Effect of age and monosodium-L-glutamate (MSG) treatment on neurotransmitter content in brain regions from male fischer-344 rats

This study examines the effect of age on the induction of the rate-limiting enzyme in gluconeogenesis, phosphoenolpyruvate carboxykinase (PEPCK), in response to fasting and refeeding in male Fischer 344 rats aged 3-18 mo. The rats were fasted for 30 h to increase the activity of PEPCK and subsequently were refed for 24 h to lower activity toward basal levels. PEPCK activity increased 2.2-fold in the 3-mo-old rats and 2.3-fold in the 18-mo-old rats during the 30-h fast. Therefore PEPCK induction during the 30-h fast was not altered with age. Similarly, refeeding resulted in a significant decrease in PEPCK activity at all ages. After the 24-h refeeding period, the rats were fasted a second time, and the time course of induction from the basal refed level was measured. In the young rats (6 mo), the activity of PEPCK increased rapidly from 18.12 +/- 1.61 to 42.66 +/- 5.94 U/g protein (P < 0.01) within 8 h of fasting. However, in the 18-mo-old rats, the initiation of the induction of PEPCK activity was delayed, and, after 12 h, PEPCK activity had increased from 17.34 +/- 1.34 to only 32.50 +/- 3.21 U/g protein (P < 0.01). Furthermore, the rate of induction appears to be decreased in the older animals. The activity after 24 h of fasting was equivalent in all four age groups (ranging from 44.72 +/- 5.38 at 3 mo to 40.18 +/- 5.42 U/g protein at 18 mo).(ABSTRACT TRUNCATED AT 250 WORDS)

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The effect of a long term (6 months) treatment with (−)deprenyl on antioxidant enzyme activities in selective brain regions in old female fischer 344 rats

Biochemical Pharmacology ◽

10.1016/0006-2952(94)90331-x ◽

1994 ◽

Vol 47 (8) ◽

pp. 1333-1338 ◽

Cited By ~ 30

Author(s):

Maria Cristina Carrillo ◽

Kenichi Kitani ◽

Setsuko Kanai ◽

Yuko Sato ◽

Kyoko Miyasaka ◽

...

Keyword(s):

Antioxidant Enzyme ◽

Enzyme Activities ◽

Brain Regions ◽

Antioxidant Enzyme Activities ◽

Fischer 344 Rats ◽

Fischer 344

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R403 – Epidermal Proliferating Cell Nuclear Antigen in Aging Rats

Otolaryngology ◽

10.1016/j.otohns.2008.05.556 ◽

2008 ◽

Vol 139 (2_suppl) ◽

pp. P178-P178 ◽

Cited By ~ 3

Author(s):

Tapan K Bhattacharyya ◽

Paula Jackson ◽

J Regan Thomas

Keyword(s):

Cell Proliferation ◽

Proliferating Cell Nuclear Antigen ◽

Nuclear Antigen ◽

Proliferation Index ◽

Fischer 344 Rats ◽

Fischer 344 ◽

Age Related ◽

Two Parameters ◽

Proliferating Cell ◽

Effect Of Age

Problem To determine if epidermal cell proliferation in colony-raised Fischer 344 rats changes with age and diet. Methods Fischer 344 rats fed ad libitum and calorie-restricted (CR) diets were obtained from the NIA colonies, and young, young adult, and old animals from both groups were used for this study (six in each group). Tissue sections from the dorsal skin (DS) and foot plate (FP) were used for immunohistochemical staining of proliferating cell nuclear antigen (PCNA). The proliferation index (PCNA-I) was computed from counts of stained and total number of keratinocytes. Simultaneous measurements of epidermal thickness were obtained from same sections. Data were analyzed with Excel and SPSS 14.0 software for statistics. Results Two-way analysis of variance (ANOVA) was applied to the data to probe the effect of age, diet, and age-diet interaction. A significant effect of age was noticed in the two parameters i.e., DS PCNA (F 3.96, P .011), FP epidermal width (F 3.37, P .021) and FP PCNA-I (F 9.0, P .000). A significant correlation between DS width and PCNA values was also noted (r 0.5, P .01). Conclusion There is a trend of reduction of PCNA positive cells with increasing age irrespective of thickness of epidermis, and this trend is more apparent in CR rats. Significance This cell proliferation study has implications in relation to CR effect on age-related disease conditions, and biogerontology. Support The study was partially funded by the 2007 Leslie Bernstein grant from AAFPRS foundation.

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Preferential Metabolic Activation of Subcortical Brain Areas by Acute Administration of Nicotine to Rats

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1990.7 ◽

1990 ◽

Vol 10 (1) ◽

pp. 48-56 ◽

Cited By ~ 34

Author(s):

Dennis McNamara ◽

Denise M. Larson ◽

Stanley I. Rapoport ◽

Timothy T. Soncrant

Keyword(s):

Visual Processing ◽

Metabolic Activation ◽

Brain Regions ◽

Acute Administration ◽

Cognitive Effects ◽

Fischer 344 Rats ◽

Thalamic Nuclei ◽

Fischer 344 ◽

Nicotine Administration ◽

Nicotine Receptors

Cerebral metabolic and behavioral effects of acutely administered nicotine were measured in rats in relation to dose. Nicotine 0.1, 1, or 10 mg/kg or vehicle was administered intraperitoneally to 3-month-old male Fischer-344 rats that had been pretreated with hexamethonium bromide 5 mg/kg i.p. to reduce peripheral autonomic effects. Regional CMRglc (rCMRglc) values were measured, using the quantitative autoradiographic [14C]-2-deoxy-d-glucose method, in 71 brain regions, beginning 3 min after nicotine or vehicle administration. Intensity of body tremor, scored by a blinded rater, was dose related and peaked at 3 min after nicotine injection. rCMRglc rose in a dose-related manner: Nicotine 0.1 mg/kg had no significant effect in any region, whereas 1 mg/kg elevated rCMRglc significantly in 21 regions (mean rise 20%) and 10 mg/kg produced generalized (56 regions) and greater (mean rise 50%) increases in rCMRglc. Nicotine 1 mg/kg activated thalamic nuclei, cerebellum, geniculate nuclei, superior colliculus, median raphe, reticular formation, and the habenulointerpeduncular pathway, but was without effect in the telencephalon. Effects of nicotine in the hindbrain were related anatomically to reported distributions of [3H]nicotine and [3H]acetylcholine but not [125I]α-bungarotoxin binding sites, implying that the former ligands label functional nicotine receptors. The pattern of change in rCMRglc after nicotine administration suggests that its cognitive effects in humans are due to augmented arousal/attention and visual processing rather than to direct neocortical or hippocampal activation.

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