Search PubMed⌕ Search

Biomedical subjects

J F Lorden

Publications and source records attributed to J F Lorden.

65 records · Page 4Linked to original sources
PubMed1977

Food intake and body weight: effects of specific and non-specific lesions in the midbrain path of the ascending noradrenergic neurons of the rat.

Bilateral injections of 4.8 or 12 microgram of 6-hydroxydopamine hydrobromide were made in the midbrain path of the ascending norepinephrine (NE) fibers. Maximum NE depletion was obtained with the 4 microgram dose. Increasing the dose did not increase NE depletion in either the hypothalamus or the telencephalon. Increases in food intake were observed following the 12 microgram dose only. Electrolytic, copper sulfate, or 5,6-dihydroxytryptamine lesions at the same site caused increases in both food intake and body weight with only moderate (-32 to -58%) decreases in NE levels. Behavioral changes were seen in only those groups in which a large amount of non-specific tissue damage was also observed. Therefore, the behavioral effects were attributed to general tissue damage in the area and not the NE fibers specifically.

5,6-Dihydroxytryptamine↗
PubMed1976

Effects of food restriction and mutation on central catecholamine levels in genetically obese mice.

Norepinephrine (NE) levels in the hypothalamus and telencephalon of genetically obese mice with the OBOB and DBDB mutations are significantly higher than those of their lean littermates. Obese mice with the viable yellow mutation failed to show this increase. Restricting the diets of OBOB animals to prevent excessive weight gain does not affect NE levels in the hypothalamus, telencephalon or brainstem.

Animals↗
PubMed1976

Effects of lesions of the gustatory necortex on taste aversion learning in the rat.

Normal rats and rats with lesions of the gustatory neocortex (GN) were compared for their ability to learn aversions to taste cues paired with toxicosis. When the taste presentation was followed immediately by toxicosis, normal rats and rats with lesions of the posterior (visual) neocortex learned aversions to sucrose, sodium chloride, quinine hydrochloride, and hydrochloric acid solutions. Rats with GN lesions learned aversions to all solutions except sucrose. In preference tests, all solutions were shown to be discriminable from water by both normal rats and rats with GN lesions. Under conditions in which a 6-hr delay separated taste presentation and toxicosis, normal rats again learned specific aversions to all four solutions, but rats with GN lesions failed to learn specific aversions to sucrose, sodium chloride, and hydrochloric acid solutions. It was shown that the ability of rats with GN lesions to learn aversions to sucrose and quinine depended on stimulus concentration; and it was proposed that the data could be accounted for by postulating a change in the threshold for taste-illness associations following GN lesions.

Animals↗
PubMedDate not supplied

Reverse-phase separation and electrochemical detection of neuropeptides.

The reverse-phase separation of neuropeptides using isocratic conditions is described. Each component of the mobile phase was examined for its ability to influence the separation of complex mixtures of neuropeptides. Manipulation of buffer strength, pH, organic modifier and column type provided sufficient flexibility to resolve closely related neuropeptides. Amperometric detection of oxidizable amino acids in the peptide sequence of a number of endogenous neuropeptides proved suitable for the identification of peptide standards and quantification of neural lobe arginine vasopressin and striatal methionine enkephalin.

Animals↗
PubMedDate not supplied

GABA levels and GAD immunoreactivity in the deep cerebellar nuclei of rats with altered olivo-cerebellar function.

Immunocytochemistry was used to examine the distribution, size, and density of glutamic acid decarboxylase immunoreactive (GAD+) puncta in two animal models with movement disorders, the genetically dystonic (dt) rat and rats with 3-acetylpyridine (3AP) lesions of the inferior olive. In both models, GAD activity is increased in the deep cerebellar nuclei (DCN) where the enzyme is localized primarily in the terminals of Purkinje cells. GABA levels were also measured in the DCN. The general distribution of GAD+ puncta in the DCN was similar in all groups. Immediately after the 3AP lesions, however, GABA levels were elevated in 3AP rats in comparison with both normal rats and age-matched dt rats. GAD+ puncta were also larger than normal in the 3AP group at this time, although the magnitude of this effect declined over a 2-week recovery period. Puncta density was decreased in the medial nucleus only in 25-day-old dt rats in comparisons with normal littermates. These findings are discussed in the context of previously reported differences in the firing rate of Purkinje cells in dt and 3AP-treated rats.

Animals↗
PubMedDate not supplied

Behavioral and endocrinological effects of single injections of monosodium glutamate in the mouse.

Treatment of neonatal mice with large, repeated doses of monosodium L-glutamate (MSG) produces a syndrome of obesity and endocrinological dysfunction generally attributed to a hypothalamic lesion. We have used single injections of MSG, administered on postnatal day four, to explore the lower end of the dose-response curve for this toxin. Major features of the MSG syndrome including hypophagia, obesity, hypoactivity, reduced pituitary protein content, decreased ovarian weight, delayed puberty and elevated plasma corticosterone levels were obtained at the highest dose. Of the variables measured, feeding disturbances and reduced pituitary and ovarian weights were the most sensitive indicators of damage. The extent of damage produced in the arcuate nucleus of the hypothalamus increased with increasing dose. A prominent lesion was also detected in the medial preoptic area of animals receiving the highest dose. Damage was not evident in other diencephalic structures associated with body weight regulation. Since little is known about the mechanisms underlying MSG obesity, a second study examined the contribution of ovarian hormones to obesity in MSG treated mice. Ovariectomy increased the body weights of animals injected with low but not high doses of MSG, suggesting that a reduction in ovarian function may contribute to the MSG obesity syndrome in the female. Measurement of hypothalamic monoamines and metabolites in these mice indicated that as with repeated doses of MSG, single injections of the toxin reduced hypothalamic dopamine levels. DOPAC levels were unchanged.

Adipose Tissue↗