PubMed · 7624985
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F F Marshall. 1995. Radical nephrectomy.. https://doi.org/10.1016/s0090-4295(99)80184-8
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Although apoptotic cellular degeneration has been reported to be extremely rapid with the use of in vitro models, the time needed to clear apoptotic neurons in the in vivo brain is unknown. In this study we used a simple morphological approach to solve this problem. Four days after adrenalectomy (ADX), all of the operated rats morphologically displayed hippocampal granule cell apoptosis that was prevented completely by corticosterone replacement immediately after ADX. Therefore, we intravenously injected the rats with corticosterone 4 d after ADX and subsequently maintained them on corticosterone replacement in saline drinking water. This corticosterone replacement could protect healthy granule cells promptly and continuously against hormone-deficient apoptosis, because the normal glucocorticoid receptor immunoreactivity within the granule cell nuclei, which disappeared after ADX, was identified 1 hr after corticosterone replacement was started, and this effect persisted for several days. However, this corticosterone treatment could not prevent the irreversible apoptosis of the already degenerated granule cells at various stages of the same progressive apoptotic process. Then we successively traced the disappearance of apoptotic granule cells throughout the hippocampus at different time points by Nissl and silver staining. Given that the apoptotic cells at the earliest stage of the degenerating process when the ADX rats received corticosterone injection were the last to disappear, the period from corticosterone injection until the disappearance of the last degenerating debris of apoptotic cells was taken to represent the time course for elimination of apoptotic neurons in vivo. We discovered that the elimination of apoptotic granule cells took 72 hr.
Lactating rats display a period of blunted hypothalamo-pituitary-adrenal (HPA) response to a variety of stressors. This hyporesponsiveness is reported to be dependent upon continuous mother-pup interactions. In this study, computer-assisted densitometric methods were used to measure levels of induced Fos-like immunoreactivity (FLI) in the hypothalamic paraventricular nucleus (PVN) of lactating and non-lactating rats. Adrenalectomy (ADX) induces elevated levels of FLI in the PVN of non-lactating rats. We have observed that, between post-partum day (pd) 4 and pd 21, the level of ADX-induced FLI in the PVN of lactating rats follows a U-shaped distribution; that the persistence of this phenomenon is dependent upon continued mother-pup interaction and that sustained mother-pup interaction beyond the end of the normal suckling period (pd 21) does not extend the period of refractoriness. We have further determined that both the non-specific neural activator Metrazole, and the glutamate agonist N-methyl-D,L-aspartate (NMA), induced smaller increases in FLI in the PVN of lactating rats compared to non-lactating cohorts, and that the suppressing effect of lactation on Metrazole-induced FLI does not extend to all brain regions. These results suggest that mechanisms responsible for the onset and maintenance of the so-called lactational stress-hyporesponsive period (LSHRP) include altered function of glutamatergic pathways.
Reproduction is adversely affected by alcohol abuse in humans and laboratory animals. In rats, alcohol exposure suppresses both luteinizing hormone (LH) and sex steroid secretion, although consensus is lacking as to which level of the hypothalamic-pituitary-gonadal (HPG) axis is primarily affected. We tested the hypothesis that acute alcohol treatment inhibits the HPG axis by blunting release of LH-releasing hormone (LHRH) in female rats, by examining the effect of this drug on the central reproductive endocrine event; i.e., the proestrous surge of gonadotropins, which triggers ovulation. In a first series of experiments, we injected alcohol at 8 A.M. and 12 P.M. on proestrus and measured plasma levels of LH, estradiol (E2), and progesterone during the afternoons of proestrus and estrus. Alcohol administration blocked the proestrous surge of LH and ovulation. In subsequent experiments, alcohol inhibited the surge of LHRH (measured by push-pull cannulation) and LHRH neuronal activation (measured by Fos labeling in LHRH neurons). Because alcohol also decreased E2 levels, we reasoned that it might have prevented positive feedback; however, alcohol retained its ability to inhibit the LH surge evoked by E2 implantation in ovariectomized females, disproving this hypothesis. Additionally, alcohol does not act via increased corticosteroid secretion, because alcohol also blocked the proestrous surge in adrenalectomized females. Last, exogenous administration of LHRH to alcohol-blocked animals evoked LH secretion and ovulation, indicating that pituitary and/or ovarian function could be restored by mimicking the hypothalamic signal. Collectively, these data indicate that in female rats, alcohol inhibits the gonadotropin surge primarily by decreasing LHRH secretion.