Chronic corticotropin-releasing factor type 1 receptor antagonism with antalarmin regulates the dopaminergic system of Fawn-Hooded rats

Lawrence, A, Parish, C, Chen, F, Lodge, D, Krstew, E, Card, K, Finkelstein, D and Horne, M 2005, 'Chronic corticotropin-releasing factor type 1 receptor antagonism with antalarmin regulates the dopaminergic system of Fawn-Hooded rats', Journal of Neurochemistry, vol. 94, no. 6, pp. 1523-1534.


Document type: Journal Article
Collection: Journal Articles

Title Chronic corticotropin-releasing factor type 1 receptor antagonism with antalarmin regulates the dopaminergic system of Fawn-Hooded rats
Author(s) Lawrence, A
Parish, C
Chen, F
Lodge, D
Krstew, E
Card, K
Finkelstein, D
Horne, M
Year 2005
Journal name Journal of Neurochemistry
Volume number 94
Issue number 6
Start page 1523
End page 1534
Total pages 12
Publisher Wiley-Blackwell Publishing
Abstract Corticotropin-releasing factor is a neuropeptide associated with the integration of physiological and behavioural responses to stress and also in the modulation of affective state and drug reward. The selective, centrally acting corticotropin-releasing factor type 1 receptor antagonist, antalarmin, is a potent anxiolytic and reduces volitional ethanol consumption in Fawn-Hooded rats. The efficacy of antalarmin to reduce ethanol consumption increased with time, suggestive of adaptation to reinforcement processes and goal-directed behaviour. The aim of the present study was to examine the effects of chronic antalarmin treatment on reward-related regions of Fawn-Hooded rat brain. Bi-daily antalarmin treatment (20 mg/kg, i.p.) for 10 days increased tyrosine hydroxylase messenger RNA expression throughout the ventral mesencephalon. Following chronic antalarmin the density of dopaminergic terminals within the basal ganglia and amygdaloid complex were reduced, as was dopamine transporter binding within the striatum. Receptor autoradiography indicated an up-regulation of dopamine D2, but no change in D1, binding in striatum, and Golgi-Cox analysis of striatal medium spiny neurones indicated that chronic antalarmin treatment increased spine density. Thus, chronic antalarmin treatment modulates dopaminergic pathways and implies that chronic treatment with drugs of this class may ultimately alter postsynaptic signaling mechanisms within the basal ganglia.
Subject Central Nervous System
DOI - identifier 10.1111/j.1471-4159.2005.03300.x
ISSN 0022-3042
Versions
Version Filter Type
Citation counts: Scopus Citation Count Cited 10 times in Scopus Article | Citations
Altmetric details:
Access Statistics: 129 Abstract Views  -  Detailed Statistics
Created: Mon, 06 Dec 2010, 14:11:00 EST by Catalyst Administrator
© 2014 RMIT Research Repository • Powered by Fez SoftwareContact us