Infusions into the oculomotor nucleus or nerve: a method of estimating the dosage at which transmitter antagonists infused intracranially produce nonspecific blocking of neural activity

Lidocaine, a local anesthetic, was first infused into the oculomotor nucleus or nerve in anesthetized rats through one barrel of a two barrel infusion needle and the extent of pupillary dilation measured. Ten to fifteen minutes after the pupillary diameter had returned to its preinfusion level, a transmitter antagonist was injected through the second barrel of the cannula and its effect on pupillary diameter measured. Lidocaine, when in close proximity to the oculomotor nucleus or nerve produced a dilation of 3 to 4 mm while saline produced no consistent change. Infusion of phentolamine (α-adrenergic), tolazoline (α-adrenergic), atropine (cholinergic), and haloperidol (dopaminergic) but not propranolol (β-adrenergic) produced increases in pupillary diameter as large as those produced by lidocaine whether infused along the nerve or into the nucleus. In a second experiment using unanesthetized rats, dilation by each of these substances and infusion methyl nitrate and propranolol induced dilation when infused into the oculomotor nucleus. In a final experiment, (dopamine) agonists produced pupillary constriction. These results suggest that pupillary control by the oculomotor nucleus is sensitive to glutamate and aspartate but not to several other well known transmitter substances. It, therefore, can serve as a useful site for the evaluation of the nonspecific suppression of neural activity caused by various transmitter antagonists as well as a variety of other excitatory and inhibitory substances.