- Title
- The effects of haloperidol treatment on the distribution of NK1 receptor immunoreactive neurons in guinea-pig brain (Short communication)
- Creator
- Tooney, Paul A.; Anderson, Wayne B.; Lynch-Frame, Ann; Chahl, Loris Avril
- Relation
- Neuroscience Letters Vol. 383, no. 1-2, p. 155-159
- Publisher
- Elsevier Science Ireland
- Resource Type
- journal article
- Date
- 2005
- Description
- Previous studies have observed increased tachykinin NK1 receptor immunoreactivity (NK1-IR) in the prefrontal cortex in subjects with schizophrenia. Since the subjects were medicated the possibility of a treatment effect could not be excluded. Thus, the present study was undertaken to determine the effect of chronic treatment with the antipsychotic drug, haloperidol, on the distribution of NK1-IR neurons in the guinea-pig brain. Guinea pigs were treated each day for 21 days with either haloperidol (1 mg/kg) or vehicle and the brains were then processed for immumohistochemistry using an NK1 receptor-specific polyclonal antibody. NK1-IR neurons and fibres were abundant in the forebrain cortex and caudate putamen and more sparsely distributed in a number of other brain regions. The relative density of NK1-IR neurons was significantly increased in the forebrain cortex, but not in the caudate putamen in guinea pigs treated with haloperidol. This study has shown that haloperidol causes region-specific changes to the density of NK1-IR neurons. Whether these changes are related to the therapeutic effects or to the side effects of haloperidol in individuals with schizophrenia, remains to be determined. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
- Subject
- tachykinins; NK1 receptor; haloperidol; schizophrenia; guinea pig; messenger RNA levels; prefrontal cortex; tachykinin NK1; substance P; neuroleptic treatment; nucleus accumbens; caudate putamen; visual cortex; rat
- Identifier
- uon:534
- Identifier
- http://hdl.handle.net/1959.13/24643
- Identifier
- ISSN:0304-3940
- Language
- eng
- Hits: 2652
- Visitors: 3137
- Downloads: 0