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11. |
Characteristics of Dopaminergic Neurons in the Aged Male Rat |
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Neuroendocrinology,
Volume 31,
Issue 3,
1980,
Page 222-227
K.T. Demarest,
G.D. Riegle,
K.E. Moore,
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摘要:
Male rats were sacrificed at 5 months (young rats) or at 24 months (aged rats). When compared with values in young rats, aged rats had higher serum concentrations of prolactin and lower concentrations of luteinizing hormone and testosterone. In the median eminence, which contains the terminals of tuberoinfundibular dopamine (DA) neurons, the concentrations of DA and dihydroxyphenylacetic acid (DOPAC), and the rate of DA synthesis (accumulation of DOPA after the inhibition of DOPA decarboxylase) were decreased in aged rats. In the striatum, which contains the terminals of nigrostriatal DA neurons, the concentration of DA was reduced, but this change was not accompanied by a decrease in DOPAC concentrations or DOPA accumulation. The decreased DA concentration observed in the median eminence and striatum of aged rats may reflect the loss of DA neurons. An attempt was made to mimic the age-related loss of nigrostriatal and tuberoinfundibular DA neurons by pretreating rats with intraventricular injections of 6-hydroxydopamine. In these animals the decrease of DA in the median eminence was accompanied by a concomitant reduction in the rate of DOPA accumulation, whereas in the striatum the concentration of DA was reduced, but DOPA accumulation remained normal. These results suggest that in aged and 6-hydroxydopamine-treated rats, the loss of nigrostriatal DA neurons is accommodated for by a compensatory increase in the activity of the remaining neurons whereas tuberoinfundibular DA neurons are unable to compensate in a similar manner.
ISSN:0028-3835
DOI:10.1159/000123078
出版商:S. Karger AG
年代:1980
数据来源: Karger
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12. |
Monosodium Glutamate Disruption of Behavioral and Endocrine Function in the Female Rat |
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Neuroendocrinology,
Volume 31,
Issue 3,
1980,
Page 228-235
Jorge F. Rodriguez-Sierra,
R. Sridaran,
Charles A. Blake,
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摘要:
Experiments weie conducted to determine the effects of neonatal administration of L-monosodium glutamate (MSG) on behavioral and endocrine function in the female rat. Administration of MSG (4 mg/kg body weight) at days 1, 3, 5, 7 and 9 in neonates results in a delay of vaginal opening (VO) and the absence of ovulation at the time of VO. However, some rats were observed to ovulate after VO if they were subjected to sequential laparotomies. MSG-treated rats also fail to exhibit compensatory ovarian hypertrophy. Ovariectomized MSG-treated rats injected with estradiol benzoate (EB) followed by a progesterone injection 2 days later did not exhibit sexual behavior to male rats, while all the control rats displayed lordosis. Chronic treatment with EB for 12 days, followed by a progesterone injection on the 12th day, resulted in a marked improvement of the sexual receptivity of the MSG-treated rats. The body weight of the MSG-treated animals was lower than that of the controls during development although the MSG animals looked obese. Food intake is normal in the MSG-treated rats, but when expressed as intake/100 g body weight, the MSG-treated rats appeared slightly hyperphagic. MSG-treated rats respond with increased food intake after ovariectomy and EB treatment suppresses the increased food intake. Thus, the control of food intake by estrogen does not seem to be affected by the MSG treatment; in fact, these animals seem to be more sensitive than control rats to the anorectic effects of EB. Neonatal MSG treatment appears to affect the neural control for the tonic secretion of gonadotropins by destroying arcuate nuclei. This undoubtedly reduces the reproductive capacity of the animals by impeding the growth and secretions of their ovaries. The findings that chronic estrogen followed by progesterone treatment can reinstate sexual receptivity in MSG-treated animals suggests that the arcuate nuclei are not needed for the expression of sexual behavior and that estrogens might remedy the fertility problems of MSG-treated animals.
ISSN:0028-3835
DOI:10.1159/000123079
出版商:S. Karger AG
年代:1980
数据来源: Karger
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13. |
Announcement |
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Neuroendocrinology,
Volume 31,
Issue 3,
1980,
Page 236-236
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PDF (67KB)
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ISSN:0028-3835
DOI:10.1159/000123080
出版商:S. Karger AG
年代:1980
数据来源: Karger
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