Molecular and behavioral effects mediated by Gs-coupled adenosine A2a, but not serotonin 5-HT4 or 5-HT6 receptors following antipsychotic administration

Ward, Raymond P.; Dorsa, Daniel M.

doi:10.1016/s0306-4522(98)00364-9

Cited by 34 publications

(13 citation statements)

References 49 publications

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“…For instance, the reversal of haloperidol-induced catalepsy by 5-HT 2 antagonists occurs independently from changes in DA release . Conversely, while 5-HT 4 antagonists reduce morphine-or haloperidol-induced striatal DA release, 5-HT 4 antagonists do not affect haloperidolinduced catalepsy and morphine-induced catatonia (De Deurwaerdère et al 2002;Ward and Dorsa 1999). Thus, although various striatal 5-HT receptors are able to affect behaviors related to striatal DA dysfunction such as dyskinesia, catalepsy, stereotypies, locomotor activity, or even addiction, the picture is still unclear Soubrié et al 1984).…”

Section: Discussionmentioning

confidence: 99%

Presynaptic control of serotonin on striatal dopamine function

Navailles

Deurwaerdère

2010

Psychopharmacology

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Section: Discussionmentioning

confidence: 99%

Presynaptic control of serotonin on striatal dopamine function

Navailles

Deurwaerdère

2010

Psychopharmacology

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“…Both increased Fos expression and NT neurotransmission in the dorsolateral striatum have been linked to the EPSE liability of APDs (Adams et al, 1997;Decker et al, 1995;Shibata et al, 1987;Ward and Dorsa, 1999). NT receptor antagonism and a genetically disrupted NT neurotransmission both decrease haloperidol-induced Fos expression in the dorsolateral CPu but do not have an effect on haloperidol-induced catalepsy .…”

Section: Discussionmentioning

confidence: 99%

Neurotensin Receptor Antagonist SR 142948A Alters Fos Expression and Extrapyramidal Side Effect Profile of Typical and Atypical Antipsychotic Drugs

Binder

Kinkead

Owens

et al. 2004

Neuropsychopharmacol

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Antipsychotic drugs (APDs) have previously been shown to alter Fos expression in a regionally specific manner. Increases in Fos expression in the nucleus accumbens (NAcc) are common to all clinically effective APDs. In contrast, APD-induced Fos expression increases in the caudate-putamen (CPu) and prefrontal cortex (PFC) are associated with the extrapyramidal side effect liability of typical APDs or the effectiveness against negative symptoms of atypical APDs, respectively. Considerable evidence suggests that the neuropeptide neurotensin (NT) mediates some of the effects of APDs. To determine whether NT neurotransmission is also involved in APD-induced Fos expression in brain regions relevant for therapeutic efficacy, the NT receptor antagonist SR 142948A (10 or 100 mg/ kg i.p.) was coadministered with APDs (haloperidol (2.0 mg/kg s.c.), olanzapine (5 mg/kg i.p.), or clozapine (20 mg/kg s.c.)). Fos expression was evaluated in the PFC, NAcc shell, dorsomedial, and dorsolateral CPu and the lateral septum. SR 142948A attenuated haloperidolinduced Fos expression in the CPu but, in contrast, increased olanzapine-induced Fos expression in this brain region. The effects of the NT receptor antagonist were paralleled by its effects on catalepsy in olanzapineFbut not haloperidolFtreated animals.

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“…This has been shown in several experimental models including rodents pretreated with D 2 receptor antagonists, reserpine, 6-OH-dopamine or MPTP or after genetic inactivation of D 2 receptors (Kanda et al, 1994;Pollack and Fink, 1995;Shiozaki et al, 1999;Ward and Dorsa, 1999;Chen et al, 2001, Ferré et al, 2001Hauber et al, 2001;Wardas et al, 2001) or MPTP-treated monkeys (Kanda et al, 1998;Grondin et al, 1999). Reserpinized mice, rats with unilateral 6-OH-dopamine lesions and MPTP-treated monkeys are well-established validated models of Parkinson's disease.…”

Section: Adenosine a 2a Receptors In The Ventral Striatum And The Acumentioning

confidence: 92%

Adenosine A2A receptors in ventral striatum, hypothalamus and nociceptive circuitry

Ferré

Diamond

Goldberg

et al. 2007

Progress in Neurobiology

127

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Adenosine A 2A receptors localized in the dorsal striatum are considered as a new target for the development of antiparkinsonian drugs. Co-administration of A 2A receptor antagonists has shown a significant improvement of the effects of L-DOPA. The present review emphasizes the possible application of A 2A receptor antagonists in pathological conditions other than parkinsonism, including drug addiction, sleep disorders and pain. In addition to the dorsal striatum, the ventral striatum (nucleus accumbens) contains a high density of A 2A receptors, which presynaptically and postsynaptically regulate glutamatergic transmission in the cortical glutamatergic projections to the nucleus accumbens. It is currently believed that molecular adaptations of the cortico-accumbens glutamatergic synapses are involved in compulsive drug seeking and relapse. Here we review recent experimental evidence suggesting that A 2A antagonists could become new therapeutic agents for drug addiction. Morphological and functional studies have identified lower levels of A 2A receptors in brain areas other than the striatum, such as the ventrolateral preoptic area of the hypothalamus, where adenosine plays an important role in sleep regulation. Although initially believed to be mostly dependent on A 1 receptors, here we review recent studies that demonstrate that the somnogenic effects of adenosine are largely mediated by hypothalamic A 2A receptors. A 2A receptor antagonists could therefore be considered as a possible treatment for narcolepsy and other sleep-related disorders. Finally, nociception is another adenosine-regulated neural function previously thought to mostly involve A 1 receptors. Although there is some conflicting literature on the effects of agonists and antagonists, which may partly be due to the lack of selectivity of available drugs, the studies in A 2A receptor knockout mice suggest that A 2A receptor antagonists might have some therapeutic potential in pain states, in particular where high intensity stimuli are prevalent.

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Molecular and behavioral effects mediated by Gs-coupled adenosine A2a, but not serotonin 5-HT4 or 5-HT6 receptors following antipsychotic administration

Cited by 34 publications

References 49 publications

Presynaptic control of serotonin on striatal dopamine function

Presynaptic control of serotonin on striatal dopamine function

Neurotensin Receptor Antagonist SR 142948A Alters Fos Expression and Extrapyramidal Side Effect Profile of Typical and Atypical Antipsychotic Drugs

Adenosine A2A receptors in ventral striatum, hypothalamus and nociceptive circuitry

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