Chronic fluoxetine treatment attenuates stressor-induced changes in temperature, heart rate, and neuronal activation in the olfactory bulbectomised rat
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2007Author
Roche, Michelle
Harkin, Andrew
Kelly, John P.
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Roche, M., Harkin, A., Kelly, J. P. (2007) 'Chronic fluoxetine treatment attenuates stressor-induced changes in temperature, heart rate, and neuronal activation in the olfactory bulbectomised rat'. Neuropsychopharmacology, 32 (6):1312-1320.
Abstract
The olfactory bulbectomized (OB) rat is a well characterized animal model that
exhibits a number of behavioural and neurochemical changes that have relevance to
clinical depression. Hyperactivity in the open field is the most widely used parameter
assessed in this model and is reversed following chronic, but not acute, antidepressant
treatment. This study investigated OB-induced alterations in heart rate, body
temperature and neuronal activation following open field exposure and the impact of
chronic treatment with fluoxetine on these parameters. Upon placement in the open
field OB rats exhibited a characteristic hyperactivity response. Heart rate and body
temperature were increased in sham-operated rats following open field exposure, a
predictable response to stress which was significantly reduced in OB rats. Moreover
bulbectomy reduced open field-induced cFOS expression in the basal nucleus of the
stria terminalis while concurrently increasing expression in the hippocampus,
amygdala, paraventricular nucleus of the thalamus and dorsal raphe nucleus. Chronic
fluoxetine treatment (10 mg/kg s.c. once daily for 5 weeks) attenuated all of these OB
associated changes. In conclusion, OB rats exhibit alterations in behaviour, body
temperature, heart rate and neuronal activation in response to open field exposure
which are reversed following chronic fluoxetine administration. These results identify
stress sensitive regions within the brain which are altered following bulbectomy and
which may underlie the abnormal behavioural and physiological changes observed in
this rodent model of depression.