Clonidine mydriasis in the cat

Summary

Both clonidine (1–100 μg/kg, i.v.) and d-amphetamine (500 μg, i.c.v.) produced mydriasis associated with depression of tonic ciliary nerve activity in the anaesthetized cat. Clonidine administration in preparations depleted of noradrenaline, dopamine and serotonin by pretreatment with reserpine (5 mg/kg, i.p.) and α-methyl-p-tyrosine (2×300 mg/kg, i.p.) resulted in a quantitatively similar mydriasis and inhibition of nerve activity. Thus it is concluded that both drugs cause pupillary dilation by inhibition of parasympathetic tone to the iris and that clonidine's action on this particular system is probably postsynaptic.

In contrast, amine depletion totally prevented amphetamine-induced mydriasis and parasympathetic nerve depression, supporting the contention that centrally administered amphetamine acts in this system by means of releasing endogenous stores of monoamines. Pretreatment with yohimbine (0.5 mg/kg, i.v.) totally blocked the effects of i.c.v. amphetamine as it does with clonidine.

These studies suggest that the pupillary dilation by i.v. clonidine and i.c.v. amphetamine is primarily the result of central inhibition of parasympathetic tone to the iris. It would appear that clonidine produces this effect by acting on postsynaptic mechanisms and that amphetamine acts indirectly through release of an endogenous inhibitory neurotransmitter. The observation that the effects of both of these compounds are blocked by yohimbine supports the suggestion that a central adrenergic inhibitory mechanism is involved.