Effects of Toluene Exposure on Signal Transduction: Toluene Reduced the Signaling via Stimulation of Human Muscarinic Acetylcholine Receptor m2 Subtypes in CHO Cells

Tsuga, Hirofumi; Haga, Tatsuya; Honma, Tetsuo

doi:10.1254/jjp.89.282

Cited by 7 publications

(7 citation statements)

References 26 publications

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“…The possible mechanism of the inhibitory effect of toluene on the efferent system could be a lipid-mediated mechanism, as mentioned by Tsuga et al (2002) and based upon in vitro observations.…”

Section: Discussionmentioning

confidence: 99%

Increase in cochlear microphonic potential after toluene administration

2007

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Section: Discussionmentioning

confidence: 99%

Increase in cochlear microphonic potential after toluene administration

2007

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“…Typically inactive, mGluRs function as autoreceptors during elevated neuronal activity to attenuate DA, GABA, glutamate, and acetylcholine release (Cartmell and Schoepp, 2000). Given the widespread influence of mGluRs and the list of ion channel and G-protein coupled receptors affected by toluene, further research is necessary to clarify the cellular sequence of events underlying any toluene-induced behavior (Bale et al, 2002;Cruz et al, 1988;Beckstead et al, 2000;Tsuga et al, 1999Tsuga et al, , 2002. Nevertheless, the above observations at the systems level are consistent with the fact that LY379268 similarly reduces the DA-dependent behavioral effects of PCP and to a lesser extent those of amphetamine (Moghaddam and Adams, 1998;Cartmell et al, 1999Cartmell et al, , 2000aClark et al, 2002).…”

Section: Ly379268 Studies and Toluenementioning

confidence: 99%

Toluene-Induced Locomotor Activity is Blocked by 6-Hydroxydopamine Lesions of the Nucleus Accumbens and the mGluR2/3 Agonist LY379268

Riegel

Ali

French

2003

Neuropsychopharmacol

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The abuse of volatile inhalants remains a prominent, yet poorly understood, form of substance abuse among youth. Nevertheless, the identification of a mechanism underlying the reinforcing properties of inhalants has been hampered by the lack of a clearly identifiable neural substrate upon which these chemicals act. One ingredient that is common to many abused inhalants is toluene, an organic solvent that is self-administered by nonhuman primates and rodents. Most drugs of abuse have been found to elicit forward locomotion in rats, an effect owing to the activation of mesoaccumbal dopamine (DA) pathways. Thus, the present study was undertaken using two different approaches to determine whether toluene-induced locomotor hyperactivity is also ultimately dependent upon DA neurotransmission in the mesolimbic nucleus accumbens (NAC). Here we report on the effects of 6-hydroxydopamine (6-OHDA) lesions of the NAC or pretreatment with the metabotropic mGlu2/3 receptor agonist LY379268 on toluene-induced locomotor activity. Both procedures, which are known to alter neurotransmission within the NAC, significantly attenuated toluene's locomotor stimulatory effects. These results provide strong support for a central mechanism of action of inhalants, which in the past has been more typically attributed to general nonspecific mechanisms throughout the brain. Moreover, as with other drugs of abuse, the NAC may be the final common pathway subserving toluene's abuse liability.

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“…Many mental and nervous diseases are related to disordered function of neurotransmitters, and neuroactive drugs act by altering neurotransmitter levels 14) . Neurochemical changes are also involved in chemical neurotoxicity 15,16) . The present study used a neurochemical approach to investigate how BPA alters brain function in second generation rats.…”

Section: Introductionmentioning

confidence: 99%

Effects of Perinatal Exposure to Bisphenol A on Brain Neurotransmitters in Female Rat Offspring

Honma¹,

Miyagawa²,

Suda³

et al. 2006

Ind Health

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Pregnant Sprague-Dawley (CD IGS) rats were orally administered doses of bisphenol A (BPA) at 4, 40, and 400 mg/kg, from gestation days 6 to postnatal day 20. Neurotransmitters such as dopamine (DA) and serotonin (5HT) were extracted from the brains of dams and female offspring, and measured using liquid chromatography. BPA at 400 mg/kg was toxic and dosed rats died. At 3 wk after birth, brain levels of 3,4-dihydroxyphenylacetic acid (DOPAC, a DA metabolite), homovanillic acid (HVA, a DA metabolite), 5HT, 5-hydroxyindoleacetic acid (5HIAA, a 5HT metabolite) in female offspring were increased and the HVA/DA ratio was high in some brain areas of BPA-treated groups as compared with controls. At the age of 6 wk, levels of choline (Ch) in BPAtreated groups at 4 and 40 mg/kg were higher than control in all of eight brain areas. No changes were observed in acetylcholine (ACh) contents. In 9-wk-old offspring, changes in monoamines and metabolites were scattered and not great. At 3 wk after delivery, levels of 5HIAA in some brain areas of dams treated with BPA were higher than in control dams. Dose dependent increases in HVA and the HVA/DA ratio of the occipital cortex, and in the HVA/DA ratio of the frontal cortex were observed. The turnover of DA and 5HT was accelerated in 3-wk-old offspring and dams. BPA possesses very weak estrogenic activity. Changes in cerebral neurotransmitters observed in offspring and dams in this study may have been related to the estrogenic activity of BPA. However, further investigation is needed to examine the contribution of hormonal activity to such neurotransmitter changes.

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Effects of Toluene Exposure on Signal Transduction: Toluene Reduced the Signaling via Stimulation of Human Muscarinic Acetylcholine Receptor m2 Subtypes in CHO Cells

Cited by 7 publications

References 26 publications

Increase in cochlear microphonic potential after toluene administration

Increase in cochlear microphonic potential after toluene administration

Toluene-Induced Locomotor Activity is Blocked by 6-Hydroxydopamine Lesions of the Nucleus Accumbens and the mGluR2/3 Agonist LY379268

Effects of Perinatal Exposure to Bisphenol A on Brain Neurotransmitters in Female Rat Offspring

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