellar ataxia by several receptor mechanisms such as nAChRs, NMDA, CB₁, adenosine, A₁ & A_2A.  Recently, strong cross tolerance between cannabinoid and nicotine and between Δ⁹-THC and nicotine was observed using cerebellar ataxia as the test response.  Currently, focus is on the subtypes of the nAChR that actually mediate the functional cross-tolerance and the role of nitric oxide signaling in the functional interaction and cross-tolerance.

Publications
Taslim, N., Al-Rejaie, S., and Dar, M.S. (2008).  Attenuation of ethanol-induced ataxia by α₄β₂ nicotinic acetylcholine receptor subtype in mouse cerebellum:  a functional interaction.  Neuroscience, 157: 204-213.

Dar, M.S. (2007). Co-modulation of acute ethanol-induced motor impairment by mouse cerebellar adenosinergic A₁ and GABA_A receptor systems.  Brain Res. Bull., 71:  287-295.

Smith, A.D. and Dar, M.S. (2007).  Behavioral cross-tolerance between repeated intracerebellar nicotince and acute Δ⁹-tetrahydrocannabinol-induced cerebellar ataxia:  role of cerebellar nitric oxide. J. Pharmacol. Exp. Ther., 322:  243-253.

Al-Rejaie, S. and Dar, M.S. (2005).  Antagonism of ethanol ataxia by intracerebellar nicotine:  possible modulation by mouse cerebellar nitric oxide and cGMP.  Brain Res. Bull., 69:  187-196.

Al-rejaie, S. and Dar, M.S. (2005).  Possible role of mouse cerebellar nitric oxide in the behavioral interaction between chronic intracerebellar nicotine and acute ethanol administration. Neuroscience, 138:  575-585.

Dar, M.S. and Meng, Z.-H. (2004).  Acute ethanol-induced adenosine diphosphate ribosylation regulates the functional activity of rat striatal pertussis toxin-sensitive G proteins.  Alcoholism: Clinical and Experimental Res., 28:  1299-1307.