Ecstasy counteracts catalepsy in rats, an anti-parkinsonian effect?

Schmidt, Werner; Mayerhofer, Andreas; Meyer, Antonia; Kovar, Karl-A.

doi:10.1016/s0304-3940(02)00823-6

Cited by 38 publications

(22 citation statements)

References 6 publications

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“…This indicates that MDMA can affect movement control in a dopamine-independent manner. A similar "antiparkinsonian" effect has been observed in rats, in which MDMA counteracted haloperidol-induced parkinsonism [63].…”

Section: Ii23 the Dopaminergic Systemsupporting

confidence: 62%

Mice in Ecstasy: Advanced Animal Models in the Study of MDMA

Stove¹,

Letter²,

Piette³

et al. 2010

CPB

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The party drug 3,4-methylenedioxymethamphetamine -better known as MDMA or ecstasy-has numerous effects on the human body, characterized by a rush of energy, euphoria and empathy. However, also a multitude of toxic/neurotoxic effects have been ascribed to MDMA, based upon case reports and studies in animals. Given the intrinsic difficulties associated with controlled studies in human beings, most of our insights into the biology of MDMA have been gained through animal studies. The vast majority of these studies utilizes a pharmacological approach to elucidate the mechanisms by which MDMA exerts its effects.Advances in genetics during the last decade have led to the development of several mouse models (transgenic or knockout) that have greatly contributed to our understanding of MDMA biology. This review provides an overview of these genetically modified animal models, in the light of some characteristic effects of MDMA, e.g. hyperlocomotion, neurotoxicity, hyperthermia, behaviour or rewarding. Without a shadow of a doubt, the next decade will bring many more advanced animal models, such as mice with site-specific deletion or rescue of genes and more genetically modified rat models. These models will further improve our knowledge on the pharmacology and toxicity of MDMA and, possibly, may assist in developing therapies coping with potential damage in abusers of MDMA and other drugs, as well as in patients suffering from specific neuronal pathologies.MDMA in advanced animal models 3

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Section: Ii23 the Dopaminergic Systemsupporting

confidence: 62%

Mice in Ecstasy: Advanced Animal Models in the Study of MDMA

Stove¹,

Letter²,

Piette³

et al. 2010

CPB

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show abstract

“…It may also account for the drug's antiparkinsonian and antidyskinetic effects in animal models of extrapyramidal disorders (Iravani et al 2003;Schmidt et al 2002). Salute and by two FIRB grants (Grants RBNE01WY7P_010 and RBNE017555_006) to N.B.M.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

Federici

Sebastianelli

Natoli

et al. 2007

Biological Psychiatry

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“…The present study shows that ghrelin increases firing rate dose dependently, and results in the burst firing at high concentrations. To demonstrate the in vivo effect of ghrelin, we utilized the catalepsy model induced by a specific D2 receptor antagonist haloperidol, which has been proven to represent a reliable model for PD and is selectively reversed by clinically effective antiparkinson drugs 45 . Based on the current understanding of neural framework in basal ganglia, degeneration of nigral dopaminergic neurons leads to dopamine depletion in the striatum, resulting in an imbalance of direct and indirect pathway and subsequent motor disorders [46][47][48] .…”

Section: Inhibition Of Voltage-dependent Kcnq/m-currents By Ghrelinmentioning

confidence: 99%

“…The degree of catalepsy was assessed by measuring the time from placement of rats until removal of one of its paws ('descent latency') with a cutoff time of 300 s (ref. 45). …”

Section: Hplc Electrochemical Detection (Hplc-ecd)mentioning

confidence: 99%

Peptide hormone ghrelin enhances neuronal excitability by inhibition of Kv7/KCNQ channels

Shi

Bian

et al. 2013

Nat Commun

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The gut-derived orexigenic peptide hormone ghrelin enhances neuronal firing in the substantia nigra pars compacta, where dopaminergic neurons modulate the function of the nigrostriatal system for motor coordination. Here we describe a novel mechanism by which ghrelin enhances firing of nigral dopaminergic neurons by inhibiting voltage-gated potassium Kv7/KCNQ/M-channels through its receptor GHS-R1a and activation of the PLC-PKC pathway. Brain slice recordings of substantia nigra pars compacta neurons reveal that ghrelin inhibits native Kv7/KCNQ/M-currents. This effect is abolished by selective inhibitors of GHSR1a, PLC and PKC. Transgenic suppression of native Kv7/KCNQ/M-channels in mice or channel blockade with XE991 abolishes ghrelin-induced hyperexcitability. In vivo, intracerebroventricular ghrelin administration causes increased dopamine release and turnover in the striatum. Microinjection of ghrelin or XE991 into substantia nigra pars compacta results in contralateral dystonic posturing, and attenuation of catalepsy elicited by systemic administration of the D2 receptor antagonist haloperidol. Our findings indicate that the ghrelin/ KCNQ signalling is likely a common pathway utilized by the nervous system.

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Ecstasy counteracts catalepsy in rats, an anti-parkinsonian effect?

Cited by 38 publications

References 6 publications

Mice in Ecstasy: Advanced Animal Models in the Study of MDMA

Mice in Ecstasy: Advanced Animal Models in the Study of MDMA

Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

Peptide hormone ghrelin enhances neuronal excitability by inhibition of Kv7/KCNQ channels

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