Sigma receptors modulate both A9 and A10 dopaminergic neurons in the rat brain: functional interaction with NMDA receptors

Iyengar, Smriti; Dilworth, Vickie M.; Mick, Steve J.; Contreras, Patricia C.; Monahan, Joseph B.; Rao, Tadimeti S.; Wood, Paul L.

doi:10.1016/0006-8993(90)90709-k

Cited by 87 publications

(23 citation statements)

References 16 publications

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“…Further support for this notion has been provided by data obtained in both A9 and AlO regions (Iyengar et al, 1990a) and in the hypothalamic-pituitary-adrenal axis (Iyengar et al, 1990b;. Neuropeptide Y (NPY), which has been reported to bind to sigma receptors (Roman et al, 1989;Bouchard et al, 1993), behaves like sigma agonists in our in vivo electrophysiological model (Monnet et al, 1992c,d) as well as in various in vivo and in vitro paradigms (Roman et al, 1989; Author for correspondence.…”

Section: Introductionsupporting

confidence: 58%

The effects of sigma ligands and of neuropeptide Y on N‐methyl‐d‐aspartate‐induced neuronal activation of CA₃ dorsal hippocampus neurones are differentially affected by pertussin toxin

Monnet

Debonnel

Bergeron

et al. 1994

British J Pharmacology

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Section: Introductionsupporting

confidence: 58%

The effects of sigma ligands and of neuropeptide Y on N‐methyl‐d‐aspartate‐induced neuronal activation of CA₃ dorsal hippocampus neurones are differentially affected by pertussin toxin

Monnet

Debonnel

Bergeron

et al. 1994

British J Pharmacology

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“…Such an effect of DTG could be the result of a direct action on dopamine neurons, as sigma receptor binding in the substantia nigra pars compacta and the striatum decreases following intrastriatal 6-hydroxydopamine lesions, suggesting that there are sigma receptors located directly on dopaminergic neurons (23). However, altered NMDA receptor function may be involved in sigma receptor-mediated increases in striatal dopamine, as 6-OHDA lesions only reduced sigma binding by about 15-30% (23), and the NMDA receptor antagonist CPP was found to block increases in striatal dopamine metabolites induced by the sigma agonists (ϩ)-SKF 10,047 and (ϩ)-pentazocine (26).…”

Section: Discussionmentioning

confidence: 99%

The Delayed Effects of DTG and MK-801 on Latent Inhibition in a Conditioned Taste-Aversion Paradigm

Turgeon¹,

Auerbach²,

Duncan-Smith³

et al. 2000

Pharmacology Biochemistry and Behavior

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. The delayed effects of DTG and MK-801 on latent inhibition in a conditioned taste-aversion paradigm. PHARMACOL BIOCHEM BEHAV 66 (3) 533-539, 2000.-The delayed effects of phencyclidine (PCP) have been shown to disrupt latent inhibition (LI) in a conditioned taste-aversion paradigm. In an attempt to understand the mechanism of this disruption, the delayed effects of the selective sigma receptor agonist 1,3-Di(2-tolyl)guanidine (DTG) and the selective NMDA receptor antagonist MK-801 on latent inhibition were assessed in the same paradigm. Water-deprived male rats were allowed access to either water (nonpreexposed; NPE) or 5% sucrose (preexposed; PE) for 30 min on 2 consecutive days. On the third day, animals were allowed access to sucrose and subsequently injected with lithium chloride. On the forth day, animals were allowed access to both sucrose and water. LI was assessed by comparing the percent sucrose consumed in PE and NPE groups on the fourth day. DTG (1.0, 5.0, or 10.0 mg/kg), MK-801 (0.5, 1.0, or 2.0 mg/kg), or vehicle was administered IP 20 h before preexposure (days 1 and 2) and conditioning (day 3). In vehicle-treated groups, PE animals consumed a significantly higher percent sucrose on the test day than NPE animals, indicating the presence of LI. DTG (10.0 mg/kg) and MK-801 (2.0 mg/kg) decreased the percent sucrose consumed by animals in the PE group to the level observed in the NPE group, indicating disrupted LI. However, this dose of MK-801 was found to produce a decrease in percent sucrose consumed in PE animals not treated with lithium chloride, indicating that the decrease observed in the LI paradigm could be due to MK-801-induced decrease in taste preference for sucrose rather than a disruption of LI. Lower doses of MK-801 that did not produce a decrease in taste preference for sucrose did not significantly disrupt LI. None of the doses of DTG tested altered taste preference for sucrose. These data suggest a role for sigma receptors in the previously observed PCP-induced disruption of LI. LATENT inhibition (LI) is the impaired acquisition of a conditioned response to a stimulus that has been previously presented without reinforcement (35). LI is thought to be a measure of an organism's capacity to ignore irrelevant stimuli, and has been demonstrated in a variety of species including humans (4,35,36). Disruption of LI has been observed in nonmedicated acute schizophrenics (4) as well as animals and humans treated with the psychotomimetic drug amphetamine (14,22,49,(64)(65)(66)(67). Medicated schizophrenic patients do not demonstrate disrupted LI (4,37). In addition, antipsychotic medications reverse amphetamine-induced disruption of LI in animals (49,68), and can enhance LI on their own (11,15). These observations suggest that the disruption of LI is a useful animal model for this specific attentional deficit seen in schizophrenia (12,15). Phencyclidine (PCP) is a drug that can produce a psychotomimetic effect in humans (3,28,38) as well as a number of behavioral and cognitive changes in animals...

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“…Secondly, because haloperidol and phencyclidine can bind to sigma-recep tors (37,38), but risperidone can not (35), it is possible that sigma-receptors may be involved in dopamine turn over. Recently, several investigators have demonstrated that sigma-receptors may play an important role in schizophrenia (37,39) and that some of the sigma-recep tor ligands have the ability to change dopamine turnover (40,41). Moreover, phencyclidine-induced head-weaving, which is partly mediated by nigrostriatal dopaminergic neuronal systems (29,30), was blocked by the sigma receptor antagonists NE-100 and BMY-14802 (42, 43) Therefore, it is possible that our present results may result from the differences in the binding affinity for sigma receptors between risperidone and haloperidol, although the roles of sigma-receptors on dopamine turnover remain to be further elucidated.…”

Section: Discussionmentioning

confidence: 99%

Effects of Risperidone on Phencyclidine-Induced Behaviors: Comparison with Haloperidol and Ritanserin

Kitaichi

Yamada

Hasegawa

et al. 1994

Japanese Journal of Pharmacology

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ABSTRACT-In this study, we investigated whether risperidone, a serotonin-S2A (5-HT21)/dopamine-D2 (D2)-receptor antagonist, inhibits phencyclidine (PCP)-induced stereotyped behaviors in comparison with haloperidol and ritanserin. Moreover, we also attempted to investigate the effects of these antipsychotics on the contents of dopamine, serotonin (5-HT) and their metabolites in rat striatum and frontal cortex. In rats, PCP (5 mg/kg, i.p.) caused hyperlocomotion and stereotyped behaviors, including sniffing, head-weaving, backpedalling and turning. Both risperidone (0.8-2.4 mg/kg, p.o.) and haloperidol (0.3-1.0 mg/kg, p.o.) inhibited these behaviors, except for backpedalling, in a dose-dependent manner. PCP (10 mg/kg, i.p.) pro duced hyperlocomotion and stereotyped behaviors, including rearing, sniffing head-twitch, backpedalling and turning. Risperidone (0.8-2.4 mg/kg, p.o.) inhibited both hyperlocomotion and PCP-induced behaviors, except for backpedalling, while ritanserin (3 -10 mg/kg, p.o.) inhibited only the head-twitch. These results suggest that risperidone may have an antipsychotic effect on schizophrenia as well as PCP psychosis in humans by exerting a mixed 5-HT2A/D2 antagonism. Neurochemically, the increasing effects of risperidone on the content of DOPAC and the ratio of DOPAC to dopamine in the striatum were lower than those of haloperidol. These findings may support the view that the extrapyramidal side effects of risperidone are lower than those of haloperidol in clinical situations.

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Sigma receptors modulate both A9 and A10 dopaminergic neurons in the rat brain: functional interaction with NMDA receptors

Cited by 87 publications

References 16 publications

The effects of sigma ligands and of neuropeptide Y on N‐methyl‐d‐aspartate‐induced neuronal activation of CA₃ dorsal hippocampus neurones are differentially affected by pertussin toxin

The effects of sigma ligands and of neuropeptide Y on N‐methyl‐d‐aspartate‐induced neuronal activation of CA₃ dorsal hippocampus neurones are differentially affected by pertussin toxin

The Delayed Effects of DTG and MK-801 on Latent Inhibition in a Conditioned Taste-Aversion Paradigm

Effects of Risperidone on Phencyclidine-Induced Behaviors: Comparison with Haloperidol and Ritanserin

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Sigma receptors modulate both A9 and A10 dopaminergic neurons in the rat brain: functional interaction with NMDA receptors

Cited by 87 publications

References 16 publications

The effects of sigma ligands and of neuropeptide Y on N‐methyl‐d‐aspartate‐induced neuronal activation of CA3 dorsal hippocampus neurones are differentially affected by pertussin toxin

The effects of sigma ligands and of neuropeptide Y on N‐methyl‐d‐aspartate‐induced neuronal activation of CA3 dorsal hippocampus neurones are differentially affected by pertussin toxin

The Delayed Effects of DTG and MK-801 on Latent Inhibition in a Conditioned Taste-Aversion Paradigm

Effects of Risperidone on Phencyclidine-Induced Behaviors: Comparison with Haloperidol and Ritanserin

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The effects of sigma ligands and of neuropeptide Y on N‐methyl‐d‐aspartate‐induced neuronal activation of CA₃ dorsal hippocampus neurones are differentially affected by pertussin toxin

The effects of sigma ligands and of neuropeptide Y on N‐methyl‐d‐aspartate‐induced neuronal activation of CA₃ dorsal hippocampus neurones are differentially affected by pertussin toxin