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|Title:||Are Estrogens Neuromodulators?|
|Authors:||Whitehead, Ann Saffron|
|Keywords:||Medical Sciences;Medical Sciences|
|Abstract:||<p>Ovulation is the result of the positive feedback action of estrogen, either alone or in combination with progesterone, and the integrated sensory input from the external environment onto the neural circuits controlling gonadotrophin secretion. During the dioestrus II in the 4-day cycling rat the ovaries secrete an increasing quantity of estrogen which stimulates neurons in the preoptic area (POA) to trigger the surge of luteinizing hormone releasing hormone into the capillaries of the hypophysical portal plexus. However, the mechanisms whereby estrogen stimulates this increased activity are, as yet, unknown.</p> <p>The binding of estrogen to specific target areas within the brain may induce changes in the metabolic function of neurons or it may directly or indirectly affect the electrical properties of neuronal membranes. The latter possibility has been tested by observing the affects of an intravenous (i.v.) injection of estrogen on the spontaneous activity and responsiveness to iontonphoretically applied putative neurotransmitters of identified preoptic neurons.</p> <p>Experiments I and II were undertaken in order to establish certain parameters of the experimental design. Experiment I demonstrated that halothone anaesthesia inhibits ovulation in the cycling rat by an action on the neuroendocrine circuits which control gonadotrophin secretion. In experiment II measurements were made of the plasma concentration of estrogen following various doses of an i.v. injection of estrogen or progesterone would stimulate an increased secretion of LH in estrogen primed ovariectomized rats. Measurements of serum LH concentrations one and five hours after the injection showed there was no stimulation of LH under these conditions.</p> <p>Experiment III was undertaken to identify neurons in the POA which are thought to implicated in a neuroendocrine circuit controlling gonadotrophin secretion and which may be target neurons for the positive feedback action of estrogen. Cells in the POA, which receive an input from the stria terminals have been identified by stimulating this pathway at its point of convergence in the amygdala. Antidromic stimulation techniques were employed to identify cells in the POA which make a direct connection with the basal hypothalamus.</p> <p>Experiment IV constitutes the major objective of the research, which was to thought to be implicated in a neuroendocrine circuit controlling gonadotrophin secretion and which may be target neurons for the positive feedback action of estrogen. Cells in the POA which receive an input from the stria terminalis have been identified by stimulating this pathway at its point of convergence in the amygdala. Antidromic stimulation techniques were employed to identify cells in the POA which make a direct connection with the basal hypothalamus.</p> <p>Experiment IV constitutes the major objective of the research, which was to investigate 1) the sensitivity of antidromically identified preoptic neurons to iontophoretically applied putative neurotransmitters; the cells were inhibited by both the cataecholamines, dopamine (DA) and norepinephrine (NE) but were unresponsive to acetylcholine applied iontophoretically; b) to test the possible membrane effects of estrogen on those antidromically identified cells. Two indices of a change of the excitability of preoptic neurons were used (i) the effects of an i.v. injection of estrogen on the rate of spontaneous activity and (ii) changes in the response of a neuron to electrophoretically applied DA or NE following the injection of estrogen or progesterone in primed and unprimed animals. The results of the first series of experiments demonstrated that estrogen can decrease the rate of spontaneous activity in identified preoptic units. Some cells showed a long lasting depression in their spontaneous activity following the steriod injection while others showed a short term decrease in the rate of unit discharge five minutes after estrogen administration. In the second series of experiments no changes were observed in the dose response curves of iontophoretically applied DA or NE thirty minutes after the steroid injection in either group of animals. The negative finding could be due to the technical limitations of this type of experiment or to the fact that estrogens do not affect the response of neurons to synaptic inputs in which these amines may function as neural transmitters.</p>|
|Appears in Collections:||Open Access Dissertations and Theses|
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