Rights statement: http://journals.cambridge.org/action/displayJournal?jid=NEU The final, definitive version of this article has been published in the Journal, Acta Neuropsychiatrica, 28 (2), pp 110-116 2016, © 2016 Cambridge University Press.
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Research output: Contribution to Journal/Magazine › Journal article › peer-review
Research output: Contribution to Journal/Magazine › Journal article › peer-review
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TY - JOUR
T1 - Long-term treatment with haloperidol affects neuropeptide S and NPSR mRNA levels in the rat brain
AU - Palasz, Artur
AU - Rojczyk, Ewa
AU - Golyszny, Milosz
AU - Filipczyk, Lukasz
AU - Worthington, John J.
AU - Wiaderkiewicz, Ryszard
N1 - http://journals.cambridge.org/action/displayJournal?jid=NEU The final, definitive version of this article has been published in the Journal, Acta Neuropsychiatrica, 28 (2), pp 110-116 2016, © 2016 Cambridge University Press.
PY - 2016/4
Y1 - 2016/4
N2 - OBJECTIVE: The brainstem-derived neuropeptide S (NPS) has a multidirectional regulatory activity, especially as a potent anxiolytic factor. Accumulating data suggests that neuroleptics affect peptidergic signalling in various brain structures. However, there is no information regarding the influence of haloperidol on NPS and NPS receptor (NPSR) expression.METHODS: We assessed NPS and NPSR mRNA levels in brains of rats treated with haloperidol using quantitative real-time polymerase chain reaction.RESULTS: Chronic haloperidol treatment (4 weeks) led to a striking upregulation of NPS and NPSR expression in the rat brainstem. Conversely, the NPSR mRNA expression was decreased in the hippocampus and striatum.CONCLUSIONS: This stark increase of NPS in response to haloperidol treatment supports the hypothesis that this neuropeptide is involved in the dopamine-dependent anxiolytic actions of neuroleptics and possibly also in the pathophysiology of mental disorders. Furthermore, our findings underline the complex nature of potential interactions between dopamine receptors and brain peptidergic pathways, which has potential clinical applications.
AB - OBJECTIVE: The brainstem-derived neuropeptide S (NPS) has a multidirectional regulatory activity, especially as a potent anxiolytic factor. Accumulating data suggests that neuroleptics affect peptidergic signalling in various brain structures. However, there is no information regarding the influence of haloperidol on NPS and NPS receptor (NPSR) expression.METHODS: We assessed NPS and NPSR mRNA levels in brains of rats treated with haloperidol using quantitative real-time polymerase chain reaction.RESULTS: Chronic haloperidol treatment (4 weeks) led to a striking upregulation of NPS and NPSR expression in the rat brainstem. Conversely, the NPSR mRNA expression was decreased in the hippocampus and striatum.CONCLUSIONS: This stark increase of NPS in response to haloperidol treatment supports the hypothesis that this neuropeptide is involved in the dopamine-dependent anxiolytic actions of neuroleptics and possibly also in the pathophysiology of mental disorders. Furthermore, our findings underline the complex nature of potential interactions between dopamine receptors and brain peptidergic pathways, which has potential clinical applications.
KW - brainstem
KW - haloperidol
KW - neuroleptics
KW - NPSR
U2 - 10.1017/neu.2015.56
DO - 10.1017/neu.2015.56
M3 - Journal article
C2 - 26467816
VL - 28
SP - 110
EP - 116
JO - Acta Neuropsychiatrica
JF - Acta Neuropsychiatrica
SN - 0924-2708
IS - 2
ER -