Amphetamine-induced hyperlocomotion in rats: Hippocampal modulation of the nucleus accumbens

White, Ilsun M.; Whitaker, Christopher J.; White, Wesley

doi:10.1002/hipo.20189

Cited by 29 publications

(32 citation statements)

References 41 publications

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“…; Figure 3). This agrees with previous data (Bardgett and Henry, 1999 ;Rouillon et al, 2007 ;White et al, 2006). In contrast with these findings, Flicker and Geyer (1982) reported that infusion of lidocaine into DH reduced basal locomotor activity.…”

Section: Histologycontrasting

confidence: 45%

“…For instance, while previous studies have reported that massive lesion of the hippocampus or the fimbria-fornix, a subcortical area that mediates most of the hippocampal output signals, increased hyperlocomotion induced by acute amphetamine (Coutureau et al, 2000 ;Mittlemann et al, 1998 ;Schaub et al, 1997 ;Wilkinson et al, 1993 ;Wolf et al, 1995), others have found a reduction of hyperlocomotion to acute amphetamine following lesion of the hippocampus or the fimbria-fornix (Burns et al, 1993 ;White et al, 2006) or no effect (Bannerman et al, 2003 ;Bardgett and Henry, 1999). Similarly, discrete excitotoxic lesion or inhibition of DH by lidocaine has been reported to increase hyperlocomotion induced by acute amphetamine, whereas inhibition of VH has been shown to block it (Burns et al, 1993 ;Caine et al, 2001 ;White et al, 2006), thereby suggesting that DH and VH may exert respectively, in normal conditions, an inhibitory and a facilitatory action on the motor-activating properties of amphetamine. However, others have found that electrolytic lesion of VH potentiated rather than reduced hyperlocomotion to acute amphetamine (Riegert et al, 2004).…”

Section: Introductionmentioning

confidence: 96%

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Modulation by the dorsal, but not the ventral, hippocampus of the expression of behavioural sensitization to amphetamine

Degoulet¹,

Rostain²,

David³

et al. 2007

Int. J. Neuropsychopharm.

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Although the dorsal hippocampus (DH) and the ventral hippocampus (VH) densely innervate the nucleus accumbens, which mediates the expression of behavioural sensitization, the respective and specific contribution of DH and VH in the expression of behavioural sensitization to amphetamine has not been investigated. In the present study, we investigated how lidocaine infused in DH or VH modulated behavioural locomotor sensitization induced by repeated administration of systemic amphetamine. Rats, well habituated to their environmental conditions and experimental protocol, were given repeated administration of systemic amphetamine. Once behavioural sensitization was developed, rats were challenged with amphetamine and infused with saline (controls) or lidocaine into DH or VH. We found that reversible inhibition by lidocaine of DH, but not VH, blocks the expression of behavioural sensitization to amphetamine. Control animals injected with saline solution do express behavioural sensitization. Our results bring new insights on the role of the hippocampus complex in the expression of behavioural sensitization, indicating that, in individuals well habituated to the drug-associated context, DH but not VH would play a key role. The results provide experimental evidence for clinical studies in human addicts that have demonstrated that exposure to environmental stimuli associated with drug-taking behaviour elicits craving and can promote relapse, and further suggest that in drug abusers, once addiction has occurred, the contextual and spatial conditions that are associated with drug consumption may play a critical role in the maintenance of drug abuse.

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Section: Histologycontrasting

confidence: 45%

Section: Introductionmentioning

confidence: 96%

Modulation by the dorsal, but not the ventral, hippocampus of the expression of behavioural sensitization to amphetamine

Degoulet¹,

Rostain²,

David³

et al. 2007

Int. J. Neuropsychopharm.

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“…3B). By modulating activity within the limbic basal ganglia, ventral hippocampal activity can drive medial striatal DA release (13,14) and behaviors mediated by this system, including the locomotor response to AMPH (23,24). Consistent with this function of the hippocampus, Ccnd2 −/− mice showed a dose-dependent increase in AMPH-induced locomotion ( Fig.…”

Section: Increases In Mesolimbic Da Neuron Population Activity and Rementioning

confidence: 65%

Interneuron precursor transplants in adult hippocampus reverse psychosis-relevant features in a mouse model of hippocampal disinhibition

Gilani

Chohan²,

Inan

et al. 2014

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

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GABAergic interneuron hypofunction is hypothesized to underlie hippocampal dysfunction in schizophrenia. Here, we use the cyclin D2 knockout (Ccnd2 −/− ) mouse model to test potential links between hippocampal interneuron deficits and psychosis-relevant neurobehavioral phenotypes. Ccnd2 −/− mice show cortical PV + interneuron reductions, prominently in hippocampus, associated with deficits in synaptic inhibition, increased in vivo spike activity of projection neurons, and increased in vivo basal metabolic activity (assessed with fMRI) in hippocampus. Ccnd2 −/− mice show several neurophysiological and behavioral phenotypes that would be predicted to be produced by hippocampal disinhibition, including increased ventral tegmental area dopamine neuron population activity, behavioral hyperresponsiveness to amphetamine, and impairments in hippocampus-dependent cognition. Remarkably, transplantation of cells from the embryonic medial ganglionic eminence (the major origin of cerebral cortical interneurons) into the adult Ccnd2 −/− caudoventral hippocampus reverses these psychosisrelevant phenotypes. Surviving neurons from these transplants are 97% GABAergic and widely distributed within the hippocampus. Up to 6 mo after the transplants, in vivo hippocampal metabolic activity is lowered, context-dependent learning and memory is improved, and dopamine neuron activity and the behavioral response to amphetamine are normalized. These findings establish functional links between hippocampal GABA interneuron deficits and psychosis-relevant dopaminergic and cognitive phenotypes, and support a rationale for targeting limbic cortical interneuron function in the prevention and treatment of schizophrenia.parvalbumin | temporal lobe-dependent cognition | neural stem cell therapy | functional magnetic resonance imaging | contextual fear conditioning P recursors of most γ-aminobutyric acid (GABA)-releasing interneurons of the cerebral cortex and the hippocampus originate in the embryonic medial ganglionic eminence (MGE) (1-3). A subpopulation of MGE-derived cells differentiates into fast-spiking, parvalbumin-expressing (PV +

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“…Moreover, vHipp activation has been shown to increase the behavioral response to amphetamine in normal rats (White et al, 2006). Therefore, we propose that the source of amphetamine hyper-responsivity may be attributed to vHipp-induced enhancement of baseline DA neuron population activity.…”

Section: Discussionmentioning

confidence: 78%

Aberrant Hippocampal Activity Underlies the Dopamine Dysregulation in an Animal Model of Schizophrenia

2007

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Evidence supports a dysregulation of subcortical dopamine (DA) system function as a common etiology of psychosis; however, the factors responsible for this aberrant DA system responsivity have not been delineated. Here, we demonstrate in an animal model of schizophrenia that a pathologically enhanced drive from the ventral hippocampus (vHipp) can result in aberrant dopamine neuron signaling. Adult rats in which development was disrupted by prenatal methylazoxymethanol acetate (MAM) administration display a significantly greater number of spontaneously firing ventral tegmental DA neurons. This appears to be a consequence of excessive hippocampal activity because, in MAM-treated rats, vHipp inactivation completely reversed the elevated DA neuron population activity and also normalized the augmented amphetamine-induced locomotor behavior. These data provide a direct link between hippocampal dysfunction and the hyper-responsivity of the DA system that is believed to underlie the augmented response to amphetamine in animal models and psychosis in schizophrenia patients.

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Amphetamine-induced hyperlocomotion in rats: Hippocampal modulation of the nucleus accumbens

Cited by 29 publications

References 41 publications

Modulation by the dorsal, but not the ventral, hippocampus of the expression of behavioural sensitization to amphetamine

Modulation by the dorsal, but not the ventral, hippocampus of the expression of behavioural sensitization to amphetamine

Interneuron precursor transplants in adult hippocampus reverse psychosis-relevant features in a mouse model of hippocampal disinhibition

Aberrant Hippocampal Activity Underlies the Dopamine Dysregulation in an Animal Model of Schizophrenia

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