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PubMed1995

The neurokinin1 receptor antagonist CP-99,994 reduces catalepsy produced by the dopamine D2 receptor antagonist raclopride: correlation with extracellular acetylcholine levels in striatum.

The ability of the substance P (NK1) receptor antagonist CP-99,994 to alter catalepsy induced by a dopamine D1 or D2 receptor antagonist and the ability of CP-99,994 to influence acetylcholine (ACh) release in the striatum were investigated in rats. Catalepsy produced by the D1 antagonist SCH 23390 (0.5 mg/kg s.c.) was not altered by CP-99,994 (0.5, 2.5, or 10 mg/kg s.c.). In contrast, catalepsy induced by the D2 antagonist raclopride (2.5 mg/kg i.p.) was attenuated by CP-99,994 (2.5 and 10 mg/kg). CP-99,994 (10 mg/kg) did not stimulate locomotion when given alone. The less active enantiomer of CP-99,994, CP-100,263 (10 mg/kg), did not alter raclopride-induced catalepsy. Both systemic administration and intrastriatal perfusion of CP-99,994 alone decreased striatal ACh release. Bilateral intrastriatal perfusion of CP-99,994 (40 and 100 microM) reduced catalepsy produced by raclopride and attenuated raclopride-induced increases in striatal ACh release. The reductions in the duration of catalepsy and decreases in striatal ACh release associated with CP-99,994 perfusion were positively correlated. These findings suggest that blockade of striatal NK1 receptors reduces catalepsy induced by a dopamine D2 antagonist, an effect mediated, at least in part, by reducing striatal ACh release. Striatal NK1 receptors, therefore, may be a new therapeutic target for developing drugs that alleviate motor side effects associated with antipsychotic treatment.

Acetylcholine↗

PubMed1982

Estrogen and haloperidol-induced versus handling-related catalepsy in male rats.

A single injection of 17 beta-estradiol valerate produces, 6-7 days later, potentiation of neuroleptic catalepsy. Multiple behavioral measures demonstrate that this effect occurs with an acute dose of haloperidol of 0.25 mg/kg IP. An even lower dose of haloperidol (0.10 mg/kg), which fails to make control rats cataleptic, produces catalepsy in estrogen-treated animals. Thus, estrogen lowers the threshold of haloperidol-induced catalepsy. Repeated testing alone induces cataleptic reactions in control rats. Estrogen suppresses such handling-related catalepsy in animals that subsequently show potentiation of catalepsy at a dose of haloperidol (0.10 mg/kg), which has virtually no effect on control rats. Thus, in these behavioral paradigms, estrogen by itself does not produce cataleptic effects, and estrogen-induced potentiation of haloperidol catalepsy is not merely additive to an antecedent, neuroleptic-like effect of this hormone. We interpret our results in terms of (1) the relationship of cataleptic reactions in normal rats to drug-induced cataleptic states; (2) the possible relevance of our behavioral results to basal ganglia disorders; and (3) the relationship of neuroleptic catalepsy to striatal DA receptors and their modulation by estrogen.

Animals↗

PubMed1976

AMT catalepsy and hypokinesia: interaction with morphine and cocaine.

Acute morphine induced a dose-dependent hypokinesia and rigidity, but only mild and non-dose-dependent catalepsy. AMT, injected 1/2 h after morphine, slightly potentiated catalepsy but not hypokinesia during 3 h after morphine; in contrast, rigidity was decreased. The behavioral changes induced by AMT were accelerated in onset and reached their usual development, although AMT toxicity and hypothermia were completely antagonized; thus, it would appear that AMT hypokinesia/catalepsy are not the consequence of toxicity. When morphine was injected 4 h after AMT, a mutual potentiation of the two drugs on hypokinesia and catalepsy was observed, although previous biochemical measurements had shown no effect of morphine on CA depletion under these conditions. Rigidity appeared to be antagonized. After 17 days of repeated injections, morphine no longer elicited hypokinesia and catalepsy, but no cross-tolerance developed to the AMT behavioral changes. A similar lack of cross-tolerance to the effects of AMT or haloperidol was observed when morphine tolerance was induced by pellet implantation. Catalepsy and hypokinesia developed in a much more pronounced way after two large i.p. doses than after small, multiple administration of AMT; this difference was accompanied by a significantly lower concentration of brain DA, but not NA in the former group. The hyperthermic response observed after a 40 mg/kg s.c. injection of morphine was reversed to hypothermia when the same dose was given 4 or 10 h after CA synthesis inhibition. Cocaine strongly antagonized AMT hypokinesia and catalepsy when given 8 1/2 h after AMT, and, although to a lesser extent, even when injected 12 1/2 h after AMT.

Animals↗

PubMed1978

Noradrenergic influences on catalepsy.

Widespread depletion of forebrain noradrenaline, produced by the intracerebral injection of 4 microgram of 6-hydroxydopamine into the fibres of the dorsal noradrenergic bundle, potentiated the catalepsy induced by 20 mg/kg of morphine and severely attenuated the catalepsy induced by two separate cholinergic agonists, arecoline and pilocarpine. It did not, however, affect haloperidol catalepsy at any of the four doses tested. These results suggest that cholinergic catalepsy may be critically dependent on an intact noradrenergic substrate, perhaps through cholinergic receptors located either presynaptically on noradrenergic terminals or on the cell bodies of origin in the locus coeruleus. Noradrenaline appears to play a modulatory role in morphine catalepsy, although other sites of action must also be involved. Ascending noradrenergic systems do not appear to influence haloperidol catalepsy.

Animals↗

PubMed1994

Effect of dizocilpine (MK-801) on the catalepsy induced by delta 9-tetrahydrocannabinol in mice.

Mice treated with delta 9-tetrahydrocannabinol (THC; 5 and 10 mg/kg i.v.) showed the catalepsy in high bar test, and median descent latencies of catalepsy were about 150 sec. Dizocilpine (MK-801, 0.05 and 0.1 mg/kg), non-competitive N-methyl-D-aspartate (NMDA) antagonist, significantly attenuated THC-induced catalepsy. Furthermore, the anticataleptic effect of MK-801 on THC-induced catalepsy was blocked by acetylcholine agonist oxotremorine (0.005 mg/kg) and dopamine antagonist haloperidol (0.01 mg/kg), but not by NMDA. Oxotremorine, haloperidol, and NMDA themselves did not affect THC-induced catalepsy at the doses used. These results suggest that the anticataleptic effect of MK-801 on THC-induced catalepsy may be developed through dopaminergic and acetylcholinergic neuronal systems.

Acetylcholine↗

PubMed1995

Persistent catalepsy associated with severe dyskinesias in rats treated with chronic injections of haloperidol decanoate.

Patients who develop persistent parkinsonism while on chronic neuroleptic therapy may be predisposed towards the development of tardive dyskinesia (TD). We investigated this issue in an animal model of TD by examining the association between catalepsy and the syndrome of neuroleptic-induced vacuous chewing movements (VCMs). VCMs were measured every 3 weeks for 33 weeks while rats received injections of haloperidol decanoate. Catalepsy was measured after the second through the seventh injections of the depot neuroleptic. There were no correlations between the severity of catalepsy scores after the second or third injections of haloperidol and the severity of the overall VCM syndrome. However, the severity of the catalepsy score following the third through seventh injections of haloperidol strongly correlated with the concurrent number of VCMs. Persistent high catalepsy scores across the six catalepsy rating sessions were strongly associated with the development of persistent severe VCMs. These findings suggest that, to the extent that persistent parkinsonian signs in humans are associated with a propensity towards the development of TD, the VCM syndrome in rats is at least a partially faithful animal model of this relationship.

Animals↗

PubMed1992

D1/D2 dopamine and N-methyl-D-aspartate (NMDA) receptor participation in experimental catalepsy in rats.

Mixed D1/D2 dopamine (DA) antagonists, perphenazine (5 mg/kg) and haloperidol (2 mg/kg) induced catalepsy in rats. SCH 23390 (1 mg/kg), a D1 DA antagonist, also produced catalepsy. Co-administration of perphenazine (0.5 mg/kg) and SCH 23390 (0.1 mg/kg), at low doses, produced a marked increase in cataleptic response. B-HT 920, a D2 agonist, reversed the cataleptogenic effects of perphenazine, haloperidol and SCH 23390. SKF 38893 (5 mg/kg) reduced the cataleptogenic effect of SCH 23390 but failed to reverse haloperidol- or perphenazine-induced catalepsy. SKF 38393 (10 mg/kg), however, protected the animals against perphenazine- induced catalepsy. Combined administration of B-HT 920 (0.1 mg/kg) and SKF 38393 (5 mg/kg) enhanced the protective effect of B-HT 920 in SCH 23390-treated animals but not in animals treated with haloperidol or perphenazine. MK-801 (0.025-0.5 mg/kg), a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, reduced the cataleptogenic effects of perphenazine, haloperidol as well as SCH 23390. The anticataleptic action of MK-801 was enhanced by scopolamine (0.1 mg/kg) but not by bromocriptine (1 mg/kg) or clonidine (0.05 mg/kg) in perphenazine-treated rats. Unlike B-HT 920 (0.1 mg/kg), SKF 38393 (5 mg/kg) potentiated the anticataleptic effect of MK-801 (0.01 mg/kg) against SCH 23390-induced catalepsy. The above data suggests D1/D2 interdependence in catalepsy and a modulatory role of D1 and D2 DA receptor stimulation on the anticataleptic effect of MK-801.

Animals↗

PubMed1999

Adenosinergic modulation of 3alpha-hydroxy-5alpha-pregnan-20-one induced catalepsy in mice.

RATIONALE: Neurosteroid 3alpha, 5alpha THP, a positive allosteric modulator of the GABA(A) receptor Cl- ionophore complex, induces catalepsy-like dopamine antagonists, adenosine agonists or GABA agonists. Adenosine and dopamine receptors are co-localized on GABAergic neurons in the striatum and regulate GABA-mediated neurotransmission. Moreover, the antagonistic interactions between specific subtypes of adenosine and dopamine receptors are involved in motor depressant or motor stimulant effects of adenosine receptor agonists or antagonists, respectively. Such interaction may modulate neurosteroid-induced catalepsy. OBJECTIVE: This study examined the modulation of 3alpha, 5alpha THP-induced catalepsy by adenosinergic agents. METHODS: Catalepsy induced by 3alpha, 5alpha THP (2-8 microg, ICV) was assessed by bar test periodically up to 3 h in mice. Adenosine A1, A2A or A3 receptor agonists or antagonists were given IP or ICV prior to 3alpha, 5alpha THP. Some animals received IP dopamine D2 receptor agonist or antagonist 30 min prior to above combination treatment. RESULTS: Adenosine A1, A2A, and A3 receptor agonists potentiated, whereas adenosine A2A receptor antagonists, but not A1 antagonists, reversed 3alpha, 5alpha THP-induced catalepsy. These effects of adenosine agonists and antagonists were abolished by prior administration of bromocriptine, the dopamine D2 receptor agonist and spiperone, the dopamine D2 receptor antagonist, respectively. CONCLUSIONS: These findings suggest specific adenosine-dopamine receptor interaction in the striatum to modulate 3alpha, 5alpha THP-induced catalepsy.

Animals↗

PubMed1988

Evidence for the independent role of GABA synapses of the zona incerta-lateral hypothalamic region in haloperidol-induced catalepsy.

Bicuculline (0.5-50 ng), injected bilaterally into the zona incerta-lateral hypothalamus (ZI-LH) of the rat, inhibited catalepsy evoked by haloperidol (1 mg/kg s.c.) in a dose-dependent manner. The same effect was obtained by injections of bicuculline directed towards the ventromedial thalamic nucleus (Vm), but then higher doses of the drug were necessary (10-50 ng). Muscimol (10-50 ng), injected into the ZI-LH, evoked a state of catalepsy almost identical to that of haloperidol. Bicuculline (50 ng) abolished the catalepsy evoked by muscimol (25 ng). Bicuculline injected into ZI-LH in doses of 0.5-2.5 ng did not change locomotor activity of rats as measured in photoresistor actometers, whereas it had a slightly stimulating effect at a dose of 5 ng. A comparison between the doses of bicuculline injected into the ZI-LH and Vm suggests that, irrespective of Vm synapses, GABA synapses of this region are involved in the mediation of haloperidol-induced catalepsy. A similar conclusion regarding the catalepsy and rigidity induced by morphine was drawn previously. It seems, therefore, that the catalepsy antagonism of bicuculline is independent of the action of the drug which promotes the locomotor stimulation.

Animals↗

PubMed1990

Lateral hypothalamus-zona incerta region as an output station for the catalepsy induced by the blockade of striatal D1 and D2 dopamine receptors.

Our previous study reported that the blockade of GABAA receptors of the lateral hypothalamus-zona incerta region (LH-ZI) by local injections of bicuculline methiodide inhibited the haloperidol-induced catalepsy. The aim of the present study was to determine (1) whether the blockade of GABAA receptors of the LH-ZI may counteract the catalepsy evoked by SCH 23390 and by sulpiride, and (2) whether the GABAA receptors of the LH-ZI affect the function of the striatal dopaminergic system. Bicuculline methiodide (2.5 and 5 ng/side) injected bilaterally into the LH-ZI inhibited in a dose-dependent manner the catalepsy induced by SCH 23390 administered peripherally (0.2 mg/kg s.c.). SCH 23390 (2 micrograms/side) and sulpiride (1 microgram/side) injected bilaterally into the rostroventral part of the striatum induced potent catalepsy. The catalepsy induced by injection of SCH 23390 (2 micrograms) and sulpiride (1 microgram) into the striatum was inhibited by bicuculline methiodide (2.5 ng and 5 ng) injected into the LH-ZI. Neither bicuculline (5 ng/side) nor muscimol (50 ng/side) injected bilaterally into the LH-ZI changed the levels of dopamine and its intraneuronal metabolite, 3,4-dihydroxyphenyl-acetic acid, or the concentration of noradrenaline and 5-hydroxyindole-acetic acid measured in the striatum and nucleus accumbens by HPLC with an electrochemical detection. It is concluded that GABAA receptors of the LH-ZI are an output station for the catalepsy induced by the blockade of the striatal D2 and D1 dopamine receptors.

Animals↗

PubMed1995

Antagonism by the 5-HT2A/C receptor agonist DOI of raclopride-induced catalepsy in the rat.

It has been shown that the administration of 5-hydroxytryptamine (5-HT)1A receptor agonists will antagonize the catalepsy induced by dopamine D1 or D2 receptor blocking agents. In the present study, administration of the 5-HT2A/C receptor agonist, 1-(2,5-dimethoxy-4-iodo)-2-aminopropane (DOI) (1 mg kg-1 s.c.), counteracted the catalepsy produced by the dopamine D2 receptor antagonist, raclopride (16 mg kg-1 s.c.), but not by the dopamine D1 receptor antagonist (R)-(+)-8-chloro-2,3,4,5-tetra-hydro-3-methyl-5-phenyl-1H-3-benzazepine (SCH 23390) (0.2 mg kg-1 s.c.). The effects of DOI on raclopride-induced catalepsy were fully antagonized by pretreatment with the 5-HT2A/C receptor antagonist, ritanserin (2 mg kg-1 s.c.). The 5-HT precursor, 5-hydroxytryptophan (5-HTP) (6.25-25.0 mg kg-1 i.p.), in combination with the peripheral 5-HTP decarboxylase inhibitor, benserazide (25 mg kg-1 i.p.), and the selective serotonin reuptake inhibitor, zimeldine (10 mg kg-1 s.c.), enhanced the catalepsy produced by a low dose of raclopride (4 mg kg-1 s.c.). It is concluded that stimulation of (postsynaptic) 5-HT2 receptors results in antagonism of the catalepsy induced by treatment with a dopamine D2, but not a D1, receptor antagonist. The fact that 5-HTP, in the presence of benserazide and zimeldine, enhanced raclopride-induced catalepsy suggests the possibility of postsynaptic 5-HT receptors acting in opposition to the 5-HT1 and 5-HT2 receptors, as regards extrapyramidal motor functions in the rat.

5-Hydroxytryptophan↗

PubMed1996

Effects of cannabinoid receptor stimulation and blockade on catalepsy produced by dopamine receptor antagonists.

The ability of cannabinoid receptor stimulation or blockade to alter catalepsy produced by dopamine D1 and D2 receptor antagonists was studied in rats. The cannabinoid receptor antagonist SR 141716A (N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-me thyl-1H- pyrazole-3-carboxamidehydrochloride) (0.5 and 2.5 mg/kg) reduced catalepsy elicited by the cannabinoid receptor agonist CP 55,940 (1 alpha,2-(R)-5-(1,1-dimethylheptyl)-2-[5-hydroxy-2-(3-hydroxypropyl ) cyclohexyl-phenol) (0.5 mg/kg). However, SR 141716A (0.5 and 2.5 mg/kg) did not decrease catalepsy produced by the dopamine D1 receptor antagonist SCH 23390 (R-(+)-7chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5- tetrahydro-1-H-3-benzazepine) (0.5 mg/kg) or the dopamine D2 receptor antagonist raclopride (S(-)-3,5-dichloro-N-(1-ethyl-2-pyrrolidinyl)-methyl-6-methoxysalicylami de) (2.5 mg/kg), suggesting that, under these conditions, endogenous cannabinoid ligands do not modulate the cataleptic effects of dopamine D1 or D2 receptor antagonists. In contrast, CP 55,940 (0.025 and 0.1 mg/kg), at doses which do not produce catalepsy when administered alone, enhanced catalepsy produced by SCH 23390 and raclopride. These results suggest that stimulation, but not blockade, of brain cannabinoid receptors modifies catalepsy behavior produced by selective dopamine D1 and D2 receptor blockade.

Animals↗

PubMed1989

Effects of repeated testing on the incidence of haloperidol-induced catalepsy in mice.

Effects of repeated testing on the incidence of haloperidol-induced catalepsy were investigated in mice. The incidence of catalepsy, evaluated with the forelimbs or hindlimbs placed on a standard horizontal bar, increased in three successive tests in mice injected with haloperidol. Catalepsy was not provoked by repeated testing in animals with saline. In a subsequent study, mice were examined for catalepsy in the forelimbs in the first two trials and then in the hindlimbs. In this procedure, the incidence of catalepsy did not increase with repeated testing. These results suggest that repeated testing increases the incidence of haloperidol-induced catalepsy but does not influence the cataleptogenic potency of the drug.

Animals↗

PubMed1989

Relative importance of the dopaminergic system in haloperidol-catalepsy and the anticataleptic effect of antidepressants and methamphetamine in rats.

The mechanisms involved in haloperidol (HPD)-catalepsy in rat and the effect of antidepressants and methamphetamine (MA) were studied. HPD-catalepsy, as measured by high bar test, lasted for 6-8 min. MA, imipramine (IMP), nomifensine (NOM) and mianserin (MIAN) reduced the duration of catalepsy on IP injection. Electrolytic lesion of the caudate-putamen (CP) and nucleus accumbens (ACC) extensively reduced HPD-catalepsy. Microinjection of MA and NOM into ACC had a similar effect. In the medial amygdala and CP, only MA displayed anticataleptic activity. Zimelidine did not reduce the duration of catalepsy. These results suggest that dopaminergic systems play a key role in mediating HPD-catalepsy and the anticataleptic activity of MA and NOM.

Animals↗

PubMed1991

Nicotine potentiates haloperidol-induced catalepsy and locomotor hypoactivity.

Nicotine was found to potentiate the catalepsy and reduced locomotion following the administration of haloperidol. The ability of various doses of nicotine (0.1, 0.2, or 0.3 mg/kg) to potentiate the catalepsy produced by haloperidol (0.1, 0.2 or 0.4 mg/kg) was investigated. Nicotine potentiated the cataleptic effects of both the 0.2 and 0.4 mg/kg doses of haloperidol, but had no effect following the lowest (0.1 mg/kg) dose of haloperidol. The nicotine potentiation of catalepsy produced by the highest dose of haloperidol was independent of the dose of nicotine used. Nicotine alone did not produce catalepsy. A second experiment evaluated the ability of nicotine to potentiate the decreases in spontaneous locomotor activity produced by haloperidol. Animals received nicotine (0.1 mg/kg) alone or in conjunction with haloperidol (0.1 or 0.4 mg/kg) and were tested in Digiscan Animal Monitors. Haloperidol produced a dose-related decrease in locomotion. Nicotine significantly potentiated the hypoactivity produced by both doses of haloperidol. These results indicated that: 1) nicotine produces a significant potentiation of both the catalepsy and locomotor decreases following haloperidol and 2) the Digiscam Animal Activity Monitors may provide a more sensitive assessment of the interaction between nicotine and haloperidol than the catalepsy bat test. These data suggest that adjunct treatment with nicotine may prove useful for treating neuroleptic responsive disorders such as Tourette Syndrome, schizophrenia and Huntington's disease.

Animals↗

PubMed1995

IL-1 beta and TNF alpha modulate delta 9-tetrahydrocannabinol-induced catalepsy in mice.

The role of the proinflammatory cytokines interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF alpha) in THC-induced catalepsy in mice was examined. Recombinant IL-1 beta (400 ng/mouse, IV) and TNF alpha (500 ng/mouse, IV) were effective in potentiating the cataleptic effect of low-dose THC (10 micrograms/mouse, IV). Recombinant IL-1 alpha and IL-6 did not potentiate catalepsy at any dose tested. Anti-IL-1 beta and anti-TNF alpha antibodies were effective in attenuating high-dose (75 micrograms/mouse) THC-induced catalepsy. Antibodies to IL-1 alpha and IL-6 had no effect on catalepsy. Early onset catalepsy (10 min postinjection) was potentiated by exogenous recombinant IL-1 beta and TNF alpha but only later catalepsy (2 h postinjection) was attenuated by antibodies to endogenous IL-1 beta or TNF alpha. This divergence of the cytokine effect suggests that these substances regulate, by different mechanisms, the early and late THC-induced cataleptic response.

Animals↗

PubMed1997

Adenosine A2 receptors modulate haloperidol-induced catalepsy in rats.

The effect of adenosine A1 and A2 receptor agonists and antagonists was investigated on haloperidol-induced catalepsy in rats. Pretreatment (i.p.) with the non-selective adenosine receptor antagonist, theophylline, or the selective adenosine A2 receptor antagonist, 3,7-dimethyl-1-propargylxanthine (DMPX), significantly reversed haloperidol-induced catalepsy, whereas the selective adenosine A1 receptor antagonists, 8-phenyltheophylline and 8-cyclopentyl-1,3-dipropylxanthine produced no effect. Similar administration of the adenosine A2 receptor agonists, 5'-(N-cyclopropyl)-carboxamidoadenosine and 5'-N-ethylcarboxamidoadenosine (NECA), and the mixed agonists with predominantly A1 site of action, N6-(2-phenylisopropyl) adenosine or 2-chloroadenosine, potentiated haloperidol-induced catalepsy. Higher doses of the adenosine agonists produced catalepsy when given alone. However, N6-cyclopentyladenosine, a highly selective adenosine A1 receptor agonist, was ineffective in these respects. The per se cataleptic effect of adenosine agonists was blocked by DMPX and the centrally acting anticholinergic agent, scopolamine. Scopolamine also attenuated the potentiation of haloperidol-induced catalepsy by adenosine agonists. Further, i.c.v. administration of NECA and DMPX produced a similar effect as that produced after their systemic administration. These findings demonstrate the differential influence of adenosine A1 and A2 receptors on haloperidol-induced catalepsy and support the hypothesis that the functional interaction between adenosine and dopamine mechanisms might occur through adenosine A2 receptors at the level of cholinergic neurons. The results suggest that adenosine A2, but not A1, receptor antagonists may be of potential use in the treatment of Parkinson's disease.

2-Chloroadenosine↗

PubMed1998

Tiapride-induced catalepsy is potentiated by gamma-hydroxybutyric acid administration.

1. The effect of administration of gammahydroxybutyrate (GHB) and tiapride, either alone or in combination, on catalepsy behavior was examined in male mice. 2. Catalepsy was measured by bar and grid tests. Two successive evaluations were carried out 30 and 60 min after injections. 3. Tiapride (175 and 200 mg/kg) and gammahydroxybutyrate (200 mg/kg) provoked an increase of catalepsy scores, exhibiting different time courses. GHB produced a marked but short lasting catalepsy with a peak of action at 30 min, while tiapride produced a catalepsy state with a peak of action at 60 min. 4. Tiapride-induced catalepsy was potentiated by gammahydroxybutyrate administration at 30 min (bar test) and 60 min (bar and grid tests). 5. These results underlie the view that GHB interacts with central dopamine D2 transmission.

Anesthetics, Intravenous↗