Adolescent γ-hydroxybutyric acid exposure decreases cortical N-methyl-d-aspartate receptor and impairs spatial learning

  title={Adolescent $\gamma$-hydroxybutyric acid exposure decreases cortical N-methyl-d-aspartate receptor and impairs spatial learning},
  author={Ratna Sircar and Ashim Kumar Basak},
  journal={Pharmacology Biochemistry and Behavior},
  • R. SircarA. Basak
  • Published 1 December 2004
  • Biology, Psychology
  • Pharmacology Biochemistry and Behavior

Effects of γ-hydroxybutyric acid on spatial learning and memory in adolescent and adult female rats

γ‐Hydroxybutyric Acid–Induced Cognitive Deficits in the Female Adolescent Rat

Exposure to GHB in adolescent female rats has a negative impact on spatial learning and memory, and in the probe trial drug‐treated rats spent less time in the quadrant where the platform was present prior to its removal than did control adolescent rats.

Anxiogenic-like effects of gamma-hydroxybutyric acid (GHB) in mice tested in the light-dark box.

It is suggested that the anxiogenic effects of GHB could be related to its ability to modulate GABA and/or dopaminergic receptors.

Improvement in γ-hydroxybutyrate-induced contextual fear memory deficit by systemic administration of NCS-382

The ability of the putative GHB receptor antagonist NCS-382 to block the disrupting effects of GHB on fear memory in adolescent rat is examined, suggesting that low-dose amnesic effects ofGHB are mediated by GHB receptors.

Neurotoxic effects induced by gammahydroxybutyric acid (GHB) in male rats.

The results show for the first time that the repeated administration of GHB, especially at very low doses, produces neurotoxic effects, which is very relevant because its abuse, especially by young persons, could produce considerable neurological alterations after prolonged abuse.

Systemic administration of gamma-hydroxybutyric acid in adolescent rat impairs contextual fear conditioning, but not cued conditioning

Results demonstrate that in the adolescent rat exposure to GHB preferentially disrupt hippocampal-dependent learning, and administration of GHB before the presentation of tone-shock pairings dose-dependently disrupted the acquisition of contextual conditioning.



Gamma-hydroxybutyric acid reducing effect on ethanol intake: evidence in favour of a substitution mechanism.

The results of the present study demonstrate that a non-sedative and anxiolytic dose of GHB effectively reduced voluntary ethanol intake in sP rats, adding further support to the hypothesis that GHB may control alcohol craving and consumption in humans by substituting for ethanol's reinforcing effects.

The stimulus properties of γ-hydroxybutyrate

It is concluded that the compound stimulus produced by GHB is most closely associated with GABAergic systems, but that minor opiate and serotonergic components are present as well.

The Role of GABAB Receptors in the Discriminative Stimulus Effects of γ-Hydroxybutyrate in Rats: Time Course and Antagonism Studies

Results implicate GABAB mechanisms in the discriminative stimulus effects of GHB and suggest that the effects of 1,4-BDL under these conditions result from its conversion to GHB, which could explain the lack of antagonism reported for NCS-382.

A specific gamma-hydroxybutyrate receptor ligand possesses both antagonistic and anticonvulsant properties.

The results suggest that NCS-382 may represent a harbinger for a new class of anticonvulsant drugs that most probably act by modifying the endogenous GHB system.

Effects of the putative antagonist NCS382 on the behavioral pharmacological actions of gammahydroxybutyrate in mice

GHB dose dependently produced depressant-like effects on learned and unlearned behavior and the putative GHB antagonist NCS382 failed to convincingly antagonize these effects.

Evaluation of the discriminative stimulus and reinforcing effects of gammahydroxybutyrate (GHB)

The data indicate that GHB is unlike PCP as a reinforcer and that neither PCP nor heroin generalize to injections of GHB, nor can injections ofGHB attenuate the discriminative stimulus effects of cocaine.