Amphetamine enhances Ca2+ entry and catecholamine release via nicotinic receptor activation in bovine adrenal chromaffin cells

Liu, Pei-Shan; Liaw, Chwen-Tzy; Lin, M. S.; Shin, Song-Huah; Kao, Lung‐Sen; Lin, Lih-Fang

doi:10.1016/s0014-2999(02)02870-4

Cited by 18 publications

(18 citation statements)

References 45 publications

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“…Although the nicotine pretreatment 'primed' the striatum through activation of nicotinic receptors, it is not known which downstream effectors might play a role in the enhanced amphetamine challenge response. Amphetamine has been shown to increase catecholamine release via nicotine receptor activation in bovine chromaffin cells, but this occurred at high micromolar concentrations of amphetamine, which would not be achieved by our in vivo doses (Liu et al 2003). Future studies will examine the molecular mechanism of these potentiated interactions.…”

Section: Discussionmentioning

confidence: 87%

Nicotine and amphetamine acutely cross-potentiate their behavioral and neurochemical responses in female Holtzman rats

et al. 2008

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Section: Discussionmentioning

confidence: 87%

Nicotine and amphetamine acutely cross-potentiate their behavioral and neurochemical responses in female Holtzman rats

et al. 2008

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“…Among the neuronal acetylcholine receptors, homomeric ␣7 nAChRs have the highest fractional Ca 2ϩ current. In fact, Liu et al (2003) found that D-amphetamine can activate ␣7 receptors in bovine chromaffin cells. They concluded that amphetamine enhances calcium entry via ␣7 nicotinic receptor activation and dose-dependently suppressed […”

mentioning

confidence: 99%

Methyllycaconitine Prevents Methamphetamine-Induced Effects in Mouse Striatum: Involvement of α7 Nicotinic Receptors

Escubedo

Chipana²,

Pérez-Sánchez³

et al. 2005

J Pharmacol Exp Ther

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In a previous study, we demonstrated that in rat striatal synaptosomes, methamphetamine (METH)-induced reactive oxygen species (ROS) production was prevented by methyllycaconitine (MLA), a specific antagonist of ␣7 neuronal nicotinic acetylcholine receptors (␣7 nAChR). The aim of this study was to test the influence of MLA on acute METH effects and neurotoxicity in mice, using both in vivo and in vitro models. MLA inhibited METH-induced climbing behavior by 50%. Acute effects after 30-min preincubation with 1 M METH also included a decrease in striatal synaptosome dopamine (DA) uptake, which was prevented by MLA. METH-induced neurotoxicity was assessed in vivo in terms of loss of striatal dopaminergic terminals (73%) and of tyrosine hydroxylase levels (by 90%) at 72 h post-treatment, which was significantly attenuated by MLA. Microglial activation [measured as 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinolinecarboxamide binding] was also present at 24 h post-treatment and was fully prevented by MLA, tending to confirm its neuroprotective activity. MLA had no effect on METH-induced hyperthermia. Additionally, flow cytometry assays showed that METH-induced ROS generation occurs inside synaptosomes from mouse striatum. This effect implied release of vesicular DA and was calcium-, neuronal nitric-oxide synthase-, and protein kinase C-dependent. MLA and ␣-bungarotoxin, but not dihydro-␤-erythroidine (an antagonist that blocks nAChR-containing ␤2 subunits), fully prevented METH-induced ROS production without affecting vesicular DA uptake. The importance of this study lies not only in the neuroprotective effect elicited by the blockade of the ␣7 nicotinic receptors by MLA but also in that it proposes a new mechanism with which to study METH-induced acute and longterm effects.

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“…The agonistic effect was verified by current measurements on HEK293 cells expressing ␣ 2 ␤␦⑀ nAChR. Interestingly, a curare-like block by amphetamine overdosage was identified to cause paralysis (Skau and Gerald, 1978;Liu et al, 2003), pointing to the same target. In contrast to the effects of amphetamine, weakness has not yet been reported for illicit ecstasy users.…”

Section: Mdma Acts On Skeletal Musclementioning

confidence: 85%

3,4-Methylenedioxymethamphetamine (Ecstasy) Activates Skeletal Muscle Nicotinic Acetylcholine Receptors

Klingler

Heffron²,

Jurkat‐Rott³

et al. 2005

J Pharmacol Exp Ther

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Adverse 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) effects are usually ascribed to neurotransmitter release in the central nervous system. Since clinical features such as fasciculations, muscle cramps, rapidly progressing hyperthermia, hyperkalemia, and rhabdomyolysis point to the skeletal muscle as additional target, we studied the effects of MDMA on native and cultured skeletal muscle. We addressed the question whether malignant hyperthermia (MH)-susceptible (MHS) muscle is predisposed to adverse MDMA reactions. Force measurements on muscle strips showed that 100 M MDMA, a concentration close to that determined in some MDMA users, regularly enhanced the sensitivity of skeletal muscle to caffeine-induced contractures but did not cause contractures on its own. The left-shift of the dose-response curve induced by MDMA was greater in normal than in MHS muscle. Furthermore, MDMA did not release Ca 2ϩ from isolated sarcoplasmic reticulum vesicles. These findings do not support the view of an MH-triggering effect on muscle. However, MDMA induced Ca 2ϩ

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Amphetamine enhances Ca2+ entry and catecholamine release via nicotinic receptor activation in bovine adrenal chromaffin cells

Cited by 18 publications

References 45 publications

Nicotine and amphetamine acutely cross-potentiate their behavioral and neurochemical responses in female Holtzman rats

Nicotine and amphetamine acutely cross-potentiate their behavioral and neurochemical responses in female Holtzman rats

Methyllycaconitine Prevents Methamphetamine-Induced Effects in Mouse Striatum: Involvement of α7 Nicotinic Receptors

3,4-Methylenedioxymethamphetamine (Ecstasy) Activates Skeletal Muscle Nicotinic Acetylcholine Receptors

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