Propranolol attenuates haloperidol-induced Fos expression in discrete regions of rat brain: possible brain regions responsible for akathisia.
Brain Res
; 802(1-2): 134-40, 1998 Aug 17.
Article
in En
| MEDLINE
| ID: mdl-9748542
ABSTRACT
Neuroleptics induce several extra-pyramidal side effects, such as akathisia, acute dystonia and parkinsonism. Although recently developed atypical neuroleptics ameliorate some of these side effects, akathisia remains a common and severely distressing adverse reaction. Several drugs are reported to be of clinical use for the pharmacological treatment of akathisia. In particular, the beta-adrenoceptor blocker, propranolol, has been widely used for the treatment of akathisia, but it does not ameliorate other extra-pyramidal side effects. To identify the neural substrates of akathisia, we investigated the effects of propranolol on haloperidol-induced Fos expression in rat brain. Haloperidol (1 mg/kg) induced Fos-positive nuclei in several regions of the brain, including the cingulate cortex area 3, piriform cortex nucleus accumbens, caudate-putamen, ventral lateral septum and parietal cortex. Pretreatment with propranolol (5 mg/kg) reduced the number of Fos-positive nuclei in the cingulate cortex area 3, the piriform cortex and area 1 of the parietal cortex. Injection of vehicle by itself tended to increase Fos expression in the cingulate cortex area 3 and the piriform cortex. Considering the functions of these brain regions, we speculate that the most plausible neural framework for haloperidol-induced akathisia involves area I of the parietal cortex, but possible roles for the cingulate cortex area 3 and the piriform cortex cannot be ruled out.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Propranolol
/
Antipsychotic Agents
/
Brain
/
Proto-Oncogene Proteins c-fos
/
Adrenergic beta-Antagonists
/
Haloperidol
Limits:
Animals
Language:
En
Journal:
Brain Res
Year:
1998
Type:
Article
Affiliation country:
Japan