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27 ème colloque de la Société de Neuroendocrinologie
Lille - 2-5 septembre 1998

 

EFFECT OF INTRACEREBROVENTRICULAR OXYTOCIN ON THE RESPONSE OF OXYTOCIN NEURONES TO STIMULATION OF THE MESENCEPHALIC VENTRAL TEGMENTUM IN THE MILK-EJECTING RAT

C. M. RICHARDSON, J. B. WAKERLEY

Dept. Anatomy, Univ. Bristol, Medical School, University Walk, Bristol BS8 1TD.

Intracerebroventricular (i.c.v.) oxytocin facilitates the milk-ejection reflex and causes increased bursting responses in oxytocin neurones (Richard et al., 1988, Physiol. Rev. 71: 331-370). We have investigated whether this facilitatory effect is associated with an increase in the excitatory response of oxytocin neurones to stimulation of the mesencephalic ventral tegmentum, a region previously implicated in the milk-ejection reflex (Wakerley et al, 1994, In Physiology of Reproduction, eds E. Knobil and J. Neill, Raven Press.).

Urethane-anaesthetised rats were prepared for recording from supraoptic oxytocin neurones during milk ejection, and implanted with a stimulating electrode in the ventral tegmentum (co-ordinates: 5.5mm behind bregma, 1.5 mm lateral, 8.0 mm deep). Following application of the pups, the response of oxytocin neurones to repetitive single shock stimulation of the ventral tegmentum (1 ms pulses, 0.2-0.5 mA, 0.3 Hz) was examined by PSTH before and after administration of i.c.v. oxytocin (2.2 ng, 1 mU).

Prior to i.c.v. oxytocin administration, oxytocin neurones (n=5) were unaffected by ventral tegmental stimulation, apart from 2 cells which showed a small inhibition (latency 12-20 msec, duration approx. 100 ms). In all 5 neurones tested, i.c.v. injection of oxytocin caused the appearance of a pronounced excitatory response (latency 100-150 ms, duration 140-220 msec). Onset and termination of this response closely correlated with the increased background firing and bursting activity associated with facilitation of the milk-ejection reflex by i.c.v. oxytocin. Subsequent injection of hypertonic saline (2 ml 1.5 M i.p.) to produce a comparable increase in background firing to that following i.c.v. oxytocin, did not induce a response to ventral tegmental stimulation. Hence modulation of the ventral tegmental response following i.c.v. oxytocin was unlikely to have resulted from a generalised increase in the excitability of oxytocin neurones.

In conclusion: i.c.v. oxytocin potentiates the response of oxytocin neurones to stimulation of mesencephalic ventral tegmentum. Potentiation of ascending excitatory input to the oxytocin neurones may provide a mechanism by which i.c.v. oxytocin facilitates the milk-ejection reflex.

 

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