Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.14.16.2 (tyrosine hydroxylase)
 14,760 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study compared tyrosine hydroxylase (TH) mRNA signal levels, relative quantity of TH protein, and the catalytic activity of TH in the tuberoinfundibular dopaminergic neurons (TIDA) of male and ovariectomized (OVEX) female rats. In addition, the effects of monosodium glutamate (MSG) neurotoxicity on these parameters of TH regulation were evaluated. Neonatal rats were injected with MSG (4 mg/g body weight) or 10% sodium chloride (controls) on alternate days for the first 10 days of life. Females were ovariectomized on day 45 of age, and all rats were used between 60 and 80 days of age. The TH mRNA signal levels, as assessed by an in situ hybridization technique, were 2-fold higher in control females than in control males, whereas the number of TH mRNA-containing cells was similar between sexes. The TH immunostainings of the TIDA perikarya in the arcuate nucleus and of the nerve terminals in the median eminence were qualitatively more intense in females than males. The catalytic activity of TH, as determined by in vitro DOPA accumulation in the stalk-median eminence, was 3-fold greater in females than males. Neonatal MSG-treatment resulted in a marked reduction in the number of TH mRNA-containing cells and TH-immunopositive cells in the arcuate nucleus of both sexes, as well as a decrease in the intensity of TH immunostaining in the median eminence. The cellular mRNA signal levels for TH were markedly reduced in females after MSG treatment, but were unchanged in males. MSG treatment reduced TH activity to 20% of control levels in females, but did not alter enzyme activity in males.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Sex-related alterations in hypothalamic tyrosine hydroxylase after neonatal monosodium glutamate treatment. 198 Jul 22

Clinical studies have demonstrated that estrogen replacement therapy suppresses stress-induced increases in plasma catecholamines. The present study determined whether normal circulating levels of estrogen can modulate hypoglycemia-induced increases in plasma epinephrine (EPI). In anesthetized female rats, insulin-induced hypoglycemia (0.25 U/kg) increased plasma EPI concentration to a significantly greater extent in 14-day ovariectomized (OVEX) rats compared to that in sham-operated controls. In 17beta-estradiol (E2)-replaced OVEX rats, the hypoglycemia-induced rise in plasma EPI was reduced significantly when compared to that in vehicle-replaced OVEX rats. OVEX and E2 replacement had no effect on tyrosine hydroxylase or phenylethanolamine N-methyltransferase mRNA levels in the adrenal medulla. In isolated adrenal medullary chromaffin cells, agonist-induced increases in intracellular Ca2+ were unaffected by 48-hr exposure to 10 nM E2. In contrast, acute (3-min) exposure to micromolar concentrations of E2 dose-dependently and reversibly inhibited agonist-induced Ca2+ transients. In addition, in OVEX rats, a constant infusion of E2 significantly reduced the insulin-induced increase in plasma EPI concentration compared to that in vehicle-infused controls. These data demonstrate that physiologic levels of circulating E2 can modulate hypoglycemia-induced increases in plasma EPI. This effect seems independent of steroid influence on adrenal medullary secretion or biosynthesis. In contrast, acute exposure to high levels of E2 can also suppress hypoglycemia-induced increases in plasma epinephrine, due at least in part to inhibition of stimulus-secretion coupling.
 ...
PMID:Modulation of hypoglycemia-induced increases in plasma epinephrine by estrogen in the female rat. 1561 87

Estrogens modulate critical homeostatic functions of the hypothalamus such as temperature regulation, sexual behavior and sleep with the most pronounced effects in rats occurring during the dark-phase. The neurochemical signals underlying estrogenic regulation of these hypothalamic functions have not been clearly identified, possibly due to the fact that previous studies have not explored the effects of estrogen treatments on neuronal signaling during the dark-phase. In the present study, ovariectomized rats received estradiol benzoate (5 microg/rat for 7 days, s.c.) and norepinephrine and dopamine levels were measured in the preoptic area of the hypothalamus across the light/dark cycle using in vivo microdialysis. Estradiol benzoate treatment increased extracellular norepinephrine and dopamine levels relative to vehicle treatment during the dark-phase. Increases in norepinephrine and dopamine were first detected by 30 min and 5.5h after lights-off, respectively. Subsequent increases in norepinephrine and dopamine were also noted throughout the 9.5-h collection period. The effect of estradiol benzoate on catecholamine release did not correlate with increases in either tyrosine hydroxylase (TH) protein expression or activity levels in the anterior hypothalamus, although a marked decrease in TH activity correlated with a rise in extracellular norepinephrine at the beginning of the dark-phase. We conclude that subchronic estradiol benzoate treatment increases extracellular catecholamine levels in the preoptic area of the hypothalamus during the dark-phase without a concomitant increase in neurotransmitter biosynthesis. The estradiol benzoate-induced increases in norepinephrine and dopamine levels in the preoptic area during the dark-phase may play an important role in modulating critical hypothalamic functions.
 ...
PMID:Estradiol increases catecholamine levels in the hypothalamus of ovariectomized rats during the dark-phase. 1957 79