MK-801, but not drugs acting at strychnine-insensitive glycine receptors, attenuate methamphetamine nigrostriatal toxicity

doi:10.1016/0006-8993(93)90135-A

Brain Research

Volume 625, Issue 1, 15 October 1993, Pages 38-44

https://doi.org/10.1016/0006-8993(93)90135-A Get rights and content

Abstract

Repeated administration of methamphetamine (METH) results in damage to nigrostriatal dopaminergic neurons. Both competitiveN-methyl-d-aspartate (NMDA) receptor antagonists and use-dependent cation channel blockers attenuate METH-induced damage. The objectives of the present study were to examine whether comparable reductions in METH-induced damage could be obtained by compounds acting at strychnine-insensitive glycine receptors on the NMDA receptor complex. Four injections of METH (5 mg/kg i.p.) resulted in a ∼70.9% depletion of striatal dopamine (DA) and ∼62.7% depletion of dihydroxyphenylacetic acid (DOPAC) content, respectively. A significant protection against METH-induced DA and DOPAC depletion was afforded by the use-dependent channel blocker, MK-801. The competitive glycine antagonist 7-chlorokynurenic acid (7-Cl-KA), the low efficacy glycine partial agonist (+)-3-amino-1-hydroxy-2-pyrrolidone ((+)-HA-966), and the high efficacy partial glycine agonist 1-aminocyclopropane-car☐ylic acid (ACPC) were ineffective against METH-induced toxicity despite their abilities to attenuate glutamate-induced neurotoxicity under both in vivo and in vitro conditions. These results indicate that glycinergic ligands do not possess the same broad neuroprotective spectrum as other classes of NMDA antagonists.

Reference (58)

BojeK.M. et al.
Strychnine-insensitive glycine receptors in embryonic chick retina: characteristics and modulation of NMDA neurotoxicity
Neurochem. Int.
(1992)
BojeK.M. et al.
Desensitization of the NMDA receptor complex by glycinergic ligands in cerebellar granule cell cultures
Brain Res.
(1993)
GreenA.R. et al.
The neurotoxic effects of methamphetamine on 5-hydroxytryptamine and dopamine in brain: evidence for the protective effect of chlormethiazole
Neuropharmacology
(1992)
Hemrick-LueckeS. et al.
MK-801 antagonism of the prolonged depletion of striatal dopamine by amphetamine in iprindole-treated rats
Life Sci.
(1992)
IkedaK. et al.
Cloning and expression of the ε4 subunit of the NMDA receptor channel
FEBS Lett.
(1992)
KoroshetzW.J. et al.
The correlation between excitatory amino acid-induced current responses and excitotoxicity in striatal cultures
Brain Res.
(1990)
McDonaldJ.W. et al.
HA-966 (1-hydroxy-3-aminopyrrolidone-2) selectively reducesN-methyl-d-aspartate (NMDA)-mediated brain damage
Neurosci. Lett.
(1989)
MillerR. et al.
High-performance liquid chromatographic assay for 1-aminocyclopropanecar☐ylic acid from plasma and brain
J. Chromatogr.
(1992)
MurakiA. et al.
MK-801, a non-competitive antagonist of NMDA receptor, prevents methamphetamine-induced decrease of striatal dopamine uptake sites in the rat striatum
Neurosci. Lett.
(1992)
NashJ.F. et al.
Methamphetamine neurotoxicity and striatal glutamate release: comparison to 3,4-methylenedioxymethamphetamine
Brain. Res.
(1992)

RansomR.W. et al.

Glycine modulation of NMDA-evoked release of [³H]acetylcholine and [³H]dopamine from rat striatal slices

Neurosci. Lett.

(1989)

SkolnickP. et al.

Blockade ofN-methyl-d-aspartate induced convulsions by 1-aminocyclopropanecar☐ylates

Life Sci.

(1989)

TrullasR. et al.

1-Aminocyclopropanecar☐ylates exhibit antidepressant and anxiolytic actions in animal models

Eur. J. Pharmacol.

(1991)

TrullasR. et al.

Anxiolytic properties of 1-aminocyclopropanecar☐ylic acid, a ligand at strychnine-insensitive glycine receptors

Pharmacol. Biochem. Behav.

(1989)

UckeleJ.E. et al.

Effect of glycine and glycine receptor antagonists on NMDA-induced brain injury

Neurosci. Lett.

(1989)

von LubitzD.K.J.E. et al.

A novel treatment of global cerebral ischemia with a glycine partial agonist

Eur. J. Pharmacol.

(1992)

BeaughardM. et al.

Effects of the putative glycine antagonist HA-966 on the neurological and histological changes induced by transient global ischemia in rats and gerbils

BristowL.J. et al.

Modulation of mesolimbic dopaminergic systems by the glycine/NMDA receptor antagonist,R-(+)-HA-966

CarterA.

Glycine antagonists: regulation of the NMDA receptor-channel complex by the strychnine-insensitive glycine site

Drugs of the Future

(1992)

CarterA.J. et al.

Agents which antagonize the NMDA receptor-channel complex in vivo also cause disturbances of motor coordination

Soc. Neurosci. Abstr.

(1992)

CorbettR. et al.

Effects of HA-966 on conflict, social interaction, and plus maze behaviors

Drug Dev. Res.

(1991)

EvoniukG.E. et al.

A rapid method for evaluating the behavioral effects of phencylidine-like dissociative anesthetics in mice

Psychopharmacology

(1991)

FosterA.C. et al.

HA-966 antagonizesN-methyl-d-aspartate receptors through a selective interaction with the glycine receptor

J. Neurosci.

(1989)

FosterA.C. et al.

Protection againstN-methyl-d-aspartate receptor-mediated neuronal degeneration in rat brain by 7-chlorokynurenate and 3-amino-1-hydroxypyrrolid-2-one, antagonists at the allosteric site for glycine

Eur. J. Neurosci.

(1990)

GibbJ.W. et al.

Influence of dopamine synthesis on methamphetamine-induced changes in striatal and adrenal tyrosine hydroxylase

Naunyn-Schmiedeberg's Arch. Pharmacol.

(1979)

GoldbergM.P. et al.

N-methyl-d-aspartate receptors mediate hypoxic neuronal injury in cortical culture

J. Pharmacol. Exp. Ther.

(1987)

HartleyD.M. et al.

7-Chlorokynurenate blocks NMDA receptor mediated neurotoxicity in murine cortical culture

Eur. J. Neurosci.

(1990)

HendersonG. et al.

Competitive antagonists and partial agonists at the glycine modulatory site of the mouseN-methyl-d-spartate receptor

J. Physiol.

(1990)

HoodW.F. et al.

N-Methyl-d-aspartate recognition site ligands modulate activity at the glycine recognition site

J. Neurochem.

(1990)

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Importantly, repeated exposure to high doses of METH has been found to cause depletion of dopamine and serotonin (5-HT) at the nerve terminals [1–5] and promote a delayed increase in extracellular glutamate concentration in different brain regions [6–8]. Importantly, blockade of NMDA receptors prevented METH effects on dopamine depletion, which suggests the critical role of glutamatergic neurotransmission in METH-induced neurotoxicity [9]. It is well known that excessive glutamate is excitotoxic [10,11].
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Research into methamphetamine-induced neurotoxicity has experienced a resurgence in recent years. This is due to (1) greater understanding of the mechanisms underlying methamphetamine neurotoxicity, (2) its usefulness as a model for Parkinson’s disease and (3) an increased abuse of the substance, especially in the American Mid-West and Japan. It is suggested that the commonly used experimental one-day methamphetamine dosing regimen better models the acute overdose pathologies seen in humans, whereas chronic models are needed to accurately model human long-term abuse. Further, we suggest that these two dosing regimens will result in quite different neurochemical, neuropathological and behavioral outcomes. The relative importance of the dopamine transporter and vesicular monoamine transporter knockout is discussed and insights into oxidative mechanisms are described from observations of nNOS knockout and SOD overexpression. This review not only describes the neuropathologies associated with methamphetamine in rodents, non-human primates and human abusers, but also focuses on the more recent literature associated with reactive oxygen and nitrogen species and their contribution to neuronal death via necrosis and/or apoptosis. The effect of methamphetamine on the mitochondrial membrane potential and electron transport chain and subsequent apoptotic cascades are also emphasized. Finally, we describe potential treatments for methamphetamine abusers with reference to the time after withdrawal. We suggest that potential treatments can be divided into three categories; (1) the prevention of neurotoxicity if recidivism occurs, (2) amelioration of apoptotic cascades that may occur even in the withdrawal period and (3) treatment of the atypical depression associated with withdrawal.
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The glycine site-specific N-methyl-d-aspartate (NMDA) antagonist 5-nitro-6,7-dichloro-2,3-quinoxalinedione (ACEA 1021, 4×30 mg/kg, ip) given 30 min before dexfenfluramine (4×15 mg/kg, ip, every 2 h) was unable to prevent dexfenfluramine-induced depletion of 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) content, and 5-HT transporter (5-HTT) density. Another glycine site-specific NMDA antagonist, R(+)-3-aminohydroxypyrrolidin-2-one [(R)-HA 966] (2×30 mg/kg, ip), given 30 min before dexfenfluramine (2×10 mg/kg, ip, 2 hourly) was also unable to prevent regional depletion of 5-HT, 5-HIAA, and 5-HTT density. However, ACEA 1021 (4×30 mg/kg, ip) given 30 min before (S)-3,4-methylenedioxymethamphetamine (MDMA, 4×10 mg/kg, 2 hourly, ip) attenuated the regional depletion of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), 5-HT, 5-HIAA content, and 5-HTT density. ACEA 1021 combined with (S)-MDMA also prevented (S)-MDMA-induced hyperthermia without causing hypothermia or preventing an (S)-MDMA-induced increase in locomotor activity.
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A conditioned place preference paradigm was used to assess the potential rewarding properties of the uncompetitive NMDA receptor antagonist, MK-801 (dizolcipine), the two competitive NMDA receptor antagonists, CGP 37849 (dl-(E)-2-amino-4-methyl-5-phosphono-3-pentonoic acid) and its (R)-enantiomer CGP 40116, as well as the partial agonist at strychnine-insensitive glycine receptors, ACPC (1-aminocyclopropanecarboxylic acid). MK-801 (0.3 mg/kg), CGP 37849 (1.25–10 mg/kg) and CGP 40116 (1.25–10 mg/kg), administered in association with either the initially non-preferred or initially preferred side of the two-arm chamber, caused a significant increase in the time spent on that side in a post-conditioning test. In contrast, ACPC did not support the conditioned place preference. Thus, the time spent on the drug-associated side following conditioning with ACPC (50–400 mg/kg) did not significantly differ from that measured in the pre-conditioning test, irrespective of whether it was associated with the initially non-preferred black side or the initially preferred white side. These results are consistent with both clinical and pre-clinical data demonstrating differences in psychopharmacological properties among compounds acting at the multiple, allosteric regulatory sites on the NMDA receptor complex. Moreover, these results indicate that the abuse potential of ACPC, which acts as a functional NMDA receptor antagonist, may be lower than that of either uncompetitive or competitive NMDA receptor antagonists.
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  1. The effects of 7-chlorokynurenic acid were studied against the epileptiform and neurotoxic effects due to the non-NMDA excitatory amino acid, kainic acid, in rat hippocampal slices.
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  2. Slice perfusion with 7-chlorokynurenic acid (100 μM), significantly (p<0.05) decreased the duration of the CA1 epileptiform bursting due to 1 μM kainic acid.
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  3. Slice perfusion with 7-chlorokynurenic acid (100 μM) significantly (p<0.05) increased the probability of recovery of the CA1 population spike after a neurotoxic concentration (12 μM) of kainic acid.
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  4. The results indicate that 7-chlorokynurenic acid affects, with a similar potency, epileptiform and neurotoxic effects due to kainic acid.
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MK-801, but not drugs acting at strychnine-insensitive glycine receptors, attenuate methamphetamine nigrostriatal toxicity

Abstract

Neurochem. Int.

Brain Res.

Neuropharmacology

Life Sci.

FEBS Lett.

Brain Res.

Neurosci. Lett.

J. Chromatogr.

Neurosci. Lett.

Brain. Res.

Neurosci. Lett.

Life Sci.

Eur. J. Pharmacol.

Pharmacol. Biochem. Behav.

Neurosci. Lett.

Eur. J. Pharmacol.

Effects of the putative glycine antagonist HA-966 on the neurological and histological changes induced by transient global ischemia in rats and gerbils

Modulation of mesolimbic dopaminergic systems by the glycine/NMDA receptor antagonist,R-(+)-HA-966

Glycine antagonists: regulation of the NMDA receptor-channel complex by the strychnine-insensitive glycine site

Drugs of the Future

Agents which antagonize the NMDA receptor-channel complex in vivo also cause disturbances of motor coordination

Soc. Neurosci. Abstr.

Effects of HA-966 on conflict, social interaction, and plus maze behaviors

Drug Dev. Res.

A rapid method for evaluating the behavioral effects of phencylidine-like dissociative anesthetics in mice

Psychopharmacology

HA-966 antagonizesN-methyl-d-aspartate receptors through a selective interaction with the glycine receptor

J. Neurosci.

Protection againstN-methyl-d-aspartate receptor-mediated neuronal degeneration in rat brain by 7-chlorokynurenate and 3-amino-1-hydroxypyrrolid-2-one, antagonists at the allosteric site for glycine

Eur. J. Neurosci.

Influence of dopamine synthesis on methamphetamine-induced changes in striatal and adrenal tyrosine hydroxylase

Naunyn-Schmiedeberg's Arch. Pharmacol.

N-methyl-d-aspartate receptors mediate hypoxic neuronal injury in cortical culture

J. Pharmacol. Exp. Ther.

7-Chlorokynurenate blocks NMDA receptor mediated neurotoxicity in murine cortical culture

Eur. J. Neurosci.

Competitive antagonists and partial agonists at the glycine modulatory site of the mouseN-methyl-d-spartate receptor

J. Physiol.

N-Methyl-d-aspartate recognition site ligands modulate activity at the glycine recognition site

J. Neurochem.