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Biomedical subjects

S Tsujii

Publications and source records attributed to S Tsujii.

29 records · Page 2Linked to original sources
PubMed1986

Effects of food deprivation and high fat diet on opioid receptor binding in rat brain.

The effect of food deprivation for 72 h or a high fat diet on [3H]naloxone binding in the discrete brain regions of male lean Zucker rats was studied. In the midbrain, both treatments increased Bmax for the high-affinity site with no change in Kd. In the cortex, the high fat diet increased Bmax for the high-affinity site. These results suggest that dietary manipulations could produce significant changes in the endogenous opioid system.

Animals↗
PubMed1986

Effect of food deprivation on opioid receptor binding in the brain of lean and fatty Zucker rats.

The effect of food deprivation on opioid receptor binding was studied in 6 brain regions of lean and fatty Zucker rats; using [3H]dynorphin A. There was no significant difference between lean and fatty rats fed ad libitum in binding parameters for any regions studied. Food deprivation increased Bmax and/or Kd for cortex, midbrain and striatum of lean rats, and the former two regions of fatty rats. These results suggest that food deprivation may influence opioid receptor binding in lean and fatty Zucker rats.

Animals↗
PubMed1985

Modulation of luteinizing hormone(LH) release by clonidine and opioid peptides in castrated male rats.

The effect of clonidine, a central alpha-adrenergic agonist, on the suppression of LH release induced by beta-endorphin or FK33-824, an endogenous opioid peptide or its synthetic analog, was investigated in castrated male rats, with or without pretreatment with reserpine. Pulsatile LH secretion was inhibited by intravenous injection of FK33-824 (400 micrograms/kg), or intraventricular injection of beta-endorphin (5 micrograms). Without pretreatment with reserpine, intraperitoneal administration of clonidine (1 mg/kg) failed to reverse the inhibition of LH release induced by these peptides. However, with pretreatment with reserpine (10 mg/kg), clonidine abolished the inhibitory effect on LH secretion induced by these peptides in castrated male rats. These data indicate that, unlike the results in ovariectomized, steroid-primed rats, pretreatment with reserpine allows the alpha-adrenergic system to act more peripherally than the opioid neuronal system in a neuronal network-regulating LH release in castrated male rats.

Animals↗
PubMed1984

Serotonin involvement in the inhibition of luteinizing hormone (LH) release during immobilization in castrated male rats.

The involvement of serotonin in mediating the inhibitory effect of immobilization stress on LH secretion in castrated male rats was examined by employing p-chlorophenylalanine (PCPA, 320 mg/kg, ip), an inhibitor of serotonin synthesis, and 5,6-dihydroxytryptamine (5,6-DHT, 50 micrograms, icv), a drug toxic to the indoleaminergic system. Immobilization stress suppressed pulsatile LH release and decreased mean plasma LH levels. Pretreatment with PCPA or 5,6-DHT apparently eliminated the inhibitory effect of immobilization stress on LH release. These results suggest the possible involvement of a serotoninergic mechanism in mediating the suppression of LH release induced by immobilization stress in castrated male rats.

Animals↗
PubMed1984

Plasma disappearance of ovine corticotrophin-releasing factor in man.

Disappearance of immunoreactive ovine corticotrophin-releasing factor (IR-oCRF) from plasma after a single intravenous injection of ovine corticotrophin-releasing factor (oCRF) was studied in man in the morning and evening. Synthetic oCRF (80 micrograms) was injected intravenously to four normal male volunteers at 0900 h or at 2200 h. Blood samples were drawn before and 2, 5, 10, 15, 30, 45, 60, 90 and 120 min after the oCRF injection. Plasma IR-oCRF was measured by a specific radioimmunoassay for OCRF. Plasma concentrations of IR-oCRF after oCRF injections in the morning and in the evening did not differ significantly (P greater than 0.05). Disappearance of IR-oCRF was modelled with a two-exponent function by using a non-linear least squares computer program. The metabolic clearance rate, the apparent initial volume of distribution, the plasma half-life for the fast component and that for the slow component calculated from all eight tests in the morning and evening were 1.49 +/- 0.05 ml/min X kg, 44.4 +/- 1.7 ml/kg, 6.8 +/- 0.7 min and 46.2 +/- 2.3 min (mean +/- SEM), respectively. This relatively long half-life may be responsible for the prolonged biological effect of oCRF administered intravenously. There were no significant differences between parameters of IR-oCRF disappearance curves in the morning and those in the evening (P greater than 0.05).

Adult↗
PubMed1984

Plasma adrenocorticotropin and cortisol responses to ovine corticotropin-releasing factor in patients with adrenocortical insufficiency due to hypothalamic and pituitary disorders.

Plasma ACTH and cortisol responses to intravenous injection of 100 micrograms synthetic ovine corticotropin-releasing factor (CRF) were studied in 4 patients with hypothalamic hypopituitarism, 2 patients with Sheehan's syndrome, 2 patients with isolated ACTH deficiency and 10 normal subjects. All 4 patients with hypothalamic hypopituitarism had exaggerated plasma ACTH responses to CRF compared to normal subjects and gradual but definite increases in plasma cortisol from low basal levels. Of 2 patients with Sheehan's syndrome, one had slight ACTH and cortisol increases after CRF injection, whereas the other had no increase in either. In 2 patients with isolated ACTH deficiency, plasma ACTH and cortisol remained undetectable (ACTH less than 10 pg/ml, cortisol less than 0.6 microgram/dl) after CRF injection. These results suggest that the CRF test is a useful tool in evaluating patients with secondary adrenocortical deficiency.

Adolescent↗
PubMed1983

Evidence for noradrenergic involvement in naloxone-induced stimulation of luteinizing hormone release in prepubertal female rats.

The effects of phenoxybenzamine an alpha-adrenergic blocker, propranolol a beta-adrenergic blocker, and diethyldithiocarbamate a noradrenaline synthesis inhibitor, on the LH increase induced by naloxone an opiate antagonist, was investigated in 25 day old female rats. Pretreatment with phenoxybenzamine or diethyldithiocarbamate suppressed the LH increase induced by naloxone, whereas pretreatment with propranolol had no significant effects on the naloxone-induced LH release. These results suggest that naloxone-induced increase in LH release is mediated via a noradrenergic mechanism.

Animals↗
PubMed1983

Plasma adrenocorticotropin and cortisol responses to intravenous injection of corticotropin-releasing factor in the morning and evening.

Plasma ACTH and cortisol responses to corticotropin-releasing factor (CRF) were determined in the morning and evening in seven normal men. Either 100 micrograms synthetic ovine CRF or saline was given intravenously at 0900 h and at 2200 h. Blood samples were collected before and 15, 30, 45, 60, 90, and 120 min after CRF or saline injection. Plasma ACTH concentrations before and after CRF injection in the morning were significantly higher (P less than 0.05) than those in the evening at all times except 45 min after injection. Plasma cortisol concentrations before and at all times after CRF injection in the morning were also significantly higher (P less than 0.05) than those in the evening. However, neither the maximum increments in plasma ACTH and cortisol above the control levels nor increments at each time point following CRF injection in the morning differed significantly from those in the evening. Increments in the area under the ACTH and cortisol concentration curves after CRF injection in the morning also did not differ significantly from those in the evening. These results suggest that the responsiveness of the pituitary to CRF in the morning and in the evening does not differ significantly, although actual values of plasma ACTH and cortisol are higher in the morning.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Effects of food deprivation and high fat diet on immunoreactive dynorphin A(1-8) levels in brain regions of Zucker rats.

The levels of immunoreactive dynorphin A(1-8) (ir-DYN8) were measured in discrete brain regions of lean Zucker rats subjected to food deprivation for 72 hr and to a high fat diet, and in fatty Zucker rats after food deprivation for 72 hr. Fatty rats showed higher concentrations of ir-DYN8 in the cortex and midbrain, when compared to lean rats fed a stock diet ad lib. Food deprivation increased ir-DYN8 levels in the cortex of lean rats and fatty rats and in the hippocampus of fatty rats, but decreased its content in the striatum of lean rats and in the midbrain of fatty rats. The high fat diet increased ir-DYN8 levels in the cortex and midbrain of lean rats. These results suggest that ir-DYN8 levels in extrahypothalamic structures of Zucker rats could be differentially modified under conditions of hereditary obesity and dietary manipulations.

Analysis of Variance↗