Estrogen receptor (ER) and ER mRNA expression and cell division induced by neonatal diethylstilbestrol (DES) exposure in male C57BL/Tw mouse genital organs were studied using immunohistochemistry, in situ hybridization, and cell counting at metaphase. A single injection of 3 micrograms DES on the day of birth induced ER in both epithelial (E) and stromal (S) cells of the epididymis and the seminal vesicles, in E cells of the ductus deferens, and in S cells of the ductus efferens and the anterior prostate 24 h after the injection. After 5 daily injections of DES, ER was induced in S cells of the ventral prostrate at 5 days of age. The staining intensity of ER increased in E cells of the epididymis and the ductus efferens at 5 days. A single injection of DES induced ER mRNA in both E and S cells of the ductus efferens, the caput epididymis, and the ductus deferens 4 to 12 h after injection of the newborn mice. A single injection of DES stimulated cell division of both E and S cells in the ductus deferens and the epididymis; cell division of S cells of the ductus efferens, the anterior prostate, and the urethra was stimulated 24 h after the injection. After 5 daily injections of DES, cell division was stimulated significantly in E and S cells of the epididymis, the ductus deferens, and the ventral prostate, and in S cells of the seminal vesicle at 5 days. At 30 days of age, mitotic rates were significantly higher in E cells of the seminal vesicles and the epididymides of mice given 5 daily injections of DES.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMedDate not supplied

A re-examination of the role of basal forebrain cholinergic neurons in spatial working memory.

The basal forebrain cholinergic system, which innervates widespread cortical and limbic structures, has traditionally been considered important for learning and memory. The use of an immunotoxin, 192 IgG-saporin, has brought this functional designation into question; selective immunolesions of basal forebrain cholinergic neurons have failed to reproduce a number of behavioral deficits that were observed with less selective lesion methods. Recent reports, however, have indicated that a mild impairment is observed in rats on a spatial working memory task after 192 IgG-saporin lesions of the rostral groups of cholinergic neurons located in the medial septal area (MSA). Those studies used a lesion protocol in which a single large volume injection of the immunotoxin was made into the MSA. In the current study, multiple small injections were made at the locations of cholinergic neurons in the MSA, producing a cholinergic depletion comparable to that reported in the earlier studies where deficits were observed. In the current study, however, rats with cholinergic lesions had no impairment in the spatial working memory task, even when delays ranging from 60 s to 8 h were imposed within a trial. The current report indicates that selective removal of cholinergic neurons in the basal forebrain may not be sufficient to produce a deficit in spatial working memory.

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PubMedDate not supplied

Circadian control of photoreceptor outer segment membrane turnover in mice genetically incapable of melatonin synthesis.

Vertebrate retinal photoreceptors periodically shed membrane from their outer segment distal tips; this material is phagocytosed and degraded by the retinal pigmented epithelium. Both a circadian oscillator and the daily light-dark cycle affect disk shedding, and the effects of both may be mediated by melatonin. To clarify melatonin's role in this process, we asked whether endogenous melatonin is required for rhythmic disk shedding in mouse retina. We analyzed disk shedding in two mouse strains: C3H, which produce melatonin in retina and pineal under the control of circadian oscillators, and C57BL/6, which do not produce melatonin. In cyclic light, both strains exhibited a robust cycle of disk phagosome content in the pigmented epithelium. Peak shedding occurred just after dawn, and trough levels occurred during the middle of the dark phase. In constant darkness, mice exhibited circadian rhythms of locomotor activity, the characteristics of which were similar between strains. Both strains also exhibited rhythmic disk shedding in constant darkness, although amplitudes of the rhythms were damped. Exogenous melatonin delivered once per day failed to reestablish high-amplitude cyclic shedding in mice held in constant darkness. Our results show that, while disk shedding in cyclic light is robustly rhythmic, neither rhythmic production of melatonin nor the circadian oscillator responsible for rhythmic locomotor activity is sufficient to drive high-amplitude rhythmic shedding in constant darkness. More importantly, melatonin is required neither for cyclic changes in the rate of disk shedding in cyclic light, nor for the circadian rhythm of disk shedding in constant darkness.

Animals↗