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Results for “YAWNING”

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At least 343 records · Page 19Linked to original sources
PubMed1988

[Effects of bifemelane on central dopaminergic and cholinergic systems in rats].

The study served to examine the effects of bifemelane on central dopaminergic-cholinergic neuronal mechanisms in rats. Bifemelane (5-20 mg/kg) evoked yawning responses, the frequency being low. Bifemelane (10 mg/kg) as well as bromocriptine (2.5 mg/kg) potentiated physostigmine (0.2 mg/kg)-, bromocriptine (2.5 mg/kg)- or apomorphine (0.1 and 0.5 mg/kg)-induced yawning but completely inhibited pilocarpine-induced yawning. Pretreatment with sulpiride (20 mg/kg) and a low dose of haloperidol (0.02 mg/kg) reversed the stimulatory effect of bifemelane on physostigmine-induced yawning and the inhibitory effect of the drug on pilocarpine-induced yawning, whereas atropine (5 mg/kg) diminished these yawning responses. SK&38393 (2.0 mg/kg), a dopamine D-1 receptor agonist, markedly potentiated bifemelane- and bromocriptine-induced yawning but inhibited physostigmine-induced yawning, and did not affect pilocarpine-induced yawning. The increased yawning responses were blocked by atropine and a low dose of haloperidol. Bifemelane (10 mg/kg) and bromocriptine (2.5 mg/kg) tended to increase apomorphine (5 mg/kg)-induced oral stereotypy, such as licking and biting, but the increase was not significant. These results suggest that the effects of bifemelane on central dopaminergic and cholinergic neurons may be similar to those of bromocriptine.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1988

The mode of action of bromocriptine following pretreatment with reserpine and alpha-methyl-p-tyrosine in rats.

The ability of bromocriptine (BRC), a selective dopamine D-2 receptor agonist, to induce yawning responses was studied in rats pretreated with reserpine and alpha-methyl-p-tyrosine (alpha-MPT). BRC (1 20 mg/kg IP) evoked yawning responses, which were pronounced at 2.5 mg/kg and characterized by the head moving downward. Higher doses of BRC (5 20 mg/kg) dose-dependently delayed the onset and peak time of yawning. A low dose of the selective D-1 dopamine receptor agonist SK&F38393 did not induce yawning but enhanced the BRC-induced response. Pretreatment with reserpine (1 and 5 mg/kg SC), alpha-MPT (100 and 300 mg/kg IP) and reserpine (1 mg/kg) plus alpha-MPT (100 mg/kg) was able to significantly reduce BRC-induced yawning. The inhibitory effects were prevented by a low dose of SK&F38393 (0.5 mg/kg IP). In particular, combined treatment with reserpine (5 mg/kg) and BRC (10 and 20 mg/kg) elicited upright fighting and jumping behaviors which were inhibited by haloperidol (1 mg/kg IP), a non-selective D-1 and D-2 receptor antagonist, SCH23390 (0.05 mg/kg SC). a selective D-1 receptor antagonist, or sulpiride (20 mg/kg IP), a potent D-2 receptor antagonist, and were potentiated by SK&F38393 (0.5 mg/kg). SCH23390 (0.05 mg/kg) decreased BRC-induced yawning and the apomorphine (low doses)-induced potentiation of BRC yawning, and prevented the apomorphine (high doses)-induced reduction of BRC yawning. SCH23390 also inhibited apomorphine-induced stereotypy and BRC-induced potentiation of apomorphine stereotypy.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1992

Behavioral effects of dilazep on cholinergic, dopaminergic, and purinergic systems in the rat.

This study examined the effects of 1,4-bis[3-(3,4,5-trimethoxy benzoyloxy)-propyl] perhydro-1,4-diazepine (dilazep; Comelian) on central dopaminergic, cholinergic, and purinergic neuronal systems in rats. Intraperitoneal injections of dilazep (1-5 mg/kg) produced yawning responses, the most effective dose being 2 mg/kg. Dilazep potentiated physostigmine-induced yawning but not pilocarpine- and bromocriptine-induced yawning. Dilazep-induced yawning was not affected by low doses of haloperidol or sulpiride, but was completely inhibited by atropine, a muscarinic M1 receptor antagonist. Dilazep-induced yawning, as well as physostigmine-induced yawning, were markedly inhibited by pretreatment with SK & F 38393, a dopamine D1 receptor agonist, and were potentiated by SCH23390, a dopamine D1 receptor antagonist that alone does not elicit yawning. Caffeine, an adenosine receptor antagonist, inhibited dilazep- and physostigmine-induced yawning responses but N6-cyclohexyl adenosine (CHA) and N6-(L-phenylisopropyl, adenosine (L-PIA), adenosine A1 receptor agonists, were inactive. These results suggest that because the effects of dilazep on central cholinergic neurons are similar to those of physostigmine dilazep may potentiate indirectly the action of endogenous acetylcholine. Cholinergic neurons activated by dilazep may be modulated by postsynaptic dopamine D1 receptor activity but may not be affected by dopamine D2 receptor activity. Furthermore, the stimulatory effects of dilazep on cholinergic neuron may not be due to an inhibition of dopamine D1 receptors via purinergic (adenosine A1 receptor) stimulation by dilazep.

Animals↗