The dopaminergic, glutamatergic, GABAergic bases for the action of amphetamine and cocaine

Karler, Ralph; Calder, Larry D.; Thai, Lam H.; Bedingfield, J.Brent

doi:10.1016/0006-8993(94)01334-e

Cited by 67 publications

(24 citation statements)

References 16 publications

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“…6 A). It has been shown that stereotyped patterns of behavior that result from drug sensitization can be blocked by antagonists or induced by agonists of the GABAergic system (Karler et al, 1995); thus, it is possible that this behavior arises as a result of the alterations in GABAergic transmission observed in the frontal cortex (Karler et al, 1997) …”

Section: Altered Neuroligin 2 Expression Leads To Spontaneous Stereotmentioning

confidence: 99%

Synaptic Imbalance, Stereotypies, and Impaired Social Interactions in Mice with Altered Neuroligin 2 Expression

Hines¹,

Wu²,

Hines³

et al. 2008

Journal of Neuroscience

168

173

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The level of excitation in the brain is kept under control through inhibitory signals mainly exerted by GABA neurons. However, the molecular machinery that regulates the balance between excitation and inhibition (E/I) remains unclear. Candidate molecules implicated in this process are neuroligin (NL) adhesion molecules, which are differentially enriched at either excitatory or inhibitory contacts. In this study, we use transgenic mouse models expressing NL1 or NL2 to examine whether enhanced expression of specific NLs results in synaptic imbalance and altered neuronal excitability and animal behavior. Our analysis reveals several abnormalities selectively manifested in transgenic mice with enhanced expression of NL2 but not NL1. A small change in NL2 expression results in enlarged synaptic contact size and vesicle reserve pool in frontal cortex synapses and an overall reduction in the E/I ratio. The frequency of miniature inhibitory synaptic currents was also found to be increased in the frontal cortex of transgenic NL2 mice. These animals also manifested stereotyped jumping behavior, anxiety, impaired social interactions, and enhanced incidence of spike-wave discharges, as depicted by EEG analysis in freely moving animals. These findings may provide the neural basis for E/I imbalance and altered behavior associated with neurodevelopmental disorders.

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Section: Altered Neuroligin 2 Expression Leads To Spontaneous Stereotmentioning

confidence: 99%

Synaptic Imbalance, Stereotypies, and Impaired Social Interactions in Mice with Altered Neuroligin 2 Expression

Hines¹,

Wu²,

Hines³

et al. 2008

Journal of Neuroscience

168

173

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“…The behavioral activating effects of AMPH are thought to depend primarily on its ability to increase dopamine release in the terminal regions of the mesoaccumbens and neostriatum [16]. In addition, by regulating dopamine release in the midbrain, glutamate also plays an important role in regulation of motor activity [32].…”

Section: Introductionmentioning

confidence: 99%

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

Chiu

2005

Brain Research Bulletin

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Repeated intermittent exposure to psychostimulants was found to produce behavioral sensitization. The present study was designed to establish a mouse model and by which to investigate whether opioidergic system plays a role in methamphetamine-induced behavioral sensitization. Mice injected with 2.5 mg/kg of methamphetamine once a day for 7 consecutive days showed behavioral sensitization after challenge with 0.3125 mg/kg of the drug on day 11, whereas mice injected with a lower daily dose (1.25 mg/kg) did not. Mice received daily injections with either 1.25 or 2.5 mg/kg of methamphetamine showed behavioral sensitization after challenge with 1.25 mg/kg of the drug on days 11, 21, and 28. To investigate the role of opioidergic system in the induction and expression of behavioral sensitization, long-acting but non-selective opioid antagonist naltrexone was administrated prior to the daily injections of and challenge with methamphetamine, respectively. Our results show that the expressions of behavioral sensitization were attenuated by pretreatment with 10 or 20 mg/kg of naltrexone either during the induction period or before methamphetamine challenge when they were tested on days 11 and 21. These results indicate that repeated injection with methamphetamine dose-dependently induced behavioral sensitization in mice, and suggest the involvement of opioid receptors in the induction and expression of methamphetamine-induced behavioral sensitization.

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“…Furthermore, it is now understood that other neurotransmitters, particularly glutamate and ␥ -aminobutyric acid (GABA), play a key role in the development and maintenance of behavioral sensitization [39,[52][53][54] . Descending glutamatergic neurons from the medial prefrontal cortex project to medium spiny neurons of the NAc and Str [55 ; for reviews, see ref.…”

Section: Changes In Gene Expression Following Recurrent Psychostimulamentioning

confidence: 99%

Augmented Constitutive CREB Expression in the Nucleus accumbens and Striatum May Contribute to the Altered Behavioral Response to Cocaine of Adult Mice Exposed to Cocaine in utero

et al. 2005

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Neuroadaptations occurring in the mesolimbic dopamine pathway following recurrent exposure to drugs of abuse have been correlated with a behavioral phenomenon known as behavioral sensitization. We have developed an animal model of prenatal cocaine exposure and, using a postnatal sensitization protocol, have examined the subsequent sensitivity of offspring to cocaine. Pregnant Swiss Webster dams were injected twice daily from embryonic day 8 to 17, inclusive, with cocaine (COC40: administered cocaine HCl at a dose of 40 mg/kg/day, and COC20: administered cocaine HCl at a dose of 20 mg/kg/day), or saline (SAL). The SPF40 group (saline pair-fed), a nutritional control group, was ‘pair-fed’ with COC40 dams. Activity was recorded for 30 min during a 3-day saline habituation, a 14-day ‘initiation’ phase, when animals received cocaine (15 mg/kg) or saline every other day, and following a 21-day ‘withdrawal’ period when all mice were challenged with cocaine. COC40 offspring, as compared with SAL controls, did not habituate to a novel environment, demonstrated increased cocaine-induced stereotypy on Coc 1 (first cocaine injection), and blunted locomotor sensitization on challenge as measured by the percentage of each animal’s baseline locomotion. Tissue samples of the nucleus accumbens (NAc) and striatum (Str) of all four prenatal treatment groups were examined to determine whether alterations in the transcription factor CREB or glutamate receptor subunit, GluR1, induced by prenatal cocaine treatment may have contributed to the altered behavioral responses. Immunoblot quantitation revealed significantly increased constitutive CREB expression in the NAc and Str of COC40 mice as compared with SAL controls. Such alterations in constitutive CREB levels may contribute to some of the behavioral differences reported in adult mice exposed to cocaine in utero.

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The dopaminergic, glutamatergic, GABAergic bases for the action of amphetamine and cocaine

Cited by 67 publications

References 16 publications

Synaptic Imbalance, Stereotypies, and Impaired Social Interactions in Mice with Altered Neuroligin 2 Expression

Synaptic Imbalance, Stereotypies, and Impaired Social Interactions in Mice with Altered Neuroligin 2 Expression

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

Augmented Constitutive CREB Expression in the Nucleus accumbens and Striatum May Contribute to the Altered Behavioral Response to Cocaine of Adult Mice Exposed to Cocaine in utero

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