M100907, a selective 5-HT2A receptor antagonist, attenuates phencyclidine-induced Fos expression in discrete regions of rat brain

Habara, Toshiyuki; Hamamura, Takashi; Miki, Masahito; Ohashi, Kazuyo; Kuroda, Shigetoshi

doi:10.1016/s0014-2999(01)00926-8

Cited by 24 publications

(17 citation statements)

References 37 publications

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“…Overall, this observation agrees with previous studies showing that acute PCP administration at the same dose as used here induced elevations in c-Fos mRNA in the PFC, RS, S1, motor cortex and MD (Kargieman et al 2007;Santana et al 2011), but not CA1 (Santana et al 2011). Studies using other doses of PCP or other non-competitive NMDAR antagonists also report c-Fos mRNA or protein elevations in these areas (Habara et al 2001 (Jackson et al 2004;Jodo et al 2005;Kargieman et al 2007;Homayoun and Moghaddam, 2007;Santana et al 2011). …”

Section: Pcp-induced C-fos-ir In the Pfc And MDsupporting

confidence: 92%

“…This is supported by previous studies (Habara et al 2001), but this finding is not consistent across all studies using NMDA antagonists (Gao et al 1998 (NAc overall); De Leonibus et al 2002 (NAc core)). We also find that PCP induces c-Fos-IR in the CA1, which has not previously been found in studies with similar or lower PCP doses (Näkki et al 1996;Gotoh et al 2002Santana et al 2011, but is in line with previous studies using stronger PCP doses or other NMDA antagonists (Näkki et al 1996;Väisänen et al 2004;Imre et al 2006) supporting this region to be involved in mechanisms underlying NMDA hypofunction.…”

Section: Pcp-induced C-fos-ir In the Pfc And MDmentioning

confidence: 58%

“…It is wellestablished that acute systemic administration of PCP increases levels of the immediate early gene (IEG) c-Fos in several areas including PFC, hippocampus, nucleus accumbens (NAc) and thalamic nuclei in rodents (Näkki et al 1996;Sato et al 1997;Griffiths et al 1999;Habara et al 2001;Gotoh et al 2002;Kargieman et al 2007;Kargieman et al 2008;Kalinichev et al 2008;Santana et al 2011;Castañe et al 2015). It has been reported that PCP-induced c-Fos mRNA occurs in GAD67-neurons in the hippocampus, amygdala, as well as somatosensory and retrosplenial cortex (Santana et al 2011).…”

Section: Introductionmentioning

confidence: 99%

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Acute phencyclidine administration induces c-Fos-immunoreactivity in interneurons in cortical and subcortical regions

et al. 2016

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Dysfunction of N-Methyl-D-aspartate receptors (NMDARS) is believed to underlie some of the symptoms in schizophrenia, and non-competitive NMDAR antagonists (including phencyclidine (PCP)) are widely used as pharmacological schizophrenia models. Furthermore, mounting evidence suggests that impaired γ-aminobutyric acid (GABA) neurotransmission contributes to the cognitive deficits in schizophrenia. Thus alterations in GABAergic interneurons have been observed in schizophrenia patients and animal models. Acute systemic administration of PCP increases levels of c-Fos in several cortical and subcortical areas, but whether such induction occurs in specific populations of GABAergic interneuron subtypes still remains to be established. Overall, our data indicate that PCP activates a wide range of cortical and subcortical brain regions and that a substantial part of this activation is present in GABAergic interneurons in certain regions. This suggests that the psychotomimetic effect of PCP may be mediated via GABAergic interneurons.

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Section: Pcp-induced C-fos-ir In the Pfc And MDsupporting

confidence: 92%

Section: Pcp-induced C-fos-ir In the Pfc And MDmentioning

confidence: 58%

Section: Introductionmentioning

confidence: 99%

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Acute phencyclidine administration induces c-Fos-immunoreactivity in interneurons in cortical and subcortical regions

et al. 2016

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“…In contrast, the selective 5-HT 2A receptor antagonist [R-( þ )-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidinemethanol] (M100907) (Kehne et al, 1996) reduces Fos expression induced by NMDA receptor antagonists (Habara et al, 2001). M100907 also reduces the elevated locomotor activity (Gleason and Shannon, 1997;Martin et al, 1997), forced swim immobility (Corbett et al, 1999), and deficit in prepulse inhibition (Varty et al, 1999) induced by NMDA receptor antagonists.…”

Section: Introductionmentioning

confidence: 99%

The Serotonin 5-HT2A Receptors Antagonist M100907 Prevents Impairment in Attentional Performance by NMDA Receptor Blockade in the Rat Prefrontal Cortex

Carli

Baviera

Invernizzi

et al. 2004

Neuropsychopharmacol

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We investigated whether 5-HT 2A receptors contribute to the control of attentional performance by glutamate NMDA receptor mechanisms in the medial prefrontal cortex (mPFC). We examined the effects of NMDA receptor blockade in the mPFC on attentional performance by infusing a competitive glutamate NMDA receptor antagonist, 3-(R)-2-carboxypiperazin-4-propyl-1-phosphonic acid (CPP) into the mPFC of rats performing a task of divided and sustained visual attention. The five-choice serial reaction time task provides indices of attentional functioning (% correct responses), executive control (measured by anticipatory and perseverative responses) and speed. A dose of 10 ng CPP injected bilaterally into the mPFC increased anticipatory and perseverative responding; 50 ng reduced accuracy. Increasing the stimulus duration alleviated the CPP-induced accuracy deficit but did not reduce its effects on anticipatory and perseverative responses. CPP at 50 ng caused motor hyperactivity whereas lower doses had no effect., a 5-HT 2A receptor antagonist, injected subcutaneously at 10 and 40 mg/kg, had no effect on accuracy but dose dependently reversed the impairment induced by 50 ng CPP. Both doses of M100907 completely abolished CPP-induced anticipatory but not perseverative over-responding. At the dose of 40 mg/kg M100907 reversed CPPinduced motor hyperactivity. This study provides evidence that the prefronto-cortical glutamate NMDA system may make an important contribution to the control of attention and executive functions. It also indicates that 5-HT 2A receptors may serve to optimize attentional selectivity and improve some aspects of executive control.

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“…Furthermore, the mGlu 2/3 receptor ligands, LY341495 and LY379268, which increase and decrease, respectively, glutamate release in vivo, were found to increase and decrease, respectively, stimulus control by LSD ). The selective 5-HT 2A antagonist, M100907, and the serotonergic atypical antipsychotic agent, clozapine, block a variety of PCPinduced effects including hyperlocomotion (Maurel-Remy et al 1995;Swanson and Schoepp 2002), deficits in pre-pulse inhibition (Yamada et al 1999), immobility in a forced swim test (Corbett et al 1999), and the expression of the immediate early gene c-fos (Habara et al 2001). Direct neurochemical support is provided by the results of studies using in vivo microdialysis.…”

Section: Introductionmentioning

confidence: 99%

Antagonism of phencyclidine-induced stimulus control in the rat by other psychoactive drugs

2008

Pharmacology Biochemistry and Behavior

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It has been observed that agents with agonist activity at 5-HT 2A receptors prevent neurotoxicity induced by the non-competitive NMDA antagonist, dizocilpine (MK-801). Subsequent behavioral studies reported complete antagonism by LSD and DOM of the stimulus effects of the related NMDA antagonist, phencyclidine [PCP]. The present study sought to extend those observations to include other psychoactive drugs. Male F-344 rats were trained in a 2-lever, fixed ratio 10, food-reinforced task with PCP (3.0 mg/kg; IP; 30 min pretreatment) as a discriminative stimulus. Tests of generalization were then conducted using the training dose of PCP in combination with a range of doses of DOM, LSD, d-amphetamine, MDMA, psilocybin, buspirone, and GHB. All of the drugs tested in combination with PCP produced a statistically significant diminution of PCP-appropriate responding but for none was antagonism complete. These data, obtained using a stimulus control model of the hallucinogenic effects of PCP, fail to support the hypothesis that LSD and DOM completely antagonize stimulus control by PCP. Instead, the data suggest complex interactions between PCP-induced stimulus control and a variety of psychoactive drugs including GHB, an agent with no known affinity for serotonergic receptors.

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M100907, a selective 5-HT2A receptor antagonist, attenuates phencyclidine-induced Fos expression in discrete regions of rat brain

Cited by 24 publications

References 37 publications

Acute phencyclidine administration induces c-Fos-immunoreactivity in interneurons in cortical and subcortical regions

Acute phencyclidine administration induces c-Fos-immunoreactivity in interneurons in cortical and subcortical regions

The Serotonin 5-HT2A Receptors Antagonist M100907 Prevents Impairment in Attentional Performance by NMDA Receptor Blockade in the Rat Prefrontal Cortex

Antagonism of phencyclidine-induced stimulus control in the rat by other psychoactive drugs

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