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J K Nishita

Publications and source records attributed to J K Nishita.

15 recordsLinked to original sources
PubMed1990

Comparison of central nervous system and peripheral pharmacodynamics to atropine pharmacokinetics.

Two experiments were designed to examine the pharmacokinetic-pharmacodynamic relationship for the central nervous system and peripheral effects of atropine. According to a random Latin square design, healthy young male volunteers were given i.m. injections containing single doses of placebo or 0.5, 1.0, 2.0 or 4.0 mg of atropine. The central nervous system tests included wheel tracking, a coordination task, and digit symbol substitution, a memory-psychomotor speed task; the physiological variable was heart rate. The pharmacokinetics of atropine were best described by a two-compartment model with very rapid first order absorption. Changes in plasma atropine levels and heart rate closely overlapped for all four doses throughout most of the time course. In contrast, the differential time course of changes in atropine levels and behavioral impairment indicates that pharmacokinetics is not the primary rate-limiting mechanism for the central nervous system effects of atropine. Alternative explanations are discussed, including differential atropine effects on peripheral M2 receptors mediating a heart rate effect and on CNS M1 receptors mediating the memory-psychomotor effect.

Adult↗
PubMed1989

Cerebral atrophy in bulimia.

The extent of cerebral atrophy in 8 consecutively chosen unmedicated bulimics and 8 normal controls was determined by magnetic resonance imaging. There was no history of anorexia nervosa or alcoholism in either group. Measures obtained included the ratio of cerebral to cranial area at the midsagittal section, as well as maximum ventricle/brain ratio in the axial plane. Sagittal cerebral/cranial ratio was significantly less in the bulimic group than in controls [0.82 +/- 0.04 (SD) versus 0.90 +/- 0.03, Z = -2.74, p = 0.006, two-tailed Mann-Whitney U-test], whereas ventricle/brain ratio was not significantly different between groups. Implications for the occurrence of cortical atrophy in normal-weight bulimics, as well as for the relative absence of ventricular enlargement in these patients, are discussed.

Adult↗
PubMed1989

Abnormalities in the response of plasma arginine vasopressin during hypertonic saline infusion in patients with eating disorders.

We examined the response of plasma arginine vasopressin (pAVP) to intravenous 5% hypertonic saline in patients with anorexia nervosa (AN) and bulimia nervosa (BN). Patients did not differ from controls in their subjective response for the onset of thirst; however, only 5 patients (3 AN and 2 BN) showed pAVP levels that were within the normal range (0.5-11.0 pg/ml) for this test. With the exception of two eating disorder (ED) patients, all others showed some nonlinear irregularities in the pattern of their secretion of pAVP in response to the hypertonic saline infusion. Seven of the ED patients showed an irregular abnormally high pAVP secretion, and three patients showed abnormally low pAVP responses. Both of these pAVP secretion abnormalities occurred in underweight and weight-recovered AN patients, as well as in BN patients. The cause and pathophysiological consequences of these abnormalities remain unresolved.

Adolescent↗
PubMed1988

Clomiphene blocks the effect of intravenous estradiol on the firing rate of rat nigral dopamine neurons.

Intravenous 17-beta-estradiol (BETA) has a potent, stereo-specific, and rapid effect on dopamine (DA) neuron firing rate in the substantia nigra compacta (SNC). Our data demonstrate that immediate intravenous pretreatment with the anti-estrogen clomiphene (CLOM) blocks the action of subsequent intravenous BETA administration. Our results provide further physiologic evidence for membrane-bound estradiol (E2) receptors within the rat brain.

Animals↗
PubMed1987

Absence of synthesis-modulating nerve terminal autoreceptors on mesoamygdaloid and other mesolimbic dopamine neuronal populations.

The present study sought to map the distribution of dopamine (DA) synthesis-modulating autoreceptors on DA nerve terminals innervating the amygdala and other limbic structures of the rat brain at a level of anatomic resolution (i.e., discrete component nuclei) commensurate with the functional organization of such structures. The biochemically estimated response of mesoamygdaloid and other limbic DA neuronal populations to conditions of minimal (gammabutyrolactone administration or surgical axotomy) and maximal (low-dose apomorphine administration) activation of nerve terminal DA autoreceptors was examined and compared to the response of mesostriatal and mesocortical DA neurons. In contrast to the caudate nucleus, nucleus accumbens, and olfactory tubercle, neither gammabutyrolactone (GBL) nor axotomy increased biochemically estimated DA synthesis (DOPA accumulation) in any of the amygdaloid nuclei, the anterior amygdaloid area, septal nuclei, or subdivisions of the interstitial (bed) nucleus of the stria terminalis. These results indicate that, similar to the medial prefrontal cortex and median eminence, DA synthesis in mesoamygdaloid and other subcortical limbic DA neuronal populations is not under the regulatory influence of tonically active, nerve terminal-localized autoreceptors. Both GBL and axotomy increased DOPA accumulation in the anterior cingulate cortex, but not in allocortical projection fields. In contrast to the differential distribution of DA synthesis-modulating terminal autoreceptors, the end-product inhibition of tyrosine hydroxylase activity appears to be a ubiquitously expressed regulatory property of DA neurons. The decrease in DA metabolism produced by the administration of a low, presumably auto-receptor-selective, dose of apomorphine exhibited a DA neuronal population distribution distinctly unlike that of the aforementioned effects of GBL or axotomy on DOPA accumulation. These results reinforce the DA neuronal population-selective distribution of synthesis-modulating autoreceptors and indicate that nerve terminal-localized autoreceptors are operative in regulating DA synthesis in only a minority of DA-innervated brain structures. Further, the demonstration of such autoreceptors is dependent upon the preparation, pharmacological tools, and functional endpoints chosen for study.

4-Butyrolactone↗
PubMed1984

Perinatal dopamine-related drugs demasculinize rats.

Administration of haloperidol, a common neuroleptic, to pregnant or lactating rats impaired the masculine sex behavior of their male offspring. Prenatal haloperidol did not affect testosterone concentrations in fetuses. Maternal administration of apomorphine, a dopamine agonist, and of alpha-methyl-p-tyrosine, an inhibitor of dopamine synthesis, also demasculinized male offspring. In both experiments other behaviors and developmental milestones were unaffected. Perinatal haloperidol, apomorphine, and alpha-methyl-p-tyrosine did not lower testosterone in adulthood. These drugs may act directly on neurons that control masculine behavior without lowering testosterone prenatally or in adulthood.

Animals↗
PubMed1984

Anorexia nervosa. Current perspectives in research.

This article is a thorough update of drug treatment studies and basic research. In their presentation of drug interventions, the authors discuss the efficacy of such psychotropic medications as neuroleptics, tricyclic antidepressants, lithium carbonate, cyproheptadine, and delta 9-tetrahydrocannabinol. An overview of new research perspectives on two new anorectogenic substances--AP, isolated from the urine of "hypothalamic" anorectics, and satietin, purified from normal serum--is presented.

Anorexia Nervosa↗