Abstract
ABSTRACT
In previous work we have determined that intracameral (IC) administration of neurotensin (NT) produces strong miosis in rabbits. However, the pharmacological mechanism of this response remains undetermined. Blockade of α and β-adrenoceptor subtypes with phenoxybenzamine and propanolol, blockade of M. muscarinic receptors with atropine or blockade of mu opioid receptors with naloxone did not affect NT-induced miosis. Of interest however was the observation that destruction of ocular dopamine (DA) nerve endings with 6-hydroxydopamine (6-OHDA) + desmethylimipramine (DMI), or blockade of D-2 DA receptors with haloperidol significantly inhibited the miotic response to IC NT.
These findings indicate that an intact iridic DA pathway is required for the expression of NT-induced miosis.
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