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MK-801 (dizocilpine) is a potent non-competitive N-methyl-[D]-aspartate (NMDA) receptor antagonist that affects cognitive function, learning, and memory. As we know, NMDA receptors are significantly involved in memory function, as well as GABA (Gamma-Aminobutyric acid) receptors. In this study, we aimed to discover the effect of GABA-B receptors in the basolateral amygdala (BLA) on MK-801-induced memory impairment. We used 160 male Wistar rats. The shuttle box was used to evaluate passive avoidance memory and locomotion apparatus was used to evaluate locomotor activity. MK-801 (0.125, 0.25, and 0.5 μg/rat), baclofen (GABA-B agonist, 0.0001, 0.001, and 0.01 μg/rat) and phaclofen (GABA-B antagonist, 0.0001, 0.001, and 0.01 μg/rat) were injected intra-BLA, after the training. The results showed that MK-801 at the dose of 0.5 μg/rat, baclofen at the doses of 0.001 and 0.01 μg/rat, and phaclofen at the doses of 0.001 and 0.01 μg/rat, impaired passive avoidance memory. Locomotor activity did not alter in all groups. Furthermore, the subthreshold dose of both baclofen (0.0001 μg/rat) and phaclofen (0.0001 μg/rat) restored the impairment effect of MK-801 (0.5 μg/rat) on memory. Also, both baclofen (0.0001 μg/rat) potentiated the impairment effect of MK-801 (0.125 μg/rat) and phaclofen (0.0001 μg/rat) potentiated the impairment effect of MK-801 (0.125 and 0.25 μg/rat) on passive avoidance memory. In conclusion, our results indicated that BLA GABA-B receptors can alter the effect of NMDA inactivation on passive avoidance memory., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Autism spectrum disorder (ASD) is an immensely challenging developmental disorder characterized primarily by two core behavioral symptoms of social communication deficits and restricted/repetitive behaviors. Investigating the etiological process and identifying an appropriate therapeutic target remain as formidable challenges to overcome ASD due to numerous risk factors and complex symptoms associated with the disorder. Among the various mechanisms that contribute to ASD, the maintenance of excitation and inhibition balance emerged as a key factor to regulate proper functioning of neuronal circuitry. In this study, we employed prenatally exposed to valproic acid (VPA) to establish a validated ASD mouse model and found impaired inhibitory gamma-aminobutyric acid (GABAergic) neurotransmission through a presynaptic mechanism in these model mice, which was accompanied with decreased GABA release and GABA-A and GABA-B receptor subunits expression. And acute administration of individual GABA-A or GABA-B receptor agonists partially reversed autistic-like behaviors in the model mice. Furthermore, acute administration of the combined GABA-A and GABA-B receptor agonists palliated sociability deficits, anxiety and repetitive behaviors in the animal model of autistic-like behaviors, demonstrating the therapeutic potential of above cocktail in the treatment of ASD., (Copyright © 2020. Published by Elsevier B.V.)

Our prior work demonstrated the involvement of the caudal granular subregion of the insular cortex in a rat model of nicotine self-administration. Recent studies in various animal models of addiction for nicotine and other drugs have identified a role for the rostral agranular subregion (RAIC). The current research was undertaken to examine the involvement of the RAIC in a rat model of nicotine self-administration. We investigated the inactivating effects of local infusions of a γ-aminobutyric acid agonist mixture (baclofen/muscimol) into the RAIC on nicotine self-administration under a fixed-ratio 5 (FR-5) schedule and on reinstatement of nicotine seeking induced by nicotine-associated cues in rats. We also evaluated the effects of RAIC inactivation on food self-administration under an FR5 schedule as a control. Inactivation of the RAIC decreased nicotine, but not food, self-administration. RAIC inactivation also prevented the reinstatement, after extinction, of nicotine seeking induced by nicotine-associated cues. Our study indicates that the RAIC is involved in nicotine-taking and nicotine-seeking in rats. Modulating insular cortex function appears to be a promising approach for nicotine dependence treatment., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Injections of the GABAA antagonist bicuculline into the medial ventral pallidum (VPm) induce marked increases in food intake, but nothing is known about the way in which these injections alter the distribution of intake in a macronutrient selection situation. We investigated this topic by adapting rats to a diet containing independent sources of protein, carbohydrate and fat, and then examining the effects of intra-VPm bicuculline on diet selection. Under these conditions, bicuculline produced a massive, preferential increase in fat intake with subjects consuming a mean of 97% of their calories from fat. Furthermore, all treated subjects ate fat before any other macronutrient, suggesting that the animals' behavior was directed selectively toward this dietary component even before consumption had begun. Similar effects were not observed following food deprivation, which exerted its largest effect on carbohydrate intake. To compare the intra-VPm bicuculline response to that seen after activation of GABA receptors in the nucleus accumbens shell (AcbSh), a major source of projections to the VPm, we conducted similar experiments with intra-AcbSh injections of muscimol and baclofen. These injections also enhanced food intake, but did not reproduce the selective preference for fat seen after intra-VPm bicuculline. These experiments provide the first demonstration of preferential enhancement of fat intake following manipulations of a nonpeptide neurotransmitter. Since mean intakes of fat under baseline conditions and after deprivation tended to be lower than those of carbohydrates, it seems unlikely that the effects of intra-VPm bicuculline are related to the intrinsic "rewarding" properties of fat, but might rather reflect the induction of a state of "fat craving.", (Copyright © 2014 Elsevier B.V. All rights reserved.)