Regional localization of dopamine and ionotropic glutamate receptor subtypes in striatolimbic brain regions

Tarazi, Frank I.; Baldessarini, Ross J.

doi:10.1002/(sici)1097-4547(19990215)55:4<401::aid-jnr1>3.0.co;2-h

Cited by 46 publications

(33 citation statements)

References 78 publications

(93 reference statements)

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“…As D 2 -like and NMDA receptors are often functionally coupled and co-localized on the same neurons in brain [52,54], these data suggest that mood stabilizers that are effective against mania suppress AA signaling coupled to both D 2 -like and NMDA receptors. In this regard lamotrigine, which is preferred for treating bipolar depression and rapid recycling, is considered to act in part by reducing presynaptic glutamate release [22].…”

Section: Discussionmentioning

confidence: 79%

Chronic Carbamazepine Administration Attenuates Dopamine D2-like Receptor-Initiated Signaling via Arachidonic Acid in Rat Brain

et al. 2008

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Observations that dopaminergic antagonists are beneficial in bipolar disorder and that dopaminergic agonists can produce mania suggest that bipolar disorder involves excessive dopaminergic transmission. Thus, mood stabilizers used to treat the disease might act in part by downregulating dopaminergic transmission. In agreement, we reported that dopamine D 2 -like receptor mediated signaling involving arachidonic acid (AA, 20:4n-6) was downregulated in rats chronically treated with lithium. To see whether chronic carbamazepine, another mood stabilizer, did this as well, we injected i.p. saline or the D 2 -like receptor agonist, quinpirole (1 mg/kg), into unanesthetized rats that had been pretreated for 30 days with i.p. carbamazepine (25 mg/kg/day) or vehicle, and used quantitative autoradiography to measure regional brain incorporation coefficients (k*) for AA, markers of signaling. We also measured brain prostaglandin E 2 (PGE 2 ), an AA metabolite. In vehicle-treated rats, quinpirole compared with saline significantly increased k* for AA in 35 of 82 brain regions examined, as well as brain PGE 2 concentration. Affected regions belong to dopaminergic circuits and have high D 2 -like receptor densities. Chronic carbamazepine pretreatment prevented the quinpirole-induced increments in k* and in PGE 2 . These findings are consistent with the hypothesis that effective mood stabilizers generally downregulate brain AA signaling via D 2 -like receptors, and that this signaling is upregulated in bipolar disorder.

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Section: Discussionmentioning

confidence: 79%

Chronic Carbamazepine Administration Attenuates Dopamine D2-like Receptor-Initiated Signaling via Arachidonic Acid in Rat Brain

et al. 2008

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“…Although most striatal NMDA receptors are post-synaptic, there is evidence of pre-synaptic NMDA receptors on corticostriatal terminals [41]. Interestingly, systemic administration of the NMDA receptor antagonist PCP increases glutamate levels in the nucleus accumbens [1].…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

When administered into the nucleus accumbens core or shell, the NMDA receptor antagonist AP-5 reinstates cocaine-seeking behavior in the rat

Famous

Schmidt

Pierce

2007

Neuroscience Letters

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Cocaine craving in human addicts can be elicited by three major factors: environmental cues associated with drug taking, a stressful life-event or re-exposure to cocaine [26]. Drug craving is modeled in rodents and non-human primates using the reinstatement model of cocaine seeking [13,19,39]. The nucleus accumbens plays a major role in mediating the reinstatement of cocaine seeking [27,36]. The nucleus accumbens receives a major dopaminergic projection from the ventral tegmental area (VTA) and glutamatergic projections from the prefrontal cortex, hippocampus and amygdala [5,34,43]. The accumbens is composed of two major subregions, the core and the shell, which have differential afferent and efferent anatomical projections [7,20,21,44]. Functionally, the accumbens shell is considered the more limbic subregion, mediating the acute effects of drug reward [8,35]. In contrast, the core is more involved in the compulsivity of drug addiction [16] and the effects of drug-associated cues [14,18,25]. In terms of cocaine priming-induced reinstatement of drug seeking, dopamine receptors play differential roles in the shell versus the core [2][3][4]. For example, infusion of dopamine receptor antagonists into the accumbens shell, but not the core, attenuates the reinstatement of cocaine-seeking behavior [2][3][4]. Similarly, dopamine receptor agonists promote the reinstatement of cocaine seeking when microinjected into the shell, but not core [4,37]. Collectively, these studies demonstrate that increased dopamine transmission in the nucleus accumbens shell, but not the core, critically mediates the reinstatement of cocaineseeking behavior.The glutamatergic projection from the medial prefrontal cortex (mPFC) to the nucleus accumbens is one of the key anatomical substrates underlying cocaine priming-induced reinstatement of drug seeking [27,37]. There are two major classes of ionotropic glutamate receptors: AMPA/kainate and NMDA. While AMPA receptors in the nucleus accumbens are critically involved in the reinstatement of cocaine-seeking behavior [9,10,30,32,40], there is evidence that NMDA receptors may also play a role. For example, systemic administration of MK-801, an NMDA receptor channel blocker, robustly reinstated cocaine seeking, without an increase in nonspecific operant responding [12, but see also 6]. In a subsequent study, it was found that intra-accumbal administration of the competitive NMDA receptor antagonist, CPP, had no effect on the reinstatement of cocaine seeking when administered either alone or prior 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 affect the content, and all legal disclaimers that apply to the journal pertain. to a systemic...

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“…In vitro experiments, which allow for a more thorough investigation of presynaptic and postsynaptic mechanisms, have supported a presynaptic locus of action for dopamine in modulating synaptic responses, because accumbens neurons do not show consistent changes in input resistance or postsynaptic currents after application of dopamine (O'Donnell and Grace, 1994;Harvey and Lacey, 1996;Nicola et al, 1996). Although dopaminergic afferents do not make clear axoaxonic synaptic contacts on excitatory terminals in the nucleus accumbens (Sesack and Pickel, 1992), dopamine may diffuse extrasynaptically (Garris et al, 1994) to act at receptors reportedly localized on descending cortical terminals in the nucleus accumbens and striatum (Tarazi and Baldessarini, 1999). Additionally, the closely apposed convergence of dopamine terminals and PFC afferents on spiny dendrites of accumbens neurons (Sesack and Pickel, 1992) provides an anatomical basis for postsynaptic integration of dopaminergic and glutamatergic signaling.…”

Section: Mechanisms Of Dopaminergic Modulation Of Pfc Inputsmentioning

confidence: 99%

Dopaminergic Modulation of Prefrontal Cortical Input to Nucleus Accumbens NeuronsIn Vivo

Brady¹,

O’Donnell²

2004

J. Neurosci.

128

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Dopaminergic transmission in the nucleus accumbens has been proposed to modulate the effects of converging excitatory inputs from the cortex, hippocampus, and amygdala. Here, we used in vivo intracellular recording in anesthetized rats to examine the response of nucleus accumbens neurons to stimulation of the prefrontal cortex (PFC) and the ventral tegmental area (VTA). The EPSP elicited in accumbens neurons by PFC stimulation was attenuated by VTA train stimulation in a pattern mimicking dopamine cell burst firing. PFC-elicited EPSPs were smaller in amplitude and faster to decay after VTA stimulation. These changes could not be explained by membrane depolarization alone, because EPSPs evoked during the sustained depolarization after VTA stimulation were significantly smaller than EPSPs evoked during spontaneously occurring up states. Furthermore, no attenuation of PFC-elicited responses was observed during depolarization produced by positive current injection through the recording electrode. Administration of a D 1 antagonist (SCH 23390; 0.5 mg/kg, i.p.) had no effect on the VTA reduction of PFC-elicited responses, whereas administration of a D 2 antagonist (eticlopride; 0.5 mg/kg, i.p.) reversed the reduction of PFC inputs when the analysis was limited to comparisons with spontaneous up states. These results suggest that the ability of PFC inputs to drive accumbens neurons is dampened by dopamine acting primarily at D 2 receptors. Along with previous reports of dopaminergic attenuation of limbic afferents to the accumbens, these findings support the hypothesis that dopamine mediates the selection and integration of excitatory inputs and thus shapes information processing in accumbens output neurons.

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Regional localization of dopamine and ionotropic glutamate receptor subtypes in striatolimbic brain regions

Cited by 46 publications

References 78 publications

Chronic Carbamazepine Administration Attenuates Dopamine D2-like Receptor-Initiated Signaling via Arachidonic Acid in Rat Brain

Chronic Carbamazepine Administration Attenuates Dopamine D2-like Receptor-Initiated Signaling via Arachidonic Acid in Rat Brain

When administered into the nucleus accumbens core or shell, the NMDA receptor antagonist AP-5 reinstates cocaine-seeking behavior in the rat

Dopaminergic Modulation of Prefrontal Cortical Input to Nucleus Accumbens NeuronsIn Vivo

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