Effect of chlorpromazine on mouse ambulatory activity sensitization caused by (+)-amphetamine

Hirabayashi, Makizo; Tadokoro, Sakutaro

doi:10.1111/j.2042-7158.1993.tb05581.x

Cited by 12 publications

(2 citation statements)

References 23 publications

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“…It is known that antipsychotic drugs such as CPZ, when taken for a long time at high doses, increase mortality in elderly patients with dementia-related psychotic symptoms 58 . CPZ has been used in the concentration ranges of 1~25 mg/kg in previous animal studies 59 – 61 . However, in our study, we used CPZ at the dose of 0.35 μg/kg body weight, much lower than the reported doses.…”

Section: Discussionmentioning

confidence: 99%

Presenilin 2 N141I mutation induces hyperactive immune response through the epigenetic repression of REV-ERBα

et al. 2022

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Hyperimmunity drives the development of Alzheimer disease (AD). The immune system is under the circadian control, and circadian abnormalities aggravate AD progress. Here, we investigate how an AD-linked mutation deregulates expression of circadian genes and induces cognitive decline using the knock-in (KI) mice heterozygous for presenilin 2 N141I mutation. This mutation causes selective overproduction of clock gene-controlled cytokines through the DNA hypermethylation-mediated repression of REV-ERBα in innate immune cells. The KI/+ mice are vulnerable to otherwise innocuous, mild immune challenges. The antipsychotic chlorpromazine restores the REV-ERBα level by normalizing DNA methylation through the inhibition of PI3K/AKT1 pathway, and prevents the overexcitation of innate immune cells and cognitive decline in KI/+ mice. These results highlight a pathogenic link between this AD mutation and immune cell overactivation through the epigenetic suppression of REV-ERBα.

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Section: Discussionmentioning

confidence: 99%

Presenilin 2 N141I mutation induces hyperactive immune response through the epigenetic repression of REV-ERBα

et al. 2022

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“…Several drugs, previously shown to inhibit the development of sensitization, have been tested whether to reverse sensitization, but so far these attempts have failed. The drugs reported not effective were a dopamine D1 receptor antagonist (SCH23390 [10,11,15]), dopamine D2 receptor antagonists (chlorpromazine [16], haloperidol [10], sulpiride [17], and nemonapride (YM‐09151‐2 [11,15,18]), and an N‐methyl‐D‐aspartate (NMDA) receptor antagonist (MK‐801 [19–21]).…”

Section: Introductionmentioning

confidence: 99%

Treatment of the Psychostimulant-Sensitized Animal Model of Schizophrenia

Shuto

Nishi

2010

CNS Neuroscience &Amp; Therapeutics

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Behavioral sensitization to psychostimulants in rodents is associated with the alteration of dopaminergic neurotransmission, and has been proposed as a useful model of schizophrenia due to its progressively intensifying, easily relapsing, and long-lasting features. Pharmacological treatments that reverse the established sensitization may have potential therapeutic values for schizophrenia. The present aim is to review pharmacological treatments that induce the reversal of established sensitization to psychostimulants. In addition, we discuss possible mechanisms for the reversal of sensitization. Reversal of sensitization is induced by chronic dopamine D1 receptor agonism, D2 or D1/D2 receptor agonism combined with mild N-methyl-D-aspartate (NMDA) receptor antagonism or serotonin (5-HT(2A) or 5-HT(3) ) receptor antagonism, 5-HT(1A) receptor agonism, and 5-HT(2A) or 5-HT(3) receptor antagonism. Chronic treatments with these drugs likely adjust altered dopaminergic neurotransmission in sensitized animals. Especially, chronic dopamine D1 receptor agonism, which may adjust mesolimbic hyperdopaminergic and mesocortical hypodopaminergic functions in sensitized animals, is an attractive therapeutic approach for schizophrenia.

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Role of neuropeptides in migraine: where do they stand in the latest expert recommendations in migraine treatment?

Samsam

Coveñas

Ahangari

et al. 2007

Drug Development Research

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Many factors have been implicated in the pathogenesis of migraine headache, including activation of the trigeminovascular system, dysfunction of: cerebral blood vessels, circulating vasoactive substances, mitochondrial energy metabolism, brain oxygenation and metabolism, platelet disorder, alterations in serotonin levels, low levels of brain tissue magnesium, altered transport of ions across the cell membrane, and inheritance and dysfunction of the brainstem periaqueductal gray matter. The headache phase of migraine is associated with cerebral vasodilation and inflammation, presumably mediated by the release of vasoactive substances and neuropeptides including CGRP (calcitonin gene-related peptide). Increased serum CGRP levels have been detected during migraine and cluster headache. One strategy to treat migraine is to inhibit the release of neuropeptides or to block their receptors. This article briefly reviews some experimental and clinical investigations focused on neuropeptide involvement in migraine. Drug Dev Res 68: 294-314, 2007.

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Effect of chlorpromazine on mouse ambulatory activity sensitization caused by (+)-amphetamine

Cited by 12 publications

References 23 publications

Presenilin 2 N141I mutation induces hyperactive immune response through the epigenetic repression of REV-ERBα

Presenilin 2 N141I mutation induces hyperactive immune response through the epigenetic repression of REV-ERBα

Treatment of the Psychostimulant-Sensitized Animal Model of Schizophrenia

Role of neuropeptides in migraine: where do they stand in the latest expert recommendations in migraine treatment?

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