The role of the frontal cortex in the mouse in behavioral sensitization to amphetamine

Karler, Ralph; Bedingfield, J.Brent; Thai, David K.; Calder, Larry D.

doi:10.1016/s0006-8993(97)00221-7

Cited by 62 publications

(39 citation statements)

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“…There are data from electrophysiological studies that point to the GABAergic interneurons as critical mediators of dopamine-glutamate interactions in the mPFC (Seamans et al, 2001;Tseng and O'Donnell, 2004; and, from other studies, that changes in GABA transmission are associated with the development of sensitization to cocaine or AMPH (Karler et al, 1997;Jayaram and Steketee, 2005). However, no investigation has shown a laminaspecific activation of inhibitory interneurons with acute or repeated exposure to drug.…”

Section: Discussionmentioning

confidence: 99%

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

“…This means that PV+ cell activation can contribute to the silencing of pyramidal neuron activity in a layer-specific manner (Gonzalez-Islas and Hablitz, 2001;Gulledge and Jaffe, 2001;Seamans et al, 2001;Tseng and O'Donnell, 2004;. Following drug administration, there are data to implicate GABA transmission in the motor stimulant response (Karler et al, 1997;Bartoletti et al, 2005); however, no studies differentiate the regional or lamina-specific effects of inhibitory interneurons.Dopaminergic terminals from VTA neurons form dense contacts onto interneurons in layers V and VI (Sesack et al, 1995) and excitatory afferents from limbic and thalamic regions innervate specific layers where they contact both PV+ interneurons and pyramidal cells (Gabbott et al, 2002;Rotaru et al, 2005;Gabbott et al, 2006). Since layer III pyramidal neurons connect the mPFC to other cortices, and layer V and VI pyramidal cells project primarily to subcortical targets (Jones, 1984;Gabbott et al, 2005), PV+ interneurons are ideally positioned to shape the receptive fields of pyramidal cells in a layer-specific manner.…”

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Differential laminar effects of amphetamine on prefrontal parvalbumin interneurons

Morshedi

Meredith

2007

Neuroscience

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The increase in excitatory outflow from the medial prefrontal cortex is critical to the development of sensitization to amphetamine. There is evidence that psychostimulant-induced changes in dopamine-GABA interactions are key to understanding the behaviorally sensitized response. The objective of this study was to characterize the effects of different amphetamine paradigms on the Fos activation of GABAergic interneurons that contain parvalbumin in the medial prefrontal cortex. Although a sensitizing, repeated regimen of amphetamine induced Fos in all cortical layers, only layer V parvalbumin-immunolabeled cells were activated in the infralimbic and prelimbic cortices. Repeated amphetamine treatment was also associated with a loss of parvalbumin immunoreactivity in layer V, but only in the prelimbic cortex. An acute amphetamine injection to naïve rats was associated with an increase in Fos, but in parvalbumin-positive neurons of the prelimbic cortex, where it was preferentially induced in layer III. These data indicate that distinct substrates mediate the response to repeated or acute amphetamine treatment. They also suggest that a sensitizing amphetamine regimen directs mPFC outflow, via changes in inhibitory neuron activation, towards subcortical centers important in reward.Keywords prelimbic cortex; infralimbic cortex; GABA; dopamine; Fos; behavioral sensitization Repeated amphetamine (AMPH) exposure in humans has been associated with long-lasting changes in behavior (Robinson and Berridge, 2000). In experimental animals, such treatment progressively augments locomotion (behavioral sensitization), an effect that persists after treatment and can be measured by a drug challenge (Wolf, 1998). Sensitization to AMPH appears to require changes in dopamine and excitatory amino acid transmission in the medial prefrontal cortex (mPFC) and ventral tegmental area (VTA) (Wolf et al., 1995;Li and Wolf, 1997;Tzschentke and Schmidt, 2000;Wolf et al., 2003). Lesions of the mPFC block the development of sensitization, whether AMPH is repeatedly injected systemically or intra-VTA (Wolf et al., 1995;Li and Wolf, 1997;Cador et al., 1999; but see Tzschentke and Schmidt, 2000). AMPH sensitization also induces region-specific increases in mPFC Fos expression (Hedou et al., 2002), although the active neurons have yet to be fully identifed.Correspondence should be addressed to Maud M. Morshedi, Department of Cellular and Molecular Pharmacology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL 60064, USA, (maud.morshedi@students.rosalindfranklin.edu). Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could ...

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Section: Discussionmentioning

confidence: 99%

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

mentioning

confidence: 99%

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Differential laminar effects of amphetamine on prefrontal parvalbumin interneurons

Morshedi

Meredith

2007

Neuroscience

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“…The EVH1 domain exhibits a high degree of similarity across Homer isoforms and is essential for Homer interactions with a proline-rich sequence (PPSPF) displayed by proteins regulating drug-induced alterations in neuronal morphology, synaptic architecture, and glutamate receptor signaling/intracellular calcium dynamics. Of particular relevance to drug-induced neuroplasticity [e.g., 20,73,74,[78][79][80][81][82][89][90][91][92][93][94][95][96][97][98][99][100][123][124][125][126][127][128][129][130], these proteins include the mGluR1a and mGluR5 subtypes of Group 1 metabotropic glutamate receptors (mGluRs) [34,102,104,107,[131][132][133][134][135][136][137], the NMDA glutamate receptor scaffolding protein Shank [38,132,138,139], the inositol-1,4,5-triphosphate (IP3) receptor, a down-stream mediator of Group1 mGluR signaling [133,[140]…”

Section: Molecular Aspects Of Homer Proteinsmentioning

confidence: 99%

“…Acamprosate, a mixed antagonist at the NMDA ionotropic glutamate receptor (iGluR) and the mGluR5 subtype of the Group1 metabotropic glutamate receptor (mGluR) [71,72], is clinically effective at treating alcoholism [73,74] and may prove to be effective for treating psychomotor stimulant and opiate addiction [75,76]. Moreover, direct pharmacological manipulation of glutamate receptors within the PFC or the NAC result in reduced behavioral responsiveness to various drugs of abuse, including cocaine [48,50,53,[77][78][79]; but see 80], alcohol [e.g., 44, 81,82], amphetamines [e.g., [83][84][85][86][87][88][89] and opiates [90-92, but see 79], and systemic administration of antagonists of glutamate receptors blocks several aspects of nicotine reward in laboratory animals [e.g., 93-100, but see 101]. Taken together, these data pose cellular factors regulating pre-and postsynaptic aspects of corticoaccumbens glutamatergic transmission as likely molecular candidates contributing to an addicted phenotype.…”

Section: Introductionmentioning

confidence: 99%

Homers regulate drug-induced neuroplasticity: Implications for addiction

Szumlinski

Ary

Lominac

2008

Biochemical Pharmacology

118

160

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Drug addiction is a chronic, relapsing disorder, characterized by an uncontrollable motivation to seek and use drugs. Converging clinical and preclinical observations implicate pathologies within the corticolimbic glutamate system in the genetic predisposition to, and the development of, an addicted phenotype. Such observations pose cellular factors regulating glutamate transmission as likely molecular candidates in the etiology of addiction. Members of the Homer family of proteins regulate signal transduction through, and the trafficking of, glutamate receptors, as well as maintain and regulate extracellular glutamate levels in corticolimbic brain regions. This review summarizes the existing data implicating the Homer family of protein in acute behavioral and neurochemical sensitivity to drugs of abuse, the development of drug-induced neuroplasticity, as well as other behavioral and cognitive pathologies associated with an addicted state.

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Both glutamate receptor antagonists and prefrontal cortex lesions prevent induction of cocaine sensitization and associated neuroadaptations

Berney

et al. 1999

Synapse

160

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Behavioral sensitization to psychomotor stimulants is accompanied by a number of alterations in the mesoaccumbens dopamine (DA) system, including DA autoreceptor subsensitivity in the ventral tegmental area (VTA) and DA D1 receptor supersensitivity in the nucleus accumbens (NAc). We investigated the role of excitatory amino acid (EAA) transmission in the induction of cocaine sensitization and these accompanying DA receptor alterations. To do so, we used three glutamate receptor antagonists, the noncompetitive NMDA receptor antagonist MK-801 (0.1 mg/kg), the competitive NMDA receptor antagonist CGS 19755 (10.0 mg/kg), and the AMPA receptor antagonist NBQX (12.5 mg/kg). Rats received daily double injections of either one of these antagonists or saline with either cocaine (15.0 mg/kg) or saline for 5 days. Cocaine sensitization was defined as an increase in horizontal locomotor activity in response to cocaine challenge (7.5 mg/kg) on the third day of withdrawal. All three antagonists prevented the induction of cocaine sensitization. Extracellular single cell recordings revealed that these antagonists also prevented the induction of DA autoreceptor subsensitivity in the VTA and DA D1 receptor supersensitivity in the NAc. To determine whether the relevant glutamate receptors were under regulation by medial prefrontal cortex (mPFC) EAA efferents, we next lesioned the mPFC bilaterally with ibotenic acid at least 7 days before repeated cocaine treatment began. These lesions also prevented the induction of cocaine sensitization and the associated neuroadaptations. Our findings indicate that glutamate transmission from mPFC to the mesoaccumbens DA system is critical for the induction of cocaine sensitization and its cellular correlates.

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The role of the frontal cortex in the mouse in behavioral sensitization to amphetamine

Cited by 62 publications

References 30 publications

Differential laminar effects of amphetamine on prefrontal parvalbumin interneurons

Differential laminar effects of amphetamine on prefrontal parvalbumin interneurons

Homers regulate drug-induced neuroplasticity: Implications for addiction

Both glutamate receptor antagonists and prefrontal cortex lesions prevent induction of cocaine sensitization and associated neuroadaptations

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