The effects of central I|1-imidazoline and A|2-adrenergic receptors on body temperature regulation in conscious rats

• Main Author: Harrigan, Tom
• Format: Others
• Language: en; en_US
• Published: 2007
• Online Access: http://hdl.handle.net/1993/1852

Clonidine, an _2-adrenergic receptor agonist, is a classic pharmacological tool used to study the sympathetic control of cardiovascular and thermoregulatory processes. Clonidine's ability to inhibit sympathetic output may be linked more to its affinity for non-adrenergic I1-imidazoline receptors than for _2-adrenoceptors. Previous research has focused on the role of medullary _2-adrenergic and I 1-imidazoline receptors in regulating blood pressure; yet, structures rostral to the brainstem also influence sympathetic output. What role I 1-imidazoline receptors located in the medulla, or those located in the region of the third ventricle, exert towards the regulation of body temperature is largely unexplored. The present study assessed the relative contributions of diencephalic and medullary _2-adrenergic and I1-imidazoline receptors on core body temperature in conscious rats. In Experiment 1, 24 rats received chronically indwelling thermistors, for recording body temperature, and intracerebroventricular (ICV)cannulae targeted to the third ventricle, an area near the hypothalamus, for drug administration. In a repeated measures design, 12 rats were pretreated with central administration of 4 [mu]l of saline or efaroxan, an I1-antagonist; 20-min later moxonidine, an I1 agonist, was centrally administered in l of 3 doses (0, 1, 10 nmol) delivered in a 4 [mu]l saline over 45-60 s. The other 12 rats were similarly pretreated with saline or SK&F 86466, an _2 -adrenergic receptor antagonist, followed 20 min later with 1 of 3 doses (0, 1, 10 nmol) of UK 14304, an a2-adrenergic receptor agonist. Body temperature was monitored at 30-min intervals for 4 hr. The result were contrary to what might have been predicted from reports of moxonidine-induced reductions in blood pressure in that 10-nmol of moxonidine increased core body temperature (>1.5C, 'p' < .02). However, the increase in body temperature was reversed with efaroxan. UK 14304 did not alter body temperature. In Experiment 2, 24 rats underwent the same procedure as described above, except the drugs were delivered to the fourth ventricle, an area near the medulla. In this case, neither moxonidine nor UK 14304 had any significant effect on body temperature. These findings support the notion that I 1-imidazoline and _2-adrenergic receptors in the diencephalon and medulla are functionally distinct, and that the thermoregulatory contribution of diencephalic I1-imidazoline receptors is different from what would be predicted from their sympathoinhibitory action exhibited in the medulla.