NMDA receptors in the medial prefrontal cortex and the dorsal hippocampus regulate methamphetamine-induced hyperactivity and extracellular amino acid release in mice

Han, Wenyan; Wang, Fangyang; Jia, Qi; Wang, Fang; Zhang, Lijia; Zhao, Siqi; Song, Ming; Wu, Chunfu; Yang, Jingyu

doi:10.1016/j.bbr.2012.03.038

Cited by 17 publications

(8 citation statements)

References 84 publications

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“…In this study, we also demonstrated that GABA transmission in the INS plays roles in decision-making in control and METH-treated rats and that reduced activity-dependent GABA release in the INS is related to alteration of decisionmaking in METH-treated animals. Consistent with the findings reported here, a previous report demonstrated that GABA release in the frontal cortex is reduced following METH treatment (41). Based on the analysis of win-stay and lose-shift behaviors in the gambling test, it is likely that METH-treated rats have a dysfunction in the neural system that controls response evoked by both positive and negative RPEs, leading to their impulsive choice behaviors.…”

Section: Discussionsupporting

confidence: 90%

Insular neural system controls decision-making in healthy and methamphetamine-treated rats

Mizoguchi

Katahira

Inutsuka

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Patients suffering from neuropsychiatric disorders such as substance-related and addictive disorders exhibit altered decisionmaking patterns, which may be associated with their behavioral abnormalities. However, the neuronal mechanisms underlying such impairments are largely unknown. Using a gambling test, we demonstrated that methamphetamine (METH)-treated rats chose a highrisk/high-reward option more frequently and assigned higher value to high returns than control rats, suggestive of changes in decisionmaking choice strategy. Immunohistochemical analysis following the gambling test revealed aberrant activation of the insular cortex (INS) and nucleus accumbens in METH-treated animals. Pharmacological studies, together with in vivo microdialysis, showed that the insular neural system played a crucial role in decision-making. Moreover, manipulation of INS activation using designer receptor exclusively activated by designer drug technology resulted in alterations to decision-making. Our findings suggest that the INS is a critical region involved in decision-making and that insular neural dysfunction results in risk-taking behaviors associated with altered decision-making.decision-making | methamphetamine | insular cortex | DREADD | motivational value D ecision-making is a key activity of everyday life. Consequently, disturbances in the ability to make appropriate decisions or anticipate their possible consequences can result in massive social, medical, and financial problems. Decision-making depends on three temporally and partially functionally distinct sets of processes: (i) assessment and formation of preferences among possible options, (ii) selection and execution of an action, and (iii) experience or evaluation of the outcome (1). These processes are thought to require an extended neural network, mainly comprising glutamatergic, serotonergic, noradrenergic, and dopaminergic pathways in the frontostriatal and limbic loops, including the cingulate cortex, orbitofrontal cortex (OFC), insular cortex (INS), striatum (St), basal ganglia, and amygdala (2). Analysis of these processes helps to distinguish which aspects of decision-making are differentially affected in various neuropsychiatric disorders (1).Poor decision-making is a symptom of several neuropsychiatric diseases, such as depression, schizophrenia, Parkinson's disease, and drug dependence (1,(3)(4)(5). Pathological decision-making in neuropsychiatric disorders is associated with an inability to make profitable long-term decisions that incorporate expectations of future outcomes (6). Thus, pathological decision-making is recognized as a core problem in neuropsychiatric disorders, and a better understanding of the mechanisms underlying altered decisionmaking should provide insights that could lead to successful treatments for these diseases.A hallmark of addiction is continuous use of substances despite negative consequences or the absence of positive consequences (7). Addicts are less able to flexibly adapt their behavior to changes in reward contingenci...

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Section: Discussionsupporting

confidence: 90%

Insular neural system controls decision-making in healthy and methamphetamine-treated rats

Mizoguchi

Katahira

Inutsuka

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…MacDonald & Chafee, ; Castner & Williams, ), greater spontaneous and MA‐induced locomotor hyperactivity (e.g. Del Arco & Mora, ; Han et al ., ), as well as greater dopamine release within both the cell body and the terminal regions of corticoaccumbens projections (e.g. Takahata & Moghaddam, ; Lorrain et al ., ; Homayoun et al ., ) in a manner consistent with observations in MA‐experienced animals (e.g.…”

Section: Discussionmentioning

confidence: 99%

“…Currently, it is difficult to reconcile the discrepancies in our extant knowledge of how NMDA receptors regulate basal extracellular glutamate within mPFC (e.g. Moghaddam et al ., ; Gruss et al ., ; Lorrain et al ., ; Zuo et al ., ; Han et al ., ) to make any firm predictions regarding how low NMDA receptor expression within PFC might contribute to or be impacted by MA‐induced glutamate sensitization within this region.…”

Section: Discussionmentioning

confidence: 99%

“…Stephans & Yamamoto, , ). However, acute, subtoxic MA injection is sufficient to impact extracellular glutamate within both the cell body and the terminal regions of excitatory corticostriatal projections (Shoblock et al ., ; Han et al ., ) that are highly implicated in addiction neurocircuitry (Koob & Volkow, ; London et al ., ). Similarly, a history of intravenous MA self‐administration in rats augmented burst firing within PFC glutamate neurons (Parsegian et al ., ) and elicited enduring changes in extracellular glutamate within both the PFC and the ventral striatum (Lominac et al ., ; Parsegian & See, ).…”

Section: Introductionmentioning

confidence: 99%

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Prefrontal glutamate correlates of methamphetamine sensitization and preference

Lominac

Quadir

Barrett

et al. 2016

Eur J of Neuroscience

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Methamphetamine (MA) is a widely abused, highly addictive, psychostimulant that elicits pronounced deficits in neurocognitive function related to hypo-functioning of the prefrontal cortex (PFC). Our understanding of how repeated methamphetamine impacts excitatory glutamatergic transmission within the PFC is limited, as is information about the relation between PFC glutamate and addiction vulnerability/resiliency. In vivo microdialysis and immunoblotting studies characterized the effects of methamphetamine (10 injections of 2 mg/kg, IP) upon extracellular glutamate in C57BL/6J mice and upon glutamate receptor and transporter expression, within the medial PFC. Glutamatergic correlates of both genetic and idiopathic variance in MA preference/intake were determined through studies of high versus low MA-drinking selectively bred mouse lines (MAHDR versus MALDR, respectively) and inbred C57BL/6J mice exhibiting spontaneously divergent place-conditioning phenotypes. Repeated methamphetamine sensitized drug-induced glutamate release and lowered indices of NMDA receptor expression in C57BL/6J mice, but did not alter basal extracellular glutamate content or total protein expression of Homer proteins, or metabotropic or AMPA glutamate receptors. Elevated basal glutamate, blunted methamphetamine-induced glutamate release and ERK activation, as well as reduced protein expression of mGlu2/3 and Homer2a/b were all correlated biochemical traits of selection for high versus low methamphetamine drinking, and Homer2a/b levels were inversely correlated with the motivational valence of methamphetamine in C57BL/6J mice. These data provide novel evidence that repeated, low-dose, methamphetamine is sufficient to perturb pre- and post-synaptic aspects of glutamate transmission within the medial PFC and that glutamate anomalies within this region may contribute to both genetic and idiopathic variance in methamphetamine addiction vulnerability/resiliency.

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“…MAP-induced sensitization and neurotoxicity, for example, can be blocked by NMDA receptor antagonists (Ohmori et al 1994; Thomas and Kuhn, 2005). The physiological mechanisms underlying the disability of memory and learning with chronic MAP treatment have largely focused on the rat hippocampus (Ohmori et al 1994;Hori et al 2010;Han et al 2012) and neostriatum (Moriguchi et al 2002). Activation of NMDA receptors in rat hippocampal slices mediates long-term potentiation (LTP) at Schaffer collateral to CA1 neuron synapses (Hori et al 2010;Swant et al 2010), and this form of synaptic plasticity is believed to be an important aspect of the early stages of the formation of some types of memory (Lynch 2004).…”

Section: Functional Changes In Piriform Cortex Pyramidal Neurons In Tmentioning

confidence: 99%

Functional changes in piriform cortex pyramidal neurons in the chronic methamphetamine-treated rat

Hori¹,

Kadota²,

Akaike³

2015

gpb

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Abstract. Chronic treatment of rats with methamphetamine (MAP) causes a range of functional changes to the central nervous system (CNS), including a toxicity that is widespread throughout the brain (Frost and Cadet 2000;Fasihpour et al. 2013). In this report, we examined the effect of chronic MAP treatment on pyramidal neurons of the rat piriform cortex, an area involved in sensory processing, associative learning and a model system for studies on synaptic plasticity. MAP treatment significantly depolarized the membrane potential and decreased neuronal input resistance. Furthermore, the voltage-dependence of both AMPA and NMDA responses was disturbed by chronic MAP treatment, and the extent of long-term potentiation (LTP) was decreased. Morphological changes of MAP-treated rat pyramidal neurons were observed as blebbing of the dendrite trees. The changes we observed represent detrimental effects on the function of piriform cortical neurons further illustrating deficits in synaptic plasticity extend beyond the hippocampus. These changes may contribute to behavioural deficits in chronic MAP-treated animals.

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NMDA receptors in the medial prefrontal cortex and the dorsal hippocampus regulate methamphetamine-induced hyperactivity and extracellular amino acid release in mice

Cited by 17 publications

References 84 publications

Insular neural system controls decision-making in healthy and methamphetamine-treated rats

Insular neural system controls decision-making in healthy and methamphetamine-treated rats

Prefrontal glutamate correlates of methamphetamine sensitization and preference

Functional changes in piriform cortex pyramidal neurons in the chronic methamphetamine-treated rat

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