Role of brain monoamine systems in the jumping behavior induced in rats by the combination of harmine and apomorphine.

Takashi, Katsuo; Kuga, Tetsurō

doi:10.1254/jjp.31.677

Cited by 5 publications

(6 citation statements)

References 10 publications

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“…In the previous paper, we suggested that activation of the dopaminergic neurons was necessary induction of the jumping behavior by HA and APO (4). The result that denerva tion of the dopaminergic neurons by 6 hydroxydopamine treatment abolished the jumping behavior induced by HA and APO confirmed this hypothesis.…”

Section: Modificationmentioning

confidence: 53%

“…HA is a potent monoamine oxidase (MAO) inhibitor (6), and it was con sidered that the elevation of brain mono amines induced by HA would be related to this behavior. However, the fact that other MAO inhibitors did not produce this be havior (4) suggested another mode of action.…”

mentioning

confidence: 99%

“…We have demonstrated that administration of harmine in combination with apomorphine (APO) induced a violent jumping in rats instead of a tremor. This behavior was induced by HA when the central dopaminergic func tion was activated by treatment with APO or L-DOPA plus benserazide (4), and the lump ing activity was correlated with the brain HA concentration (5). HA is a potent monoamine oxidase (MAO) inhibitor (6), and it was con sidered that the elevation of brain mono amines induced by HA would be related to this behavior.…”

mentioning

confidence: 99%

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Involvement of GABAergic systems and benzodiazepine receptors in the jumping behavior induced by harmine and apomorphine in rats.

Moroi

Takashi²,

Kuga

1988

Jpn.J.Pharmacol

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Abstract-Harmine(HA) induces a jumping behavior in rats when the central dopaminergic function has been activated.Possible involvement of the GABAergic systems and the benzodiazepine receptors (BZA-R) in the jumping behavior induced by HA and apomorphine (APO) was investigated. Pretreatment with GABAergic agonists, muscimol (0.05-0.2 mg/kg) and diazepam (0.2-1.0 mg/kg), and an tagonists, picrotoxin (0.1-0.5 mg/kg) and bicuculline (0.1-0.5 mg/kg), suppressed the jumping behavior in a dose-dependent manner in rats treated with HA (10 mg/ kg) and APO (2 mg/kg).After treatment with 2, 5 or 10 mg/kg of HA in combi nation with 2 mg/kg of APO, a decrease in 3H-diazepam binding to the brain regional membranes was observed in the corpus striatum (CS) in a dose-dependent manner, but not in the other brain regions.The decrease in the 3H-diazepam binding to the CS membranes was proportional to the increase in the HA levels in the CS, and the HA levels were correlated with the intensity of jumping behavior. Pretreatment with Ro 15-1788, an antagonist of BZA-R, suppressed the jumping behavior induced by HA and APO. These results indicated the involvement of the GABAergic systems in the jumping behavior and suggested that HA induced the jumping behavior partly as a result of interacting with the BZA-R.

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Section: Modificationmentioning

confidence: 53%

mentioning

confidence: 99%

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confidence: 99%

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Involvement of GABAergic systems and benzodiazepine receptors in the jumping behavior induced by harmine and apomorphine in rats.

Moroi

Takashi²,

Kuga

1988

Jpn.J.Pharmacol

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“…Measurement of jumping activity: The jumping behavior was assessed according to the method described in the previous paper (5). Groups of 5 rats were placed in the observation cage (41 x 25 X 15 cm) at least 30 min before injections of drugs to allow for adaptation to the new environment.…”

Section: Methodsmentioning

confidence: 99%

“…We have reported that administration of harmine in combination with apomorphine induces violent jumping in rats instead of a tremor. This behavior was induced by harmine when the central dopaminergic system was activated by apomorphine or L-DOPA plus benserazide, and the intensity of the jumping behavior depended on the dose of harmine administered (5). Harmine microinjected into the caudate nucleus as well as by subcu taneous injection caused a tremor in rats (1), and harmaline, an analog of (9-carboline, induced a tremor which depended on harmaline concentration in the brain (6).…”

Section: Harminementioning

confidence: 99%

Estimation of harmine and its derivatives by HPLC : Correlation of brain harmine levels with jumping behavior in rats.

Moroi

Kuga

1987

Jpn.J.Pharmacol

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Abstract-Brainharmine was simply and sensitively determined by high perfor mance liquid chromatography (HPLC), and the relationship between brain harmine concentrations and the jumping behavior induced by harmine and apomorphine was investigated. The concentration of harmine and the peak height in HPLC showed a good correlation, and the detection limit was 0.05 pmole harmine.In rats treated with 2, 5 and 10 mg/kg of harmine, the concentrations of harmine in the brain cortex were 9.0, 21.3 and 43.1 nmole/g tissue (wet wt.), respectively. The regional brain harmine concentrations and the jumping activity measuring by a scoring system increased with increasing doses of harmine administered, and there was a direct relation between the harmine concentrations and the jumping activity. This relation was observed in washed membranes in which about 40% of the harmine in whole homogenate was present. Tissue subfractionation showed that 30% of the harmine in whole brain homogenates was in the P2 fraction, and of this, 70% was located in the synaptosomes. The brain homogenate did not metabolize harmine and no metabolite was detected in the brain 10 min after treat ment with harmine and apomorphine.These results suggest that harmine itself, but not its metabolites, may be responsible for inducing the jumping behavior and that the jumping activity is correlated with brain harmine concentrations.

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Interaction of β-carbolines with central dopaminergic transmission in mice: structure-activity relationships

Pimpinella

Palmery

1995

Neuroscience Letters

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Role of brain monoamine systems in the jumping behavior induced in rats by the combination of harmine and apomorphine.

Cited by 5 publications

References 10 publications

Involvement of GABAergic systems and benzodiazepine receptors in the jumping behavior induced by harmine and apomorphine in rats.

Involvement of GABAergic systems and benzodiazepine receptors in the jumping behavior induced by harmine and apomorphine in rats.

Estimation of harmine and its derivatives by HPLC : Correlation of brain harmine levels with jumping behavior in rats.

Interaction of β-carbolines with central dopaminergic transmission in mice: structure-activity relationships

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