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Biomedical subjects

C B Pert

Publications and source records attributed to C B Pert.

At least 145 records · Page 8Linked to original sources
PubMed1980

Bombesin: receptor distribution in brain and effects on nociception and locomotor activity.

The radioreceptor assay was used to examine the distribution of bombesin receptors in the rat brain. The highest concentrations of receptors appeared to be associated with limbic forebrain and midbrain structures such as the hippocampus, amygdala, hypothalamus and the periaqueductal gray matter. The caudate-putamen of the extrapyramidal motor system and the forebrain also exhibited high bombesin binding. Intraventricular injections of bombesin (0.1, 1.0 and 10 microgram) produced a dose-dependent increase in locomotor activity in rats. Injections of bombesin into the periaqueductal gray matter produced an antinociceptive reaction in the hot-plate as well as the tail-flick test. This apparent analgesia was not antagonized by naloxone.

Animals↗
PubMed1980

Increase in pituitary melanocyte-stimulating hormone activity of genetically obese (ob/ob) mice.

Melanocyte-stimulating hormone (MSH) activity was measured in the pituitaries of genetically obese and lean control mice using the frog skin bioassay. Obese mice pituitaries demonstrated very significantly elevated levels of biologically active MSH when compared to their lean littermates. These results support the hypothesis that the elevated levels of pituitary hormones found in obese mice possesses true biological activity.

Adrenocorticotropic Hormone↗
PubMed1980

Naltrexone reduces weight gain, alters "beta-endorphin", and reduces insulin output from pancreatic islets of genetically obese mice.

Naltrexone, an opiate antagonist, was administered to young obese (ob/ob) and lean mice for five weeks. Animals had continuous access to food and received 10 mg/kg SC twice daily with equivalent volumes of saline given to controls. The effects on body weight, and pituitary and plasma levels of beta-endorphin-like material were measured. Naltrexone-injected obese animals gained weight more slowly over the first three weeks while the weight gain of lean animals was not affected by naltrexone. Plasma levels of beta-endorphin were shown to be significantly higher in untreated ob/ob mice and this difference increased with age (4-20 weeks). With naltrexone treatment, plasma levels in +/? mice rose and exceeded those in ob/ob. Saline treatment appeared to be a stress, and pituitary beta-endorphins rose 4-6 fold in ob/ob compared with +/?. While naltrexone reduced the levels of ob/ob pituitary towards normal, no effect on beta-endorphin levels in pituitary of lean mice was obtained. In vitro studies of effects of the opiate antagonists, naloxone, on insulin secretion by isolated islets provided additional evidence of resistance of lean mice to naloxone relative to ob/ob. (IRI secretion fell only in naloxone treated ob/ob islets). These observations support the contention that this form of genetic obesity is characterized by elevated endogenous opiate levels and an increased sensitivity to opiate antagonists such as naltrexone or naloxone.

Animals↗
PubMed1980

In vitro autoradiography of opiate receptors in rat brain suggests loci of "opiatergic" pathways.

Slide-mounted sections of unfixed frozen rat brain can be labeled in vitro with [3H]naloxone to show the mu-like ligand selectivity characterized in previous studies. We have developed an autoradiographic technique using hot paraformaldehyde vapors to prevent diffusion of ligands with reversible binding. Resolution at the light level is sufficient to detect concordance between receptor patterns and terminal fields of axonal projections marked by tract-tracing techniques. The opiate receptor distribution suggests the existence of widespread intrinsic and several longer multisynaptic "opiatergic pathways within sensory and limbic circuits. One multisynaptic pathway may link olfactory structures with limbic circuits in the amygdala and habenula. Another may lie in limbic cortical structures. Opiate receptors are numerous also in sensory systems, and within primary sensory nuclei (visual, auditory, olfactory, somatic) they are found superficially in laminated structures. Together, the opiate receptors are well placed to control incoming sensory and subsequent limbic information processing.

Animals↗
PubMed1979

Vasoactive intestinal polypeptide: specific binding to rat brain membranes.

The binding of radiolabeled vasoactive intestinal polypeptide (VIP) to rat brain membranes was investigated. Specific binding of 125I-labeled VIP was reversible and saturable (Bmax = 2.2 pmol/g of wet tissue). Brain membranes exhibited a high affinity for 125I-labeled VIP (KD = 1 nM) at a single class of noninteracting sites. Binding of 125I-labeled VIP paralleled its immunohistochemical localization, being enriched in cerebral cortex, hippocampus, striatum, and thalamus, with the notable exception of the hypothalamus, which had low levels of binding. The density of sites was greater in synaptosomal fractions relative to mitochondrial or nuclear fractions. Secretin and partial sequences of it and VIP inhibited binding to brain membranes with an order of potency similar to that found in other systems. The findings suggest the existence of a unique new class of brain receptors.

Animals↗
PubMed1978

beta-Endorphin is associated with overeating in genetically obese mice (ob/ob) and rats (fa/fa).

Small doses of the opiate antagonist naloxone selectively abolished overeating in genetically obese mice (ob/ob) and rats (fa/fa). Elevated concentrations of the naturally occurring opiate beta-endorphin were found in the pituitaries of both obese species and in the blood plasma of the obese rats. Brain levels of beta-endorphin and Leu-enkephalin were unchanged. These data suggest that excess pituitary beta-endorphin may play a role in the development of the overeating and obesity syndrome.

Animals↗
PubMed1978

Long-term treatment with lithium prevents the development of dopamine receptor supersensitivity.

Long-term treatment of rats with haloperidol produced an increased sensitivity to the locomotor and stereotypic effect of apomorphine. This behavioral dopaminergic supersensitivity was accompanied by increased binding of [3H] spiroperidol in the striatum. Rats treated concurrently with lithium and haloperidol failed to develop both behavioral sensitivity to apomorphine and increased striatal dopamine receptor binding. The ability of lighium to prevent recurrent manicdepressive episodes may be related, in part, to its ability to stabilize dopaminergic receptor sensitivity.

Animals↗