Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias. Effects of clozapine, haloperidol, loxapine and chlorpromazine
| ISSN: |
1432-2072
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|---|---|
| Keywords: |
Tardive Dyskinesia ; Dopamine Receptor Hypersensitivity ; Apomorphine Response ; Homovanillic Acid ; Tolerance ; Clozapine ; Haloperidol ; Chlorpromazine ; Loxapine
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| Source: |
Springer Online Journal Archives 1860-2000
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| Topics: |
Medicine
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| Notes: |
Abstract The present study has compared the abilities of clozapine, haloperidol, chlorpromazine and loxapine to induce dopamine (DA)-receptor hypersensitivity in rats, as measured by the apomorphine response after withdrawal of the antipsychotic drugs. Haloperidol, chlorpromazine and loxapine, but not clozapine, potentiated the apomorphine response during 1–2 weeks after withdrawal. Clozapine, given prior to apomorphine, reduced the responses of the haloperidol and loxapine groups to the control level. The effects of haloperidol and clozapine were quantified in rats with unilateral striatal lesions. Biochemical investigations showed that tolerance developed to the increase in striatal homovanillic acid (HVA) after chronic treatment with haloperidol, chlorpromazine and loxapine, whereas clozapine (20 mg/kg p.o.) failed to affect the HVA content, and no tolerance developed to the increase seen at 80 mg/kg. Cross-tolerance to the rise in HVA was seen with haloperidol, chlorpromazine and loxapine, but chronic pretreatment with clozapine failed to affect the rise in HVA induced by a single dose of the former compounds. On the basis of these results, it is predicted that tardive dyskinesias are unlikely to develop after this drug, and that clozapine may attenuate or abolish neuroleptic-induced tardive dyskinesias.
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| Type of Medium: |
Electronic Resource
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| URL: |
| _version_ | 1798295935881576448 |
|---|---|
| autor | Sayers, A. C. Bürki, H. R. Ruch, W. Asper, H. |
| autorsonst | Sayers, A. C. Bürki, H. R. Ruch, W. Asper, H. |
| book_url | http://dx.doi.org/10.1007/BF00421063 |
| datenlieferant | nat_lic_papers |
| hauptsatz | hsatz_simple |
| identnr | NLM200760912 |
| issn | 1432-2072 |
| journal_name | Psychopharmacology |
| materialart | 1 |
| notes | Abstract The present study has compared the abilities of clozapine, haloperidol, chlorpromazine and loxapine to induce dopamine (DA)-receptor hypersensitivity in rats, as measured by the apomorphine response after withdrawal of the antipsychotic drugs. Haloperidol, chlorpromazine and loxapine, but not clozapine, potentiated the apomorphine response during 1–2 weeks after withdrawal. Clozapine, given prior to apomorphine, reduced the responses of the haloperidol and loxapine groups to the control level. The effects of haloperidol and clozapine were quantified in rats with unilateral striatal lesions. Biochemical investigations showed that tolerance developed to the increase in striatal homovanillic acid (HVA) after chronic treatment with haloperidol, chlorpromazine and loxapine, whereas clozapine (20 mg/kg p.o.) failed to affect the HVA content, and no tolerance developed to the increase seen at 80 mg/kg. Cross-tolerance to the rise in HVA was seen with haloperidol, chlorpromazine and loxapine, but chronic pretreatment with clozapine failed to affect the rise in HVA induced by a single dose of the former compounds. On the basis of these results, it is predicted that tardive dyskinesias are unlikely to develop after this drug, and that clozapine may attenuate or abolish neuroleptic-induced tardive dyskinesias. |
| package_name | Springer |
| publikationsjahr_anzeige | 1975 |
| publikationsjahr_facette | 1975 |
| publikationsjahr_intervall | 8024:1975-1979 |
| publikationsjahr_sort | 1975 |
| publisher | Springer |
| reference | 41 (1975), S. 97-104 |
| schlagwort | Tardive Dyskinesia Dopamine Receptor Hypersensitivity Apomorphine Response Homovanillic Acid Tolerance Clozapine Haloperidol Chlorpromazine Loxapine |
| search_space | articles |
| shingle_author_1 | Sayers, A. C. Bürki, H. R. Ruch, W. Asper, H. |
| shingle_author_2 | Sayers, A. C. Bürki, H. R. Ruch, W. Asper, H. |
| shingle_author_3 | Sayers, A. C. Bürki, H. R. Ruch, W. Asper, H. |
| shingle_author_4 | Sayers, A. C. Bürki, H. R. Ruch, W. Asper, H. |
| shingle_catch_all_1 | Sayers, A. C. Bürki, H. R. Ruch, W. Asper, H. Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias. Effects of clozapine, haloperidol, loxapine and chlorpromazine Tardive Dyskinesia Dopamine Receptor Hypersensitivity Apomorphine Response Homovanillic Acid Tolerance Clozapine Haloperidol Chlorpromazine Loxapine Tardive Dyskinesia Dopamine Receptor Hypersensitivity Apomorphine Response Homovanillic Acid Tolerance Clozapine Haloperidol Chlorpromazine Loxapine Abstract The present study has compared the abilities of clozapine, haloperidol, chlorpromazine and loxapine to induce dopamine (DA)-receptor hypersensitivity in rats, as measured by the apomorphine response after withdrawal of the antipsychotic drugs. Haloperidol, chlorpromazine and loxapine, but not clozapine, potentiated the apomorphine response during 1–2 weeks after withdrawal. Clozapine, given prior to apomorphine, reduced the responses of the haloperidol and loxapine groups to the control level. The effects of haloperidol and clozapine were quantified in rats with unilateral striatal lesions. Biochemical investigations showed that tolerance developed to the increase in striatal homovanillic acid (HVA) after chronic treatment with haloperidol, chlorpromazine and loxapine, whereas clozapine (20 mg/kg p.o.) failed to affect the HVA content, and no tolerance developed to the increase seen at 80 mg/kg. Cross-tolerance to the rise in HVA was seen with haloperidol, chlorpromazine and loxapine, but chronic pretreatment with clozapine failed to affect the rise in HVA induced by a single dose of the former compounds. On the basis of these results, it is predicted that tardive dyskinesias are unlikely to develop after this drug, and that clozapine may attenuate or abolish neuroleptic-induced tardive dyskinesias. 1432-2072 14322072 Springer |
| shingle_catch_all_2 | Sayers, A. C. Bürki, H. R. Ruch, W. Asper, H. Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias. Effects of clozapine, haloperidol, loxapine and chlorpromazine Tardive Dyskinesia Dopamine Receptor Hypersensitivity Apomorphine Response Homovanillic Acid Tolerance Clozapine Haloperidol Chlorpromazine Loxapine Tardive Dyskinesia Dopamine Receptor Hypersensitivity Apomorphine Response Homovanillic Acid Tolerance Clozapine Haloperidol Chlorpromazine Loxapine Abstract The present study has compared the abilities of clozapine, haloperidol, chlorpromazine and loxapine to induce dopamine (DA)-receptor hypersensitivity in rats, as measured by the apomorphine response after withdrawal of the antipsychotic drugs. Haloperidol, chlorpromazine and loxapine, but not clozapine, potentiated the apomorphine response during 1–2 weeks after withdrawal. Clozapine, given prior to apomorphine, reduced the responses of the haloperidol and loxapine groups to the control level. The effects of haloperidol and clozapine were quantified in rats with unilateral striatal lesions. Biochemical investigations showed that tolerance developed to the increase in striatal homovanillic acid (HVA) after chronic treatment with haloperidol, chlorpromazine and loxapine, whereas clozapine (20 mg/kg p.o.) failed to affect the HVA content, and no tolerance developed to the increase seen at 80 mg/kg. Cross-tolerance to the rise in HVA was seen with haloperidol, chlorpromazine and loxapine, but chronic pretreatment with clozapine failed to affect the rise in HVA induced by a single dose of the former compounds. On the basis of these results, it is predicted that tardive dyskinesias are unlikely to develop after this drug, and that clozapine may attenuate or abolish neuroleptic-induced tardive dyskinesias. 1432-2072 14322072 Springer |
| shingle_catch_all_3 | Sayers, A. C. Bürki, H. R. Ruch, W. Asper, H. Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias. Effects of clozapine, haloperidol, loxapine and chlorpromazine Tardive Dyskinesia Dopamine Receptor Hypersensitivity Apomorphine Response Homovanillic Acid Tolerance Clozapine Haloperidol Chlorpromazine Loxapine Tardive Dyskinesia Dopamine Receptor Hypersensitivity Apomorphine Response Homovanillic Acid Tolerance Clozapine Haloperidol Chlorpromazine Loxapine Abstract The present study has compared the abilities of clozapine, haloperidol, chlorpromazine and loxapine to induce dopamine (DA)-receptor hypersensitivity in rats, as measured by the apomorphine response after withdrawal of the antipsychotic drugs. Haloperidol, chlorpromazine and loxapine, but not clozapine, potentiated the apomorphine response during 1–2 weeks after withdrawal. Clozapine, given prior to apomorphine, reduced the responses of the haloperidol and loxapine groups to the control level. The effects of haloperidol and clozapine were quantified in rats with unilateral striatal lesions. Biochemical investigations showed that tolerance developed to the increase in striatal homovanillic acid (HVA) after chronic treatment with haloperidol, chlorpromazine and loxapine, whereas clozapine (20 mg/kg p.o.) failed to affect the HVA content, and no tolerance developed to the increase seen at 80 mg/kg. Cross-tolerance to the rise in HVA was seen with haloperidol, chlorpromazine and loxapine, but chronic pretreatment with clozapine failed to affect the rise in HVA induced by a single dose of the former compounds. On the basis of these results, it is predicted that tardive dyskinesias are unlikely to develop after this drug, and that clozapine may attenuate or abolish neuroleptic-induced tardive dyskinesias. 1432-2072 14322072 Springer |
| shingle_catch_all_4 | Sayers, A. C. Bürki, H. R. Ruch, W. Asper, H. Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias. Effects of clozapine, haloperidol, loxapine and chlorpromazine Tardive Dyskinesia Dopamine Receptor Hypersensitivity Apomorphine Response Homovanillic Acid Tolerance Clozapine Haloperidol Chlorpromazine Loxapine Tardive Dyskinesia Dopamine Receptor Hypersensitivity Apomorphine Response Homovanillic Acid Tolerance Clozapine Haloperidol Chlorpromazine Loxapine Abstract The present study has compared the abilities of clozapine, haloperidol, chlorpromazine and loxapine to induce dopamine (DA)-receptor hypersensitivity in rats, as measured by the apomorphine response after withdrawal of the antipsychotic drugs. Haloperidol, chlorpromazine and loxapine, but not clozapine, potentiated the apomorphine response during 1–2 weeks after withdrawal. Clozapine, given prior to apomorphine, reduced the responses of the haloperidol and loxapine groups to the control level. The effects of haloperidol and clozapine were quantified in rats with unilateral striatal lesions. Biochemical investigations showed that tolerance developed to the increase in striatal homovanillic acid (HVA) after chronic treatment with haloperidol, chlorpromazine and loxapine, whereas clozapine (20 mg/kg p.o.) failed to affect the HVA content, and no tolerance developed to the increase seen at 80 mg/kg. Cross-tolerance to the rise in HVA was seen with haloperidol, chlorpromazine and loxapine, but chronic pretreatment with clozapine failed to affect the rise in HVA induced by a single dose of the former compounds. On the basis of these results, it is predicted that tardive dyskinesias are unlikely to develop after this drug, and that clozapine may attenuate or abolish neuroleptic-induced tardive dyskinesias. 1432-2072 14322072 Springer |
| shingle_title_1 | Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias. Effects of clozapine, haloperidol, loxapine and chlorpromazine |
| shingle_title_2 | Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias. Effects of clozapine, haloperidol, loxapine and chlorpromazine |
| shingle_title_3 | Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias. Effects of clozapine, haloperidol, loxapine and chlorpromazine |
| shingle_title_4 | Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias. Effects of clozapine, haloperidol, loxapine and chlorpromazine |
| sigel_instance_filter | dkfz geomar wilbert ipn albert fhp |
| source_archive | Springer Online Journal Archives 1860-2000 |
| timestamp | 2024-05-06T09:44:06.991Z |
| titel | Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias. Effects of clozapine, haloperidol, loxapine and chlorpromazine |
| titel_suche | Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias. Effects of clozapine, haloperidol, loxapine and chlorpromazine |
| topic | WW-YZ |
| uid | nat_lic_papers_NLM200760912 |