PMID- 24613977
OWN - NLM
STAT- MEDLINE
DCOM- 20141212
LR  - 20140415
IS  - 1872-7549 (Electronic)
IS  - 0166-4328 (Linking)
VI  - 266
DP  - 2014 Jun 1
TI  - Neuropeptide S counteracts 6-OHDA-induced motor deficits in mice.
PG  - 29-36
LID - S0166-4328(14)00144-2 [pii]
LID - 10.1016/j.bbr.2014.03.002 [doi]
AB  - Neuropeptide S (NPS) is a 20-aminoacid peptide that selectively activates a 
      G-protein coupled receptor named NPSR. Preclinical studies have shown that NPSR 
      activation promotes anxiolysis, hyperlocomotion, arousal and weakfullness. 
      Previous findings suggest that dopamine neurotransmission plays a role in the 
      actions of NPS. Based on the close relationship between dopamine and Parkinson 
      disease (PD) and on the evidence that NPSR are expressed on brain dopaminergic 
      nuclei, the present study investigated the effects of NPS in motor deficits 
      induced by intracerebroventricular (icv) administration of the dopaminergic 
      neurotoxin 6-OHDA in the mouse rotarod test. 6-OHDA injection evoked motor 
      deficits and significantly reduced tyrosine hidroxylase (TH)-positive cells in 
      the substantia nigra (SN) and ventral tegmental area. However, a positive 
      correlation was found only between the motor performance of 6-OHDA-injected mice 
      and the number of TH-positive cells in SN. The systemic administration of 
      l-DOPA+benserazide (25+6.25 mg/kg) counteracted 6-OHDA-induced motor deficits in 
      mice. Similar to L-DOPA, the icv injection of NPS (0.1 and 1 nmol) reversed motor 
      deficits evoked by 6-OHDA. In conclusion, NPS attenuated 6-OHDA-induced motor 
      impairments in mice assessed in the rota-rod test. We discussed the beneficial 
      actions of NPS based on a putative facilitation of dopaminergic neurotransmission 
      in the brain. Finally, these findings candidate NPSR agonists as a potential 
      innovative treatment for PD.
CI  - Copyright (c) 2014 Elsevier B.V. All rights reserved.
FAU - Didonet, Julia J
AU  - Didonet JJ
AD  - Behavioral Pharmacology Laboratory, Department of Biophysics and Pharmacology, 
      Federal University of Rio Grande do Norte, Natal, RN, Brazil.
FAU - Cavalcante, Judney C
AU  - Cavalcante JC
AD  - Laboratory of Neuroanatomy, Department of Morphology, Biosciences Center, Federal 
      University of Rio Grande do Norte, Natal, RN, Brazil.
FAU - Souza, Lisiane de S
AU  - Souza Lde S
AD  - Behavioral Pharmacology Laboratory, Department of Biophysics and Pharmacology, 
      Federal University of Rio Grande do Norte, Natal, RN, Brazil.
FAU - Costa, Miriam S M O
AU  - Costa MS
AD  - Laboratory of Neuroanatomy, Department of Morphology, Biosciences Center, Federal 
      University of Rio Grande do Norte, Natal, RN, Brazil.
FAU - Andre, Eunice
AU  - Andre E
AD  - Department of Pharmacology, Federal University of Parana, Curitiba, PR, Brazil.
FAU - Soares-Rachetti, Vanessa de P
AU  - Soares-Rachetti Vde P
AD  - Behavioral Pharmacology Laboratory, Department of Biophysics and Pharmacology, 
      Federal University of Rio Grande do Norte, Natal, RN, Brazil.
FAU - Guerrini, Remo
AU  - Guerrini R
AD  - Department of Chemistry and Pharmaceutical Sciences, University of Ferrara, 
      Ferrara, Italy.
FAU - Calo', Girolamo
AU  - Calo' G
AD  - Department of Medical Sciences, Section of Pharmacology, and National Institute 
      of Neuroscience, University of Ferrara, Ferrara, Italy.
FAU - Gavioli, Elaine C
AU  - Gavioli EC
AD  - Behavioral Pharmacology Laboratory, Department of Biophysics and Pharmacology, 
      Federal University of Rio Grande do Norte, Natal, RN, Brazil. Electronic address: 
      egavioli@hotmail.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140311
PL  - Netherlands
TA  - Behav Brain Res
JT  - Behavioural brain research
JID - 8004872
RN  - 0 (Adrenergic Agents)
RN  - 0 (Dopamine Agents)
RN  - 0 (NPSR1 protein, human)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 46627O600J (Levodopa)
RN  - 8HW4YBZ748 (Oxidopamine)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
SB  - IM
MH  - Adrenergic Agents/*toxicity
MH  - Analysis of Variance
MH  - Animals
MH  - Area Under Curve
MH  - Disease Models, Animal
MH  - Dopamine Agents/therapeutic use
MH  - Female
MH  - Levodopa/therapeutic use
MH  - Mice
MH  - Movement Disorders/*drug therapy/*etiology
MH  - Oxidopamine/*toxicity
MH  - Receptors, G-Protein-Coupled/*therapeutic use
MH  - Rotarod Performance Test
MH  - Substantia Nigra/metabolism/pathology
MH  - Tyrosine 3-Monooxygenase/metabolism
OTO - NOTNLM
OT  - 6-OHDA
OT  - Dopamine
OT  - Motor activity
OT  - Mouse
OT  - Neuropeptide S
OT  - Parkinson disease
EDAT- 2014/03/13 06:00
MHDA- 2014/12/17 06:00
CRDT- 2014/03/12 06:00
PHST- 2014/01/25 00:00 [received]
PHST- 2014/02/28 00:00 [revised]
PHST- 2014/03/03 00:00 [accepted]
PHST- 2014/03/12 06:00 [entrez]
PHST- 2014/03/13 06:00 [pubmed]
PHST- 2014/12/17 06:00 [medline]
AID - S0166-4328(14)00144-2 [pii]
AID - 10.1016/j.bbr.2014.03.002 [doi]
PST - ppublish
SO  - Behav Brain Res. 2014 Jun 1;266:29-36. doi: 10.1016/j.bbr.2014.03.002. Epub 2014 
      Mar 11.