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M Shanabrough

Publications and source records attributed to M Shanabrough.

25 records · Page 2Linked to original sources
PubMed1986

Reproductive failure due to experimentally induced constant estrus does not alter the LH-RH fiber density in the median eminence of the rat.

The effects of anterior hypothalamic deafferentation on luteinizing hormone releasing hormone (LH-RH) fiber density in the mediobasal hypothalamus (MBH) were compared to those of a number of nonsurgical treatments which give rise to anovulatory sterility (injections of estradiol valerate, exposure to constant light, or neonatal androgen administration) in the female rat. All of the treatments used (surgical and nonsurgical) disrupted the normal 4-day pattern of estrous cyclicity. Bilateral anterior hypothalamic deafferentation markedly reduced the packing density of LH-RH fibers in the MBH. Unilateral deafferentation reduced the number of fibers on the ipsilateral side of the MBH by 31-64% and on the contralateral side by 15-40%. In contrast, none of the three nonsurgical treatments had any significant effect on the LH-RH fiber density. Electron microscopic examination revealed no morphologic, or distribution differences in MBH LH-RH fibers between control females and animals rendered anovulatory by the nonsurgical experimental procedures. These results demonstrate that estrogen, androgen, and constant light induced anovulatory sterility are not associated with any overt change in the number or morphology of LH-RH immunoreactive fibers in the MBH, suggesting that the primary lesion responsible for the failure of normal estrous cyclicity in such animals resides in the systems responsible for regulating the activity of the LH-RH neurons rather than in the LH-RH neurons themselves.

Afferent Pathways↗
PubMed1985

Intrinsic tyrosine hydroxylase (TH) immunoreactive axons synapse with TH immunopositive neurons in the rat arcuate nucleus.

Synaptic connections were demonstrated between tyrosine hydroxylase (TH) immunoreactive axons and dendrites in the arcuate nucleus of the rat, by electron microscopic immunocytochemistry. These connections were primarily found in the lateral part of the nucleus. The results of two types of medial-dorsal-lateral surgical de-afferentation suggest that the TH-TH contacts represent intrinsic connections.

Animals↗
PubMed1985

Estrogen responsive cells in the arcuate nucleus of the rat contain glutamic acid decarboxylase (GAD): an electron microscopic immunocytochemical study.

Twenty-one days after ovariectomy (OVX) an increased frequency of lamellar cytoplasmic organelles, termed 'whorl' bodies (WB), was observed in neurons of the rat arcuate nucleus (AN). When estradiol valerate (2 mg s.c.) was injected either at the time of OVX or one week later, the frequency of WB at 21 days was reduced. The estrogen treatment resulted in a concomitant rise in the frequency of 'nematosomes' (NS), filamentous electron-dense cytoplasmic structures. In the medial part of the AN glutamic acid decarboxylase (GAD) immunopositive symmetric (Gray II) synapses were observed in contact with WB- and NS-containing cells. After colchicine treatment, GAD immunoreactivity was observed in the WB- and NS-containing perikarya in the medial AN. Some of the NS-containing cells in the lateral AN of the colchicine-pretreated animals remained immunonegative for GAD.

Animals↗
PubMed1985

Application of avidin-ferritin and peroxidase as contrasting electron-dense markers for simultaneous electron microscopic immunocytochemical labelling of glutamic acid decarboxylase and tyrosine hydroxylase in the rat arcuate nucleus.

A pre-embedding immunostaining procedure was developed using ferritin and peroxidase to enable simultaneous electron microscopic localization of two antigens in the same tissue section. This method was used to study the anatomic relationship between glutamic acid decarboxylase (GAD) immunoreactive axons and tyrosine hydroxylase (TH) - containing neurons of the rat arcuate nucleus. The findings provide ultrastructural evidence that GAD-immunoreactive terminals establish symmetric (Gray II) synapses on TH-reactive neurons.

Animals↗
PubMedDate not supplied

Estrogen, synaptic plasticity and hypothalamic reproductive aging.

Unlike primates who undergo ovarian failure and loss of sex steroids at the end of reproduction, aging rodents undergo constant vaginal estrus followed by constant diestrus and finally anestrus, which indicates the absence of responsive ovarian follicles. The latter state is analogous to menopause in women. The timing of the appearance of constant estrus is determined by many factors including estrogen exposure in the brain during development and the number of times that the animal gets pregnant. The chief site of this reproductive aging in rat brains is the arcuate nucleus of the hypothalamus. The transition from normal cycles to constant estrus parallels the females' gradually decreased ability to respond to administered estradiol with a cycle of inhibition followed by disinhibition of gonadotrophin-releasing hormone. Evidence has accumulated indicating this to be due to a loss of the rat's ability to respond to markedly elevated estradiol with the usual arcuate nucleus neuro-glial plasticity that supports the estrogen-induced gonadotrophin surge (EIGS). Just as male rats are not capable of an EIGS, aged females loose this ability through repeated EIGS. Experiments indicate that in male rats the hypothalamic synaptology that develops as a result of exposure to testicular androgens in the perinatal period (brain sexual differentiation) is a result of conversion of testosterone from the testes to estrogen in the brain and is therefore due to early estrogen exposure. Aging females appear to reach a synaptology similar to males and constant estrus as a result of repeated exposure to ovarian estrogens during their reproductive careers. The relative role of aging and hormonal factors remains unclear. Morphological evidence is presented that indicates the above effects of estrogen involve changes in hypothalamic arcuate nucleus neurons and glia, including changes in the organization of perikaryal membranes as well as arcuate nucleus synaptology and the load of peroxidase in the astroglia. A possible role for free radicals (reactive oxygen species) in hypothalamic reproductive aging has been proposed. Such a mechanism is supported by evidence that the anti-oxidant vitamin E delays the onset of constant estrus and the accumulation of glial peroxidase in aging female rats. However, since the synaptology and peroxidase load in constant estrus females is independent of the age at which the constant estrus occurs, it appears that the role of (repeated) estradiol exposure is more deterministic of hypothalamic failure than is aging, per se.

Aging↗