Abstract
1. Administration of bromocriptine (0.1–2.5 mg/kg, i.p.) to mice produced hypothermia.
2. Pretreatment with the
α
1-adrenoceptor blocker, prazosin (2.0 mg/kg, i.p.) or the
α
2-adrenoceptor antagonist yohimbine (2.5 mg/kg, i.p.) had no effect on this response.
3. The inhibitor of catecholamine synthesis,
α-methyl-
p-tyrosine, and the muscarinic antagonist, atropine (10 mg/kg, i.p.) failed to alter the hypothermia.
4. Pretreatment with the dopamine (DA) receptor antagonists haloperidol (0.02 mg/kg, i.p.) or
cis-flupenthixol (0.01 mg/kg, i.p.) completely blocked this response while
trans-flupenthixol (0.05 mg/kg, rmi.p.) was inactive.
5. Depletion of 5-HT in the brain by
p-chlorophenylalanine reduced the hypothermic response.
6. Similarly, pretreatment with the serotonergic (5-HT) receptor blocker ketanserin (1 mg/kg, i.p.) attenuated the hypotermia and at a dose of 2 mg/kg (i.p.) it completely blocked the hypothermic response.
7. Methysergide (5 mg/kg, i.p.) was also effective in antagonizing the hypothermia.
8. It was concluded that both DA and 5-HT mechanisms are involved in bromocriptine-induced hypothermia in mice.