GHB – Induced Cognitive Deficits During Adolescence and the Role of NMDA Receptor

Author(s): R. Sircar, L-C. Wu, K. Reddy, D. Sircar, A. K. Basak

Journal Name: Current Neuropharmacology

Volume 9 , Issue 1 , 2011

Become EABM
Become Reviewer
Call for Editor


We have earlier reported that γ-hydroxybutyric acid (GHB) disrupts the acquisition of spatial learning and memory in adolescent rats. GHB is known to interact with several neurotransmitter systems that have been implicated in cognitive functioning. The N-methyl-D-aspartate receptor (NR) -type of glutamate receptor is considered to be an important target for spatial learning and memory. Molecular mechanisms governing the neuroadptations following repeated GHB treatment in adolecent rats remain unknown. We examined the role of NMDA receptor in adolescent GHB-induced cognitive deficit. Adolescent rats were administered with GHB on 6 consecutive days, and surface-expressed NMDA receptor subunits levels were measured. GHB significantly decreased NR1 levels in the frontal cortex. Adolescent GHB also significantly reduced cortical NR2A subunit levels. Our findings support the hypothesis that adolescent GHB-induced cogntive deficits are associated with neuroadaptations in glutamatergic transmission, particulaly NR functioning in the frontal cortex.

Keywords: Addiction, juvenile, cognitive function, glutamatergic, radioligand binding, western blot, NR subunit, GHB, presynaptic terminal, NR subunit, GHB, NMDA receptor, NMDA receptor antagonists

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2011
Published on: 01 March, 2012
Page: [240 - 243]
Pages: 4
DOI: 10.2174/157015911795017038

Article Metrics

PDF: 32