Potentiation of choroidal vasodilation following repetitive stimulation of the nucleus of Edinger-Westphal in pigeon

Y. Zagvazdin, M. E C Fitzgerald, Anton Reiner

Research output: Contribution to journalArticle

Abstract

Purpose. Activation of the nucleus of Edinger-Westphal (EW), the input to the ciliary ganglion (CG) via the oculomotor nerve, elicits vasodilation of the choroidal blood vessels in pigeon (Fitzgerald et al., 1990). Tetanic stimulation of the oculomotor nerve is known to cause potentiation of evoked postsynaptic potentials in the CG of birds (Martin & Pilar, 1964). In this study, we sought to determine whether the phenomenon of "post-tetanic" potentiation in the CG is reflected in an increased choroidal vasodilatory response and whether ganglionic transmission accounts for this effect. Methods. Choroidal blood flow (ChBF) was measured transclerally using the laser Doppler technique in pigeons anesthetized by urethane or ketamine and xylazine. Stimulation to induce choroidal vasodilation (anodal puses 0.5-1 ms duration, 50-200 μA amplitude at 50-75 Hz for 5 seconds) was applied with a stereotaxically positioned electrode and repeated 1-3 times with an interval of 30-60 seconds. Neuroeffector (atropine, the NOS inhibitor L-NAME) and ganglionic (hexamethonium) blocking agents were infused intravenously to verify the mechanism of potentiation. All brains were subsequently processed histologically to confirm the accuracy of electrode placement. Results. Repeated stimulation resulted in more pronounced vasodilation under both types of anesthesia. The increase in the amplitude of the vasodilatory response varied between 10-60%. The potentiation persisted after atropine. The vasodilatory response was diminished following administration of L-NAME, but post-tetanic potentiation of the response was still observed. Hexamethonium attenuated or suppressed the increase in ChBF and the potentiation of vasodilation following stimulation of EW. Conclusions. A potentiation of the vasodilatory response in the choroid following repeated stimulation of EW is demonstrated by this study. The increase in the efficacy of synaptic transmission through the CG appears to be the mechanism of this effect. The vasodilatory response potentiation may be useful for adaptive control of ChBF.

Original languageEnglish (US)
JournalInvestigative Ophthalmology and Visual Science
Volume37
Issue number3
StatePublished - Feb 15 1996

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Parasympathetic Ganglia
Columbidae
Vasodilation
Oculomotor Nerve
Hexamethonium
NG-Nitroarginine Methyl Ester
Atropine
Electrodes
Ganglionic Blockers
Xylazine
Synaptic Potentials
Choroid
Urethane
Ketamine
Evoked Potentials
Synaptic Transmission
Hair
Birds
Blood Vessels
Lasers

All Science Journal Classification (ASJC) codes

  • Ophthalmology

Cite this

Potentiation of choroidal vasodilation following repetitive stimulation of the nucleus of Edinger-Westphal in pigeon. / Zagvazdin, Y.; Fitzgerald, M. E C; Reiner, Anton.

In: Investigative Ophthalmology and Visual Science, Vol. 37, No. 3, 15.02.1996.

Research output: Contribution to journalArticle

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title = "Potentiation of choroidal vasodilation following repetitive stimulation of the nucleus of Edinger-Westphal in pigeon",
abstract = "Purpose. Activation of the nucleus of Edinger-Westphal (EW), the input to the ciliary ganglion (CG) via the oculomotor nerve, elicits vasodilation of the choroidal blood vessels in pigeon (Fitzgerald et al., 1990). Tetanic stimulation of the oculomotor nerve is known to cause potentiation of evoked postsynaptic potentials in the CG of birds (Martin & Pilar, 1964). In this study, we sought to determine whether the phenomenon of {"}post-tetanic{"} potentiation in the CG is reflected in an increased choroidal vasodilatory response and whether ganglionic transmission accounts for this effect. Methods. Choroidal blood flow (ChBF) was measured transclerally using the laser Doppler technique in pigeons anesthetized by urethane or ketamine and xylazine. Stimulation to induce choroidal vasodilation (anodal puses 0.5-1 ms duration, 50-200 μA amplitude at 50-75 Hz for 5 seconds) was applied with a stereotaxically positioned electrode and repeated 1-3 times with an interval of 30-60 seconds. Neuroeffector (atropine, the NOS inhibitor L-NAME) and ganglionic (hexamethonium) blocking agents were infused intravenously to verify the mechanism of potentiation. All brains were subsequently processed histologically to confirm the accuracy of electrode placement. Results. Repeated stimulation resulted in more pronounced vasodilation under both types of anesthesia. The increase in the amplitude of the vasodilatory response varied between 10-60{\%}. The potentiation persisted after atropine. The vasodilatory response was diminished following administration of L-NAME, but post-tetanic potentiation of the response was still observed. Hexamethonium attenuated or suppressed the increase in ChBF and the potentiation of vasodilation following stimulation of EW. Conclusions. A potentiation of the vasodilatory response in the choroid following repeated stimulation of EW is demonstrated by this study. The increase in the efficacy of synaptic transmission through the CG appears to be the mechanism of this effect. The vasodilatory response potentiation may be useful for adaptive control of ChBF.",
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N2 - Purpose. Activation of the nucleus of Edinger-Westphal (EW), the input to the ciliary ganglion (CG) via the oculomotor nerve, elicits vasodilation of the choroidal blood vessels in pigeon (Fitzgerald et al., 1990). Tetanic stimulation of the oculomotor nerve is known to cause potentiation of evoked postsynaptic potentials in the CG of birds (Martin & Pilar, 1964). In this study, we sought to determine whether the phenomenon of "post-tetanic" potentiation in the CG is reflected in an increased choroidal vasodilatory response and whether ganglionic transmission accounts for this effect. Methods. Choroidal blood flow (ChBF) was measured transclerally using the laser Doppler technique in pigeons anesthetized by urethane or ketamine and xylazine. Stimulation to induce choroidal vasodilation (anodal puses 0.5-1 ms duration, 50-200 μA amplitude at 50-75 Hz for 5 seconds) was applied with a stereotaxically positioned electrode and repeated 1-3 times with an interval of 30-60 seconds. Neuroeffector (atropine, the NOS inhibitor L-NAME) and ganglionic (hexamethonium) blocking agents were infused intravenously to verify the mechanism of potentiation. All brains were subsequently processed histologically to confirm the accuracy of electrode placement. Results. Repeated stimulation resulted in more pronounced vasodilation under both types of anesthesia. The increase in the amplitude of the vasodilatory response varied between 10-60%. The potentiation persisted after atropine. The vasodilatory response was diminished following administration of L-NAME, but post-tetanic potentiation of the response was still observed. Hexamethonium attenuated or suppressed the increase in ChBF and the potentiation of vasodilation following stimulation of EW. Conclusions. A potentiation of the vasodilatory response in the choroid following repeated stimulation of EW is demonstrated by this study. The increase in the efficacy of synaptic transmission through the CG appears to be the mechanism of this effect. The vasodilatory response potentiation may be useful for adaptive control of ChBF.

AB - Purpose. Activation of the nucleus of Edinger-Westphal (EW), the input to the ciliary ganglion (CG) via the oculomotor nerve, elicits vasodilation of the choroidal blood vessels in pigeon (Fitzgerald et al., 1990). Tetanic stimulation of the oculomotor nerve is known to cause potentiation of evoked postsynaptic potentials in the CG of birds (Martin & Pilar, 1964). In this study, we sought to determine whether the phenomenon of "post-tetanic" potentiation in the CG is reflected in an increased choroidal vasodilatory response and whether ganglionic transmission accounts for this effect. Methods. Choroidal blood flow (ChBF) was measured transclerally using the laser Doppler technique in pigeons anesthetized by urethane or ketamine and xylazine. Stimulation to induce choroidal vasodilation (anodal puses 0.5-1 ms duration, 50-200 μA amplitude at 50-75 Hz for 5 seconds) was applied with a stereotaxically positioned electrode and repeated 1-3 times with an interval of 30-60 seconds. Neuroeffector (atropine, the NOS inhibitor L-NAME) and ganglionic (hexamethonium) blocking agents were infused intravenously to verify the mechanism of potentiation. All brains were subsequently processed histologically to confirm the accuracy of electrode placement. Results. Repeated stimulation resulted in more pronounced vasodilation under both types of anesthesia. The increase in the amplitude of the vasodilatory response varied between 10-60%. The potentiation persisted after atropine. The vasodilatory response was diminished following administration of L-NAME, but post-tetanic potentiation of the response was still observed. Hexamethonium attenuated or suppressed the increase in ChBF and the potentiation of vasodilation following stimulation of EW. Conclusions. A potentiation of the vasodilatory response in the choroid following repeated stimulation of EW is demonstrated by this study. The increase in the efficacy of synaptic transmission through the CG appears to be the mechanism of this effect. The vasodilatory response potentiation may be useful for adaptive control of ChBF.

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