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Biomedical subjects

N J Laping

Publications and source records attributed to N J Laping.

39 records · Page 3Linked to original sources

Prolactin induces yawning and the stretch-yawning syndrome in young adult male rats.

Herein we report that subcutaneous injection of low doses of ovine prolactin (oPRL) induce yawning in young adult male rats. The most effective dose of oPRL in evoking yawning was 0.25 microgram/kg body weight (5.2 yawns/60 min at 1000 hr vs 0.3 in control animals). Doses of 0.025, 0.05, 2.5, 25, and 250 micrograms/kg were less effective. Interestingly, yawning in response to oPRL changes over the course of one circadian cycle with highest frequency at 1600 hr (11 yawns/80 min vs 2 yawns/80 min in animals injected with boiled oPRL). The onset of yawning in most oPRL-treated rats began approximately 40 min after oPRL injection, whereas with apomorphine the latency to the response was about 10 min. These results indicate that oPRL in addition to other hypophysial peptides such as ACTH and MSH can stimulate yawning. It is proposed that PRL after initial activation of the nigrostriatal dopamine system secondarily induces yawning by inhibition of this system via an autoreceptor-mediated negative feedback mechanism. This may explain the long latency to the response.

Animals↗

Aging alters opiate inhibition of potassium (K+)-stimulated dopamine release from the corpus striatum of male rats.

The effect of Leu-enkephalin (Leu-ENK), Met-enkephalin (Met-ENK), and naloxone on potassium (K+)-evoked endogenous dopamine (DA) release from striatal tissue fragments was examined in young (2-4 month) and old (20-25 month) male rats. The K(+)-evoked DA release was significantly lower in old compared to young animals. Leu-ENK significantly reduced K(+)-evoked DA release in young animals, but neither opiate affected DA release in old animals. Naloxone, which had no effect in young animals, raised the K(+)-evoked DA response in old animals to levels seen in young control preparations. These results suggest that the age-dependent decrease in K(+)-evoked DA release may in part be due to a stronger opiate inhibitory tonus in the CS of older rats.

Age Factors↗

GFAP mRNA increases with age in rat and human brain.

Glial fibrillary acidic protein (GFAP) mRNA was examined by RNA blot hybridization in three age groups of two cohorts of male F-344 rats and in 47 human postmortem brain samples. GFAP mRNA increased in the hippocampus and striatum of 24 versus 6- to 7-month-old rats. Another astrocytic molecular marker, glutamine synthetase mRNA, did not change with age in rat brain. Rat GFAP mRNA prevalence was inversely correlated with serum testosterone but not correlated with serum corticosterone. In human hippocampus, frontal and temporal cortex, GFAP mRNA also increased in older (60-79 years) compared with middle-aged (25-59 years) individuals. In contrast, mitochondrial cytochrome oxidase subunit 1 mRNA did not change between age groups in any region. By combining the three regions for further analysis, GFAP mRNA increased with age irregardless of gender, alcoholism in the middle-aged group, or whether brains were classified as normal or neuropathologic (excluding Alzheimer's disease pathology). These data indicate that increased GFAP protein or GFAP-immunoreactive astrocytes in rats and humans may result from transcriptional or post-transcriptional regulation and extend the number to three species (including mouse) showing an increase in GFAP mRNA with age. Factors that are known to regulate GFAP mRNA expression in young brains are considered as possible causes of age-related increases.

Adult↗