Dopaminergic agonists administered into the nucleus accumbens: Effects on extracellular glutamate and on locomotor activity

Dalia, Asad; Uretsky, Norman J.; Wallace, Lane J.

doi:10.1016/s0006-8993(97)01518-7

Cited by 57 publications

(41 citation statements)

References 33 publications

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“…In an interesting report, Kalivas et al declared that SCH 23390 and sulpiride restore the amphetamine-induced glutamate level decrease in NAc suggesting the involvement of presynaptic dopamine receptors in this phenomenon [36]. Furthermore, Dalia et al indicated that dopamine increases the extracellular glutamate levels in the NAc [18]. Meanwhile, activation of glutamate receptor increases the dopamine release in the NAc [31].…”

Section: Effects Of Intra-nac Shell Nmda Administration On Anxiolyticmentioning

confidence: 99%

Original article Involvement of D 2 /D 2 dopamine antagonists upon open-arms exploratory behaviours induced by intra-nucleus accumbens shell administration of N-methyl-D-aspartate

Razavi¹,

Haeri-Rohani²,

Eidi³

et al. 2014

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Section: Effects Of Intra-nac Shell Nmda Administration On Anxiolyticmentioning

confidence: 99%

Original article Involvement of D 2 /D 2 dopamine antagonists upon open-arms exploratory behaviours induced by intra-nucleus accumbens shell administration of N-methyl-D-aspartate

Razavi¹,

Haeri-Rohani²,

Eidi³

et al. 2014

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“…The ionotropic glutamate receptors are classified into three types, that is, N-methyl-D-aspartic acid (NMDA), α-amino-3-hydro-5-methyl-4-isoxazolpropionic acid (AMPA), and kainate receptors (30). Glutamatergic agonists have been found to enhance dopamine release in the Nacc, possibly via non-NMDA receptors (31), whereas accumbal dopamine has been found to increase extracellular glutamate levels in the Nacc (32). In behavioral studies, agonists of the glutamatergic ionotropic receptors, AMPA and NMDA receptors, have been found to stimulate locomotor activity when injected into the Nacc, and drugs that inhibit dopaminergic neurotransmission have been found to inhibit these effects (33,34).…”

Section: Glutamatementioning

confidence: 99%

“…It has been suggested that stimulation of presynaptic dopaminergic receptors on glutamatergic terminals elicits contraversive pivoting identical to that elicited by stimulation of AMPA receptors in the Nacc shell (32,35) because accumbal dopamine is known to increase the release of accumbal glutamate (32).…”

Section: Glutamatementioning

confidence: 99%

Nucleus Accumbens and Dopamine-Mediated Turning Behavior of the Rat: Role of Accumbal Non-dopaminergic Receptors

et al. 2012

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Abstract. Accumbal dopamine plays an important role in physiological responses and diseases such as schizophrenia, Parkinson's disease, and depression. Since the nucleus accumbens contains different neurotransmitters, it is important to know how they interact with dopaminergic function: this is because modifying accumbal dopamine has far-reaching consequences for the treatment of diseases in which accumbal dopamine is involved. This review provides a summary of these interactions, and our current knowledge about them are as follows: A) AMPA receptors are required for dopamine-dependent behavior and vice versa; NMDA receptors modulate the activity at the level of AMPA and/or dopamine D 1 receptors. B) GABA A , but not GABA B , receptors inhibit dopamine-dependent behavior. C) Nicotinic receptors are required for dopamine-dependent behavior, whereas muscarinic receptors inhibit dopamine-dependent behavior. D) α-Adrenoceptors inhibit dopamine-dependent behavior in contrast to β-adrenoceptors, which potentiate this behavior. E) μ-and δ 2 -opioid receptors elicit behavior that requires an intact dopaminergic function and δ 2 -opioid receptors modulate dopamine-dependent behavior. F) Orexin 2 receptors play an important, modifying role in dopamine-dependent behavior. G) Somatostatin receptors potentiate dopamine-dependent behavior. It is suggested that modulation of the above-mentioned nondopaminergic receptors provide new tools to control physiological functions as well as diseases mediated by accumbal dopamine.

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“…Following stimulant drug administration, D1 and D3 receptors exert opposing effects on intracellular signaling pathways and gene expression through opposite regulatory effects on extracellular signalregulated kinase (ERK) activity and expression of Fos family genes (Zhang et al, 2004). Behaviorally, although acute concurrent D1/D2 dopamine receptor activation stimulates rodent locomotion (Dalia et al, 1998;Dreher and Jackson, 1989), D3 receptor stimulation inhibits both novelty-stimulated locomotion Xu et al, 1997;Menalled et al, 1999;Ekman et al, 1998;Accili et al, 1996) and AMPH-stimulated locomotion (Waters et al, 1993). One model, as presented in this paper, suggests the loss of a D3 receptor-mediated 'brake' on these behaviors would be expressed as the emergence of augmented locomotor response to novelty and AMPH in rodents, and might also be expressed as paranoid psychotic symptoms in humans.…”

Section: Dopamine and Behavioral Sensitizationmentioning

confidence: 99%

Behavioral Sensitization, Alternative Splicing, and D3 Dopamine Receptor-Mediated Inhibitory Function

Richtand

2006

Neuropsychopharmacol

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Behavioral sensitization, the progressive and enduring augmentation of certain behaviors following repetitive drug use, alters rodent locomotion in a long-standing manner. The same dopamine pathways playing an important role in drug dependence and psychosis also play a critical role in sensitization. Individual dopamine receptor subtypes have markedly different functional responses to stimulation, with D3 dopamine receptor stimulation inhibiting rodent locomotion. The D3 receptor has highest affinity of the dopamine receptor subtypes for dopamine, and is occupied to a greater degree following stimulant drug administration. D3 receptor activity may be regulated through the expression of an alternatively spliced, truncated receptor isoform (termed 'D3nf') altering receptor localization and function via dimerization with the full-length subunit. The expected physiological response to repetitive drug administration is tolerance. Tolerance of D3 receptor inhibition of locomotion would contribute to sensitization to stimulant drugs. We hypothesize that repetitive D3 receptor stimulation contributes to the development of behavioral sensitization through decreased responsivity of D3-receptor-mediated locomotor inhibition. Increased D3nf expression may direct altered receptor localization and subsequent release of D3-receptormediated inhibition, contributing to the expression of sensitization. These hypotheses follow directly from the affinities of the receptor subtypes for dopamine; dopamine concentrations following stimulant administration; the effects of individual dopamine receptor subtype stimulation on locomotion; and the expected homeostatic response of the system to perturbation by drug. Clarifying these mechanisms underlying sensitization may suggest new interventions for neuropsychiatric conditions in which dopamine plays an important role, including psychosis, drug dependence, and Parkinson's disease. This information may also elucidate a previously unrecognized mechanism regulating receptor trafficking and desensitization.

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Dopaminergic agonists administered into the nucleus accumbens: Effects on extracellular glutamate and on locomotor activity

Cited by 57 publications

References 33 publications

Original article Involvement of D 2 /D 2 dopamine antagonists upon open-arms exploratory behaviours induced by intra-nucleus accumbens shell administration of N-methyl-D-aspartate

Original article Involvement of D 2 /D 2 dopamine antagonists upon open-arms exploratory behaviours induced by intra-nucleus accumbens shell administration of N-methyl-D-aspartate

Nucleus Accumbens and Dopamine-Mediated Turning Behavior of the Rat: Role of Accumbal Non-dopaminergic Receptors

Behavioral Sensitization, Alternative Splicing, and D3 Dopamine Receptor-Mediated Inhibitory Function

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