Effects of granisetron, a 5-HT3 receptor antagonist, on morphine-induced potentiation of brain stimulation reward

Rompré, Pierre‐Paul; Injoyan, Rita; Hagan, Jim J.

doi:10.1016/0014-2999(95)00497-1

Cited by 10 publications

(5 citation statements)

References 38 publications

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“…Previous studies have demonstrated that systemic administration of a range of doses (0.025-0.2 mg kg -1 ) of ondansetron does not result in any changes in VTA self-stimulation thresholds (Greenshaw 1993a,b), neither does this drug affect medial forebrain bundle self-stimulation (Dunn et al 1991;Gilbert et al 1992;Herberg et al 1993). A recent study reported that granisetron, another 5-HT 3 receptor antagonist, attenuated the reward-enhancing effects of morphine on self-stimulation of a caudal mesencephalic site above the VTA (Rompré et al 1995). In that study, a small increase in thresholds was observed following a 0.003 mg kg -1 dose of granisetron.…”

Section: Discussionmentioning

confidence: 95%

Nicotine-induced decreases in VTA electrical self-stimulation thresholds: blockade by haloperidol and mecamylamine but not scopolamine or ondansetron

Иванова

Greenshaw

1997

Psychopharmacology

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The effects of repeated daily injections of (-)-nicotine (+) hydrogen tartrate (mg kg-1 s.c.) on electrical self-stimulation of the ventral tegmental area were investigated. Nicotine reduced the frequency required to maintain half-maximal response rates with animals responding in rate-frequency threshold tests. Under these conditions, nicotine induced an increase in the total number of self-stimulation responses per session, but had no statistically significant effects on the maximal response rate. These effects of nicotine were observed by the second day of administration of this drug. Acute injections of the D2-like dopamine receptor antagonist haloperidol (0.03 mg kg-1 s.c.) and of the nicotinic acetylcholine receptor antagonist mecamylamine (1 mg kg-1 s.c.) attenuated the effects of nicotine, indicating that the observed effects involve stimulation of D2-like dopamine receptors as a result of nicotinic receptor activation. The muscarinic acetylcholine receptor antagonist scopolamine (3 mg kg-1 s.c.) and the serotonin 5-HT3 receptor antagonist ondansetron (0.01 and 0.1 mg kg-1 s.c.) did not alter the effects of nicotine. The results of this study indicate that repeated daily administration of (-)-nicotine increases the rewarding effects of electrical self-stimulation of the ventral tegmental area. These data are consistent with the proposal that repeated daily injections of nicotine positively effect a mesolimbic dopaminergic substrate of reward.

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Section: Discussionmentioning

confidence: 95%

Nicotine-induced decreases in VTA electrical self-stimulation thresholds: blockade by haloperidol and mecamylamine but not scopolamine or ondansetron

Иванова

Greenshaw

1997

Psychopharmacology

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“…However, the effects of SERT KO are rather complex and can also increase the rewarding effects of cocaine (Sora et al , 1998; Hall et al , 2002; Hall et al , Submitted). This should not be surprising given the diverse effects that pharmacological treatments aimed at specific serotonin receptor subtypes have on drug reward, including both increases and decreases in the rewarding effects of diverse classes of addictive drugs (Carboni et al , 1989; Fadda et al , 1991; Higgins et al , 1992a; Higgins et al , 1992b; Bisaga et al , 1993; Kostowski et al , 1993; Lu et al , 1994; McMillen et al , 1994; Tomkins et al , 1994a; Tomkins et al , 1994b; Rompre et al , 1995; Tomkins et al , 1995; Parsons et al , 1998; Wilson et al , 1998; Fletcher & Korth, 1999; Harrison et al , 1999; Maurel et al , 1999; Tomkins & O'Neill, 2000; Fletcher et al , 2004). Indeed, under some circumstances (e.g.…”

Section: Introductionmentioning

confidence: 99%

Cocaine-conditioned locomotion in dopamine transporter, norepinephrine transporter and 5-HT transporter knockout mice

Hall

Randall-Thompson

et al. 2009

Neuroscience

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The behavioral effects of cocaine are affected by gene knockout of the dopamine transporter (DAT), the serotonin transporter (SERT) and the norepinephrine transporter (NET). The relative involvement of each of these transporters varies depending on the particular behavioral response to cocaine considered, as well as on other factors such as genetic background of the subjects. Interestingly, the effects of these gene knockouts on cocaine induced locomotion are quite different from those on reward assessed in the conditioned place preference paradigm. To further explore the role of these genes in the rewarding effects of cocaine, the ability of five daily injections of cocaine to induce conditioned locomotion was assessed in DAT, SERT and NET knockout (KO) mice. Cocaine increased locomotor activity acutely during the initial conditioning session in SERT KO and NET KO, but not DAT KO, mice. Surprisingly, locomotor responses in the cocaine-paired subjects diminished over the 5 conditioning sessions in SERT KO mice, while locomotor responses increased in DAT KO mice, despite the fact that they did not demonstrate any initial locomotor responses to cocaine. Cocaine-induced locomotion was unchanged over the course of conditioning in NET KO mice. In the post-conditioning assessment, conditioned locomotion was not observed in DAT KO mice, and was reduced in SERT KO and NET KO mice. These data reaffirm the central role of dopamine and DAT in the behavioral effects of cocaine. Furthermore, they emphasize the polygenic basis of cocaine mediated behavior and the non-unitary nature of drug reward mechanisms, particularly in the context of previous studies that have shown normal cocaine conditioned place preference in DAT KO mice.

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“…For example, doses of the 5-HT 3 receptor antagonist granisetron (Kytril ® ) that did not systematically alter ICSS threshold when tested alone attenuated the threshold-lowering effects of morphine. 38 Similarly, dopamine D 3 receptor-preferring antagonists such as SB-277011-A and NGB 2904 appear to reverse the effects of cocaine on ICSS threshold values, consistent with their ability to attenuate the effects of cocaine in other types of procedures. 39,40 Other reports also have pointed to glutamatergic or GABAergic ligands, for example, the metabotropic glutamate mGlu5 receptor antagonist MPEP or the GABA B receptor antagonist baclofen (Kemstro ® and Lioresal ® ), as promising candidate medications on the basis of their ability to attenuate cocaine's threshold-lowering effects in ICSS procedures.…”

Section: Indirect Assays For Medications Development Intracranial Selmentioning

confidence: 70%

Development of Medications for Heroin and Cocaine Addiction and Regulatory Aspects of Abuse Liability Testing

Rocha

Bergman

Comer

et al. 2008

Animal and Translational Models for CNS Drug Discovery

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Effects of granisetron, a 5-HT3 receptor antagonist, on morphine-induced potentiation of brain stimulation reward

Cited by 10 publications

References 38 publications

Nicotine-induced decreases in VTA electrical self-stimulation thresholds: blockade by haloperidol and mecamylamine but not scopolamine or ondansetron

Nicotine-induced decreases in VTA electrical self-stimulation thresholds: blockade by haloperidol and mecamylamine but not scopolamine or ondansetron

Cocaine-conditioned locomotion in dopamine transporter, norepinephrine transporter and 5-HT transporter knockout mice

Development of Medications for Heroin and Cocaine Addiction and Regulatory Aspects of Abuse Liability Testing

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