From this neuropharmacological and electrical stimulation experiments and from other observations and also in view of the knowledge acquired on the distribution of LHRH neurons, the existence of an NE synapse lying in the preoptic or anterior hypothalamic area which makes contact with LHRH neurons and which mediates the increased release of LHRH and LH which occurs during the preovulatory discharge of gonadotrophins or in response to removal of steroid negative feedback may be postulated. However one possibility that should be considered is that the mechanism(s) therefore attributed to NE may be considered in part to brain E. Caution should be exercised in trying to apply to primates the knowledge obtained in rodents on the action of catecholamine neurons in the phasic activation of gonadotrophin release. In the rat the MBH regulate tonic gonadotrphic secretion and more rostral areas initiate the cyclic ovulatory discharge whereas in the rhesus monkey the major component of the regulation of the phasic and tonic control of the gonadotrophic secretion appears to be present in the MBH-hypophysial unit. Thus, monkey would not required norepinephrinergic connection from the preoptic area to the MBH for the ovulatory trigger. Pharmacological blockers of the ovulation in rat, such as pentobarbital reserpine or phenoxybenzamine did not interfere with the positive feedback action of estrogen on gonadotrophic release in the monkey. In the human, it has been recently reported that blockade of DA receptors by pimozide or of NE synthesis by fusaric acid significantly reduced the midcycle surge of LH without significantly effecting the FSH burst. Extention of these neuropharmacological studies to human is awaited with interest.
|Number of pages||10|
|Journal||Acta Europaea Fertilitatis|
|Publication status||Published - Dec 1 1977|
ASJC Scopus subject areas
- Obstetrics and Gynaecology