The effect of methamphetamine on the release of acetylcholine in the rat striatum

Taguchi, Kyoji; Atobe, Jun; Kato, Masaaki; Chuma, Toichiro; Chikuma, Toshiyuki; Shigenaga, Toshiro; Miyatake, Tadashi

doi:10.1016/s0014-2999(98)00653-0

Cited by 16 publications

(14 citation statements)

References 25 publications

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“…Hyperthermia is known to play an important role in the toxic effects of Meth (Bowyer et al, 1992). Meth may cause hyperthermia through an increase in ACh release (Taguchi et al, 1998), because there is evidence that ACh is involved in thermoregulation (Crawshaw, 1973). Because MLA did not alter Meth-induced hyperthermia, the effects of MLA on the acute increases in extracellular glutamate and the long-term decreases in DA and 5-HT terminal markers after Meth probably are caused by its pharmacological properties that are distinct from the role of ACh in thermoregulation.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, there is evidence that systemic Meth administration causes an acute increase in extracellular acetylcholine in the rat striatum (Taguchi et al, 1998), and exposure to Meth increases ␣7 nACh receptor binding sites in differentiated PC-12 cells (Garcia-Ratés et al, 2007). In addition, activation of the ␣7 nACh receptor mediates the Meth-induced production of reactive oxygen species in isolated rat striatal synaptosomes .…”

Section: Introductionmentioning

confidence: 99%

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Regulation of Glutamate Release by α7 Nicotinic Receptors: Differential Role in Methamphetamine-Induced Damage to Dopaminergic and Serotonergic Terminals

Northrop

Smith

Yamamoto

et al. 2010

J Pharmacol Exp Ther

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Regulation of glutamate release is an important underlying mechanism in mediating excitotoxic events such as damage to dopamine (DA) and serotonin (5-HT) neurons observed after exposure to methamphetamine (Meth). One way to regulate glutamate release may be through the modulation of ␣7 nicotinic acetylcholine (nACh) receptors. Meth administration is known to increase acetylcholine release; however, it is unknown whether Meth increases glutamate release and causes long-term damage to both DA and 5-HT terminals through the activation of ␣7 nACh receptors. To test this hypothesis, the ␣7 nACh receptor antagonist, methyllycaconitine (MLA), was administered before the administration of repeated doses of Meth while simultaneously monitoring extracellular striatal glutamate with in vivo microdialysis. In addition, the subsequent longterm decreases in markers of dopaminergic and serotonergic terminals, including DA reuptake transporter (DAT), serotonin reuptake transporter (SERT), vesicular monoamine transporter-2, vesicular DA, and vesicular 5-HT content in the rat striatum, were measured. The results show that MLA pretreatment prevented Meth-induced increases in striatal glutamate and protected against the subsequent long-term decreases in striatal DAT and vesicular DA content without affecting the hyperthermia produced by Meth. In contrast, the Meth-induced decreases in striatal SERT immunoreactivity and vesicular 5-HT content were not affected by MLA. This suggests that the ␣7 nACh receptor differentially mediates glutamate-dependent damage to DA but not 5-HT terminals in a manner that is independent of hyperthermia. Furthermore, antagonism of ␣7 nACh receptors may be a possible therapeutic strategy for decreasing extracellular glutamate and preventing the excitotoxic damage observed in other DA-related neurodegenerative disorders.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Regulation of Glutamate Release by α7 Nicotinic Receptors: Differential Role in Methamphetamine-Induced Damage to Dopaminergic and Serotonergic Terminals

Northrop

Smith

Yamamoto

et al. 2010

J Pharmacol Exp Ther

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“…This alteration in the balance between a4b2 and a6b2 receptor subtypes is consistent with the suggestion that nicotine upregulates a4b2 nAChRs by increasing assembly of b2 with a4 subunits and consequently reducing assembly of b2 with a6 subunits (Kuryatov et It is interesting to speculate that an upregulation of a4b2 nAChR expression/signaling afforded by nicotine at the time of METH treatment may have contributed to neuroprotection. Importantly, METH causes acetylcholine release and thus indirectly activates nAChRs (Tsai and Chen, 1994;Taguchi et al, 1998;Dobbs and Mark, 2008). a4b2 nAChRs are found on dopaminergic terminals and increase tonic DA release when they are activated (Meyer et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Chronic Nicotine Exposure Attenuates Methamphetamine-Induced Dopaminergic Deficits

Vieira-Brock

McFadden

Nielsen

et al. 2015

J Pharmacol Exp Ther

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Repeated methamphetamine (METH) administrations cause persistent dopaminergic deficits resembling aspects of Parkinson's disease. Many METH abusers smoke cigarettes and thus selfadminister nicotine; yet few studies have investigated the effects of nicotine on METH-induced dopaminergic deficits. This interaction is of interest because preclinical studies demonstrate that nicotine can be neuroprotective, perhaps owing to effects involving a4b2 and a6b2 nicotinic acetylcholine receptors (nAChRs). This study revealed that oral nicotine exposure beginning in adolescence [postnatal day (PND) 40] through adulthood [PND 96] attenuated METH-induced striatal dopaminergic deficits when METH was administered at PND 89. This protection did not appear to be due to nicotine-induced alterations in METH pharmacokinetics. Short-term (i.e., 21-day) high-dose nicotine exposure also protected when administered from PND 40 to PND 61 (with METH at PND 54), but this protective effect did not persist. Short-term (i.e., 21-day) high-dose nicotine exposure did not protect when administered postadolescence (i.e., beginning at PND 61, with METH at PND 75). However, protection was engendered if the duration of nicotine exposure was extended to 39 days (with METH at PND 93). Autoradiographic analysis revealed that nicotine increased striatal a4b2 expression, as assessed using [125 I]epibatidine. Both METH and nicotine decreased striatal a6b2 expression, as assessed using [125 I]aconotoxin MII. These findings indicate that nicotine protects against METH-induced striatal dopaminergic deficits, perhaps by affecting a4b2 and/or a6b2 expression, and that both age of onset and duration of nicotine exposure affect this protection.

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“…Intranigral injection of SP has been shown to increase striatal DA and glutamate release that can be blocked by NK-1 receptor antagonists (Reid et al 1990a;1990b), and a parallel study in our lab showed that NK-1 receptor antagonist significantly reduced cocaine-evoked release of DA (Noailles and Angulo 2002). Moreover, METH has been shown to increase acetylcholine release in the striatum, possibly via a D1 and/or NMDA receptor mechanism (Taguchi et al 1998), which is mediated indirectly through local release of SP acting at NK-1 receptors on striatal cholinergic interneurons (Anderson et al 1994). Thus, the increased release of SP by METH and the consequent signaling through the NK-1 receptor would hypothetically lead to a neurotransmitter imbalance that ultimately triggers the release of excitatory amino acids in the striatum.…”

Section: Discussionmentioning

confidence: 99%

Neurokinin‐1 (NK‐1) receptor antagonists abrogate methamphetamine‐induced striatal dopaminergic neurotoxicity in the murine brain

Cadet

Angulo

2002

Journal of Neurochemistry

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Methamphetamine (METH) is an addictive substance that also causes extensive neural degeneration in the central nervous system. Because METH augments striatal substance P (SP) levels, we hypothesized that this neuropeptide plays a role in methamphetamine-induced toxicity and neural damage in the striatum. In this study we present evidence demonstrating that signaling through the neurokinin-1 (NK-1) receptor by SP plays an important role in methamphetamine-induced toxicity in the striatum. We tested the effects of the selective NK-1 receptor antagonists WIN-51,708 and L-733,060 on several markers of dopaminergic terminal toxicity in the mouse striatum. Administration of NK-1 receptor antagonist prevented the loss of dopamine transporters assessed by autoradiography and western blotting, the loss of tissue dopamine assessed by high-pressure liquid chromatography, and the loss of tyrosine hydroxylase, as well as the induction of glial fibrillary acidic protein determined by western blotting. Pre-treatment with NK-1 receptor antagonist had no effect on METH-induced hyperthermia. Pre-exposure of mice to either of the NK-1 receptor antagonists alone was without effect on all of these neurochemical markers. These results provide the first evidence that tachykinins, particularly SP, acting through NK-1 receptors, play a crucial role in the pathogenesis of nigrostriatal dopaminergic terminal degeneration induced by METH. This finding could lead to novel therapeutic strategies to offset drug addictions as well as in the treatment of a number of disorders including Parkinson's and Huntington's diseases.

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The effect of methamphetamine on the release of acetylcholine in the rat striatum

Cited by 16 publications

References 25 publications

Regulation of Glutamate Release by α7 Nicotinic Receptors: Differential Role in Methamphetamine-Induced Damage to Dopaminergic and Serotonergic Terminals

Regulation of Glutamate Release by α7 Nicotinic Receptors: Differential Role in Methamphetamine-Induced Damage to Dopaminergic and Serotonergic Terminals

Chronic Nicotine Exposure Attenuates Methamphetamine-Induced Dopaminergic Deficits

Neurokinin‐1 (NK‐1) receptor antagonists abrogate methamphetamine‐induced striatal dopaminergic neurotoxicity in the murine brain

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