Enhanced effect of dopaminergic stimulation on prepulse inhibition in mice deficient in the alpha subunit of Gz View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2005-10-12

AUTHORS

M. van den Buuse, S. Martin, J. Brosda, K. J. Leck, K. I. Matthaei, I. Hendry

ABSTRACT

RationaleGz is a member of the Gi G protein family associated with dopamine D2-like receptors; however, its functions remain relatively unknown. The aim of the present study was to investigate prepulse inhibition (PPI) of acoustic startle, locomotor hyperactivity and dopamine D2 receptor binding in mice deficient in the α subunit of Gz.MethodsWe used automated startle boxes to assess startle and PPI after treatment with saline, amphetamine, apomorphine or MK-801. We used photocell cages to quantitate locomotor activity after amphetamine treatment. Dopamine D2 receptor density was determined by autoradiography.ResultsStartle responses and baseline PPI were not different between the Gαz knockout mice and wild-type controls (average PPI 46±4 vs 49±3%, respectively). Amphetamine treatment caused a marked disruption of PPI in Gαz knockouts (average PPI 22±2%), but less so in controls (average PPI 42±3%). Similar genotype-dependent responses were seen after apomorphine treatment (average PPI 23±3% vs 40±3%), but not after MK-801 treatment (average PPI 29±5 vs 33±2%). Amphetamine-induced locomotor hyperactivity was greater in Gαz knockouts than in controls. There was no difference in the density of dopamine D2 receptors in nucleus accumbens.ConclusionsMice deficient in the α subunit of Gz show enhanced sensitivity to the disruption of PPI and locomotor hyperactivity caused by dopaminergic stimulation. These results suggest a possible role for Gz in neuropsychiatric illnesses with presumed dopaminergic hyperactivity, such as schizophrenia. More... »

PAGES

358-367

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00213-005-0181-6

DOI

http://dx.doi.org/10.1007/s00213-005-0181-6

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1003350144

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16220329


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