Therapeutic potential of nicotine for methamphetamine-induced impairment of sensorimotor gating

Involvement of pallidotegmental neurons

Hiroyuki Mizoguchi, Sawako Arai, Hiroyuki Koike, Daisuke Ibi, Hiroyuki Kamei, Toshitaka Nabeshima, Hyoung Chun Kim, Kazuhiro Takuma, Kiyofumi Yamada

Research output: Contribution to journalArticle

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Abstract

Introduction: We have previously found that a disruption to prepulse inhibiton (PPI) induced by methamphetamine (METH) is associated with impaired functioning of pallidotegmental neurons, which play a crucial role in PPI of the startle reflex, through the activation of gamma-aminobutyric acid type B receptors in pedunculopontine tegmental neurons in mice. Objectives: Here, we examined the effect of nicotine on METH-induced impairment of PPI of the startle reflex focusing on dysfunctional pallidotegmental neurons and the neural system. Results: Nicotine (0.15-0.5 mg/kg) ameliorated the deficit in PPI induced by acute METH, and the ameliorating effect of nicotine was antagonized by nicotinic receptor antagonists such as methyllycaconitine and dihydro-β-erythroidine. The acute METH-induced disruption of PPI was accompanied by suppression of c-Fos expression in the lateral globus pallidus (LGP) as well as its induction in the caudal pontine reticular nucleus (PnC) in mice subjected to the PPI test. Nicotine-induced amelioration of PPI deficits in METH-treated mice was accompanied by a reversal of the changes in c-Fos expression in both the LGP and PnC to the basal level. Conclusions: Nicotine is effective in ameliorating the impairment of PPI caused by METH, which may be associated with normalization of the pallidotegmental neurons.

Original languageEnglish
Pages (from-to)235-243
Number of pages9
JournalPsychopharmacology
Volume207
Issue number2
DOIs
Publication statusPublished - 01-12-2009
Externally publishedYes

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Sensory Gating
Methamphetamine
Nicotine
Neurons
Startle Reflex
Globus Pallidus
Therapeutics
Nicotinic Antagonists
GABA Receptors
Nicotinic Receptors
Basal Ganglia

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

Mizoguchi, Hiroyuki ; Arai, Sawako ; Koike, Hiroyuki ; Ibi, Daisuke ; Kamei, Hiroyuki ; Nabeshima, Toshitaka ; Kim, Hyoung Chun ; Takuma, Kazuhiro ; Yamada, Kiyofumi. / Therapeutic potential of nicotine for methamphetamine-induced impairment of sensorimotor gating : Involvement of pallidotegmental neurons. In: Psychopharmacology. 2009 ; Vol. 207, No. 2. pp. 235-243.
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Therapeutic potential of nicotine for methamphetamine-induced impairment of sensorimotor gating : Involvement of pallidotegmental neurons. / Mizoguchi, Hiroyuki; Arai, Sawako; Koike, Hiroyuki; Ibi, Daisuke; Kamei, Hiroyuki; Nabeshima, Toshitaka; Kim, Hyoung Chun; Takuma, Kazuhiro; Yamada, Kiyofumi.

In: Psychopharmacology, Vol. 207, No. 2, 01.12.2009, p. 235-243.

Research output: Contribution to journalArticle

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AU - Mizoguchi, Hiroyuki

AU - Arai, Sawako

AU - Koike, Hiroyuki

AU - Ibi, Daisuke

AU - Kamei, Hiroyuki

AU - Nabeshima, Toshitaka

AU - Kim, Hyoung Chun

AU - Takuma, Kazuhiro

AU - Yamada, Kiyofumi

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N2 - Introduction: We have previously found that a disruption to prepulse inhibiton (PPI) induced by methamphetamine (METH) is associated with impaired functioning of pallidotegmental neurons, which play a crucial role in PPI of the startle reflex, through the activation of gamma-aminobutyric acid type B receptors in pedunculopontine tegmental neurons in mice. Objectives: Here, we examined the effect of nicotine on METH-induced impairment of PPI of the startle reflex focusing on dysfunctional pallidotegmental neurons and the neural system. Results: Nicotine (0.15-0.5 mg/kg) ameliorated the deficit in PPI induced by acute METH, and the ameliorating effect of nicotine was antagonized by nicotinic receptor antagonists such as methyllycaconitine and dihydro-β-erythroidine. The acute METH-induced disruption of PPI was accompanied by suppression of c-Fos expression in the lateral globus pallidus (LGP) as well as its induction in the caudal pontine reticular nucleus (PnC) in mice subjected to the PPI test. Nicotine-induced amelioration of PPI deficits in METH-treated mice was accompanied by a reversal of the changes in c-Fos expression in both the LGP and PnC to the basal level. Conclusions: Nicotine is effective in ameliorating the impairment of PPI caused by METH, which may be associated with normalization of the pallidotegmental neurons.

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