The effects of GABAA and NMDA receptors in the shell–accumbens on spatial memory of METH-treated rats

Heysieattalab, Soomaayeh; Naghdi, Nasser; Zarrindast, Mohammad‐Reza; Haghparast, Abbas; Mehr, Shahram Ejtemaei; Khoshbouei, Habibeh

doi:10.1016/j.pbb.2015.12.008

Cited by 19 publications

(13 citation statements)

References 64 publications

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“…The MA treated mice exhibited a lower asymptotic performance level for % correct scores and an increase in the number of reference and working memory errors compared to mice given control treatment. This is consistent with several other studies reporting spatial memory deficits following a short abstinence period ( Camarasa et al, 2010 ; Heysieattalab et al, 2016 ; Williams et al, 2003 ). Others have shown that chronic use of MA can actually stave off MA-induced deficits, which can then be initiated following long-periods of abstinence.…”

Section: Discussionsupporting

confidence: 93%

Chronic voluntary oral methamphetamine induces deficits in spatial learning and hippocampal protein kinase Mzeta with enhanced astrogliosis and cyclooxygenase-2 levels

Avila

Zanca

Shor

et al. 2018

Heliyon

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Methamphetamine (MA) is an addictive drug with neurotoxic effects on the brain producing cognitive impairment and increasing the risk for neurodegenerative disease. Research has focused largely on examining the neurochemical and behavioral deficits induced by injecting relatively high doses of MA [30 mg/kg of body weight (bw)] identifying the upper limits of MA-induced neurotoxicity. Accordingly, we have developed an appetitive mouse model of voluntary oral MA administration (VOMA) based on the consumption of a palatable sweetened oatmeal mash containing a known amount of MA. This VOMA model is useful for determining the lower limits necessary to produce neurotoxicity in the short-term and long-term as it progresses over time. We show that mice consumed on average 1.743 mg/kg bw/hour during 3 hours, and an average of 5.23 mg/kg bw/day over 28 consecutive days on a VOMA schedule. Since this consumption rate is much lower than the neurotoxic doses typically injected, we assessed the effects of long-term chronic VOMA on both spatial memory performance and on the levels of neurotoxicity in the hippocampus. Following 28 days of VOMA, mice exhibited a significant deficit in short-term spatial working memory and spatial reference learning on the radial 8-arm maze (RAM) compared to controls. This was accompanied by a significant decrease in memory markers protein kinase Mzeta (PKMζ), calcium impermeable AMPA receptor subunit GluA2, and the post-synaptic density 95 (PSD-95) protein in the hippocampus. Compared to controls, the VOMA paradigm also induced decreases in hippocampal levels of dopamine transporter (DAT) and tyrosine hydroxylase (TH), as well as increases in dopamine 1 receptor (D1R), glial fibrillary acidic protein (GFAP) and cyclooxygenase-2 (COX-2), with a decrease in prostaglandins E2 (PGE2) and D2 (PGD2). These results demonstrate that chronic VOMA reaching 146 mg/kg bw/28d induces significant hippocampal neurotoxicity. Future studies will evaluate the progression of this neurotoxic state.

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Section: Discussionsupporting

confidence: 93%

Chronic voluntary oral methamphetamine induces deficits in spatial learning and hippocampal protein kinase Mzeta with enhanced astrogliosis and cyclooxygenase-2 levels

Avila

Zanca

Shor

et al. 2018

Heliyon

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“…CD38 is important for learning and memory outside of social contexts as measured by Morris water-maze, contextual fear conditioning, and novel object recognition tasks (14). Given that dopamine signaling in the striatum is important for the performance of each of these tasks (48)(49)(50)(51)(52)(53)(54), the learning and memory deficits seen in Cd38KO mice may be explained by the impaired dopaminergic signals observed here in the FSCV experiments. Apart from the human imaging study (20) and microdialysis study (12) previously noted, few studies have directly examined the role of CD38 in dopamine signaling itself.…”

Section: Discussionmentioning

confidence: 74%

A role for the CD38 rs3796863 polymorphism in alcohol and monetary reward: evidence from CD38 knockout mice and alcohol self-administration, [11C]-raclopride binding, and functional MRI in humans

Lee

Shin

Deschaine

et al. 2019

The American Journal of Drug and Alcohol Abuse

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Background: Cluster of differentiation 38 (CD38) is a transmembrane protein expressed in dopaminergic reward pathways in the brain, including the nucleus accumbens (NAc). The GG genotype of a common single nucleotide polymorphism (SNP) within CD38, rs3796863, is associated with increased social reward. Objective: Examine whether CD38 rs3796863 and Cd38 knockout (KO) are associated with rewardrelated neural and behavioral phenotypes. Methods: Data from four independent human studies were used to test whether rs3796863 genotype is associated with: (1) intravenous alcohol self-administration (n = 64, 30 females), (2) alcohol-stimulated dopamine (DA) release measured using 11 C-raclopride positron emission tomography (n = 22 men), (3) ventral striatum (VS) response to positive feedback measured using a card guessing functional magnetic resonance imaging (fMRI) paradigm (n = 531, 276 females), and (4) resting state functional connectivity (rsfc) of the VS (n = 51, 26 females). In a fifth study, we used a mouse model to examine whether cd38 knockout influences stimulated DA release in the NAc core and dorsal striatum using fast-scanning cyclic voltammetry. Results: Relative to T allele carriers, G homozygotes at rs3796863 within CD38 were characterized by greater alcohol self-administration, alcohol-stimulated dopamine release, VS response to positive feedback, and rsfc between the VS and anterior cingulate cortex. High-frequency stimulation reduced DA release among Cd38 KO mice had reduced dopamine release in the NAc. Conclusion: Converging evidence suggests that CD38 rs3796863 genotype may increase DArelated reward response and alcohol consumption.

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“…Baclofen and the positive allosteric modulators of GABA B receptor have shown to inhibit METH‐induced conditioned place preference (CPP) (Li et al, ; Voigt et al, ). Previously, we have shown that pre‐training intra‐shell NAc injection of muscimol prevented METH‐induced impairment in a spatial memory task (Morris Water Maze), while intra‐NAc infusion of an NMDA receptor agonist in METH treated rats increased memory impairment (Heysieattalab et al, ). In this study, we tested the effects of pharmacological manipulations of GABA A or NMDA receptors (agonist or antagonist) in the shell region of the nucleus accumbens on METH‐ elicited alterations in DG‐LTP.…”

Section: Introductionmentioning

confidence: 84%

“…Rats received systemic injection of saline or METH and intra‐shell NAc infusions of muscimol (0.005 µg/rat) or bicuculline (0.2 µg/rat, 1 week after systemic injection, Azizbeigi et al, ; Heysieattalab et al, ) prior to baseline recording. The experimental groups were: Saline‐muscimol, METH‐muscimol, Saline‐bicuculline, and METH‐bicuculline (Table ).…”

Section: Methodsmentioning

confidence: 99%

Methamphetamine‐induced enhancement of hippocampal long‐term potentiation is modulated by NMDA and GABA receptors in the shell–accumbens

Heysieattalab

Naghdi

Hosseinmardi

et al. 2016

Synapse

Self Cite

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Addictive drugs modulate synaptic transmission in the meso-corticolimbic system by hijacking normal adaptive forms of experience-dependent synaptic plasticity. Psychostimulants such as METH have been shown to affect hippocampal synaptic plasticity, albeit with a less understood synaptic mechanism. METH is one of the most addictive drugs that elicit long-term alterations in the synaptic plasticity in brain areas involved in reinforcement learning and reward processing. Dopamine transporter (DAT) is one of the main targets of METH. As a substrate for DAT, METH decreases dopamine uptake and increases dopamine efflux via the transporter in the target brain regions such as nucleus accumbens (NAc) and hippocampus. Due to cross talk between NAc and hippocampus, stimulation of NAc has been shown to alter hippocampal plasticity. In this study, we tested the hypothesis that manipulation of glutamatergic and GABA-ergic systems in the shell-NAc modulates METH-induced enhancement of long term potentiation (LTP) in the hippocampus. Rats treated with METH (four injections of 5 mg/kg) exhibited enhanced LTP as compared to saline-treated animals. Intra-NAc infusion of muscimol (GABA receptor agonist) decreased METH-induced enhancement of dentate gyrus (DG)-LTP, while infusion of AP5 (NMDA receptor antagonist) prevented METH-induced enhancement of LTP. These data support the interpretation that reducing NAc activity can ameliorate METH-induced hippocampal LTP through a hippocampus-NAc-VTA circuit loop. Synapse 70:325-335, 2016. © 2016 Wiley Periodicals, Inc.

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The effects of GABAA and NMDA receptors in the shell–accumbens on spatial memory of METH-treated rats

Cited by 19 publications

References 64 publications

Chronic voluntary oral methamphetamine induces deficits in spatial learning and hippocampal protein kinase Mzeta with enhanced astrogliosis and cyclooxygenase-2 levels

Chronic voluntary oral methamphetamine induces deficits in spatial learning and hippocampal protein kinase Mzeta with enhanced astrogliosis and cyclooxygenase-2 levels

A role for the CD38 rs3796863 polymorphism in alcohol and monetary reward: evidence from CD38 knockout mice and alcohol self-administration, [11C]-raclopride binding, and functional MRI in humans

Methamphetamine‐induced enhancement of hippocampal long‐term potentiation is modulated by NMDA and GABA receptors in the shell–accumbens

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