5-HT1B/D receptor agonist, SKF99101H, induces locomotor hyperactivity in the guinea pig

O’Neill, Michael F.; Dobson, David; Sanger, Graham J

doi:10.1016/s0014-2999(00)00345-9

Cited by 4 publications

(5 citation statements)

References 25 publications

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“…For example, 5-HT 1B receptor activation has been shown to enhance the motor stimulant Neumaier et al, 2002), interoreceptive Cunningham, 1995, 1997;Filip et al, 2001Filip et al, , 2002Filip et al, , 2003, conditioning (Cervo et al, 2002;Neumaier et al, 2002), reinforcing (Parsons et al, 1998), and neurochemical (Parsons et al, 1999) effects of cocaine. It is important to note that although 5-HT 1B agonist administration produces behavioral effects similar to some aspects of cocaine administration [e.g., increased locomotion (Chaouloff et al, 1999;O'Neill et al, 2000) and partial substitution for cocaine in discrimination tests Cunningham, 1995, 1997;Filip et al, 2001Filip et al, , 2003], these agonists themselves produce a conditioned place aversion (Cervo et al, 2002) and do not support operant drug selfadministration behavior in animals previously trained to self-administer cocaine (Parsons et al, 1998). Thus, the potentiating effects of 5-HT 1B agonists on some aspects of cocaine-induced behavior (e.g., place conditioning and operant reinforcement) seem to reflect a facilitation of the behavioral effects of cocaine rather than an additive effect of behaviors produced by the 5-HT 1B agonists and cocaine individually.…”

Section: Discussionmentioning

confidence: 99%

Serotonin1B Receptors in the Ventral Tegmental Area Modulate Cocaine-Induced Increases in Nucleus Accumbens Dopamine Levels

O’Dell¹,

Parsons²

2004

The Journal of Pharmacology and Experimental Therapeutics

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Previous work has demonstrated that peripheral serotonin 1B (5-HT 1B ) receptor agonist administration facilitates the behavioral and neurochemical effects of cocaine. This study used dual probe microdialysis to investigate whether activation of serotonin 1B (5-HT 1B ) receptors in the ventral tegmental area (VTA) alters the ability of peripherally administered cocaine to elevate dopamine (DA) levels in the ipsilateral nucleus accumbens (NAcc) of drug-naive Wistar rats. Intra-VTA administration of the selective 5-HT 1B agonist 1,4-dihydro-3-(1,2,3,6-tetrahydro-4-pyridinyl)-5H-pyrrolo [3,2-b]pyridin-5-one dihydrochloride (CP 93,129) by reverse dialysis produced a dose-dependent (30 and 100 M) potentiation of cocaine-induced (10 mg/kg i.p.) increases in NAcc DA efflux and concurrent cocaine-induced decreases in VTA GABA efflux. There was no effect of either local CP 93,129 or peripheral cocaine on VTA glutamate efflux. Intra-VTA administration of the 5-HT 1A/7 receptor agonist 8-hydroxy-2-dipropylaminotetralin (8-OH-DPAT; 100 M) did not alter cocaine-induced alterations in NAcc DA or VTA GABA, suggesting that the effects of CP 93,129 were not mediated through 5-HT 1A receptors. Moreover, the effects of intra-VTA CP 93,129 (100 M) on both cocaine-induced increases in NAcc DA levels and cocaine-induced decreases in VTA GABA levels were reversed by coadministration of the selective 5-HT 1B receptor antagonist 3-[3-(dimethylamine)propyl]-4-hydroxy-N-[4-(4-pyridinyl] phenyl] benzamide dihydrochloride (GR 55562; 300 M). In the absence of cocaine, intra-VTA CP 93,139 produced an increase in NAcc DA and decrease in VTA GABA levels. However, intra-VTA GR 55562 alone had no effect on any of our neurochemical measures. These findings indicate that activation of VTA 5-HT 1B receptors potentiates cocaine-induced increases in NAcc DA levels by enhancing the ability of cocaine to decrease VTA GABA efflux.The reinforcing effects of cocaine are mediated, in large part, by the mesolimbic dopamine (DA) pathway that originates in the ventral tegmental area (VTA) and terminates in several forebrain structures, including the nucleus accumbens (NAcc; Koob et al., 1994;Wise 1996). Several lines of evidence indicate that 5-hydroxytryptamine (serotonin) (5-HT) systems heavily modulate mesolimbic DA activity. Indeed, the VTA receives a dense serotonergic innervation, and serotonergic manipulations in the VTA modulate the behavioral and neurochemical effects produced by cocaine (for review, see Walsh and Cunningham, 1997).A growing body of evidence indicates that 5-HT 1B receptors play an important role in modulating the behavioral, neurochemical, and cellular effects of cocaine Cunningham, 1995, 1997;Parsons et al., 1998Parsons et al., , 1999Rocha et al., 1998;Castanon et al., 2000;Przegalinski et al., 2001). Although the neural mechanisms involved in these processes have not been elucidated, several recent studies implicate the VTA as an important locus for the modulatory influence of 5-HT 1B receptors on cocaine-induced behavior...

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Section: Discussionmentioning

confidence: 99%

Serotonin1B Receptors in the Ventral Tegmental Area Modulate Cocaine-Induced Increases in Nucleus Accumbens Dopamine Levels

O’Dell¹,

Parsons²

2004

The Journal of Pharmacology and Experimental Therapeutics

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“…First, these antagonists show marked selectivity for 5-HT 1B receptors. Second, they blocked induction of citalopram-induced LA at doses little influencing basal LA and corresponding to those active in other models of 5-HT 1B receptormediated activity (Skingle et al 1996;Harrison et al 1999;Millan et al 1999cMillan et al , 2000O'Neill et al 2000). Notably, comparable doses attenuate the induction of hyperactivity by the 5-HT 1B agonist, RU24969 (Cheetham and Neal 1993;O'Neill et al 1996O'Neill et al , 2000O'Neill and Parameswaran 1997;Chaouloff et al 1999).…”

Section: -Ht 1b Receptorsmentioning

confidence: 97%

“…Second, they blocked induction of citalopram-induced LA at doses little influencing basal LA and corresponding to those active in other models of 5-HT 1B receptormediated activity (Skingle et al 1996;Harrison et al 1999;Millan et al 1999cMillan et al , 2000O'Neill et al 2000). Notably, comparable doses attenuate the induction of hyperactivity by the 5-HT 1B agonist, RU24969 (Cheetham and Neal 1993;O'Neill et al 1996O'Neill et al , 2000O'Neill and Parameswaran 1997;Chaouloff et al 1999). Third, 5-HT 1B receptors likewise mediate the induction of LA by MDMA (McCreary et al 1999;Bankson andCunningham 2002a, 2002b;Fletcher et al 2002) which elicits a pattern of locomotion behaviourally similar, and showing cross-tolerance, to 5-HT 1B agonists (Callaway and Geyer 1992;Callaway et al 1992;Rempel et al 1993).…”

Section: -Ht 1b Receptorsmentioning

confidence: 97%

“…Moreover, they interact with mesolimbic dopaminergic pathways in the facilitation of locomotor behaviour (Parsons et al 1999;Yan and Yan 2001) and there is evidence for a role of dopaminergic mechanisms in the induction of LA by 5-HT 1B agonists (Oberlander et al 1987;Cheetham and Neal 1993;O'Neill et al 2000). However, the interrelationship between 5-HT 1B receptors and mesolimbic DA release is complex (Harrison et al 1999;Parsons et al 1999;Bronsert et al 2001).…”

Section: -Ht 1b Receptorsmentioning

confidence: 99%

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Blockade of serotonin 5-HT 1B and 5-HT 2A receptors suppresses the induction of locomotor activity by 5-HT reuptake inhibitors, citalopram and fluvoxamine, in NMRI mice exposed to a novel environment: a comparison to other 5-HT receptor subtypes

et al. 2003

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“…This action probably reflects disinhibition of mesolimbic dopaminergic pathways via inhibition of GABAergic interneurones (Johnson et al 1992) and likely underlies potentiation of cocaine-induced reinforcement by engagement of 5-HT 1B receptors (Rocha et al 1998;Parsons et al 1998;Belzung et al 2000;-though see Fletcher and Korth 1999a, b). It is also related to the positive influence of 5-HT 1B receptors upon motor behavior (Rempel et al 1993;Skingle et al 1996;Chaouloff et al 1999;O'Neill et al 2000). Moreover, 5-HT 1B receptors reduce hippocampal release of acetylcholine suggesting an inhibitory influence upon cognitive-attentional processes (Maura et al 1989;Buhot 1997; Barnes and Sharp 1999;Malleret et al 1999;Meneses 1999;.…”

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confidence: 96%

Inverse Agonist Properties of Antipsychotic Agents at Cloned, Human (h) Serotonin (5-HT)1B and h5-HT1D Receptors

Audinot

2001

Neuropsychopharmacology

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The actions of diverse antipsychotics at cloned h5-HT(1B) and h5-HT(1D) receptors were examined employing [3H]-GR125,743 and [35S]-GTPgammaS for determination of affinities and efficacies, respectively. Compared with hD(2) receptors, haloperidol, chlorpromazine and olanzapine showed markedly (>100-fold) lower affinity for h5-HT(1D) and h5-HT(1B) receptors at which they expressed inverse agonist properties. Clozapine, risperidone and ocaperidone likewise behaved as inverse agonists at h5-HT(1B) and h5-HT(1D) receptors but their affinities were only approximately 10-fold lower than at hD(2) receptors. Moreover, ziprasidone, S16924 and ORG5222 interacted at h5-HT(1B) and h5-HT(1D) receptors with affinities similar to hD(2) sites. While S16924 and ORG5222 were inverse agonists at h5-HT(1B) and h5-HT(1D) sites, ziprasidone was an inverse agonist at h5-HT(1D) receptors yet a partial agonist at h5-HT(1B) receptors. These actions of antipsychotics were abolished by the selective, neutral antagonist, S18127. In conclusion, with the exception of ziprasidone, all antipsychotics were inverse agonists at h5-HT(1B) and h5-HT(1D) receptors, although they differed markedly in their potency at these sites as compared to hD(2) receptors.

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5-HT1B/D receptor agonist, SKF99101H, induces locomotor hyperactivity in the guinea pig

Cited by 4 publications

References 25 publications

Serotonin1B Receptors in the Ventral Tegmental Area Modulate Cocaine-Induced Increases in Nucleus Accumbens Dopamine Levels

Serotonin1B Receptors in the Ventral Tegmental Area Modulate Cocaine-Induced Increases in Nucleus Accumbens Dopamine Levels

Blockade of serotonin 5-HT 1B and 5-HT 2A receptors suppresses the induction of locomotor activity by 5-HT reuptake inhibitors, citalopram and fluvoxamine, in NMRI mice exposed to a novel environment: a comparison to other 5-HT receptor subtypes

Inverse Agonist Properties of Antipsychotic Agents at Cloned, Human (h) Serotonin (5-HT)1B and h5-HT1D Receptors

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