摘要:

The role that opiate peptides play in suckling-induced prolactin (PRL) release was examined in 10-day post-partum lactating rats. The opiate receptor antagonist naloxone (NAL) suppressed suckling-induced PRL release in a dose-dependent manner and a large dose abolished the response. These results suggest either that opiate neurons are situated in the neuronal pathway mediating this neuroendocrine response, or alternatively, that opiate neurons are situated such that they can modulate neuronal transmission in this pathway. It is suggested that NAL blocks a tonic, inhibitory β-endorphinergic input to the tuberoinfundibular dopaminergic (TIDA) neurons, hence, NAL administration in effect stimulates the TIDA neurons and in this way overrides the suckling response. Intravenous, bolus administration of β-en-dorphin (β-END) produced a PRL response that was similar to the suckling response in terms of latency of onset and duration while the magnitude of the β-END-induced response was 2-fold greater than that produced by the suckling stimulus. NAL abolished β-END-induced PRL release at a much lower dose than that required to inhibit suckling-induced PRL release. This suggests that the neural mediation of the suckling response involves a mechanism in addition to the one inhibited by opiate receptor bloc

ISSN:0028-3835    

DOI:10.1159/000124448

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The accumulation of [8-arginine]vasopressin (AVP) in brain areas inside the blood-brain barrier (thalamus-hypothalamus, amygdala with overlying temporal cortex, hippocampus and cerebral cortex) and outside the blood-brain barrier (median eminence of the hypothalamus and area postrema) was measured after subcutaneous injection of the hormone. The plasma concentrations of AVP peaked at 5 min after subcutaneous injection and declined in a biphasic manner over the next 115 min. The concentration of AVP in brain tissue samples peaked at 20 min after the subcutaneous injection of AVP; the decline of AVP in the areas protected by the blood-brain barrier followed the time course seen for plasma. The concentration of AVP in the brain areas not so protected also peaked at 20 min but these declined at rates that differed from other brain areas and plasma. The concentration of AVP in the plasma and in most brain areas depended on the dose administered, while those in the median eminence and in the area postrema did not. Water deprivation for 24 and 48 h significantly elevated both the plasma AVP concentration and the concentration of AVP in the hypothalamus and in the amygdala-temporal cortex samples. The increases in AVP after water deprivation are limited to these two regions and are quantitatively much lower than after peripheral administration. Furthermore, when the brains of anesthetized rats were perfused free of blood, there were no changes in regional brain AVP content after subcutaneous treatment with 5,000 ng/kg of AVP, except for the median eminence. These data suggest that circulating AVP does not enter the parenchyma of brain areas protected by the blood-brain barrier in sufficient quantities to be detected by our assay. The penetration of AVP into areas not protected by the blood-brain barrier may be due to differences in the specialized cellular components located there. These results support the hypothesis that centrally and peripherally derived AVP may each act on different substrates to effect body function.

ISSN:0028-3835    

DOI:10.1159/000124449

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The levels of dynorphin, α-neoendorphin and β-endorphin immunoreactivity (ir-DYN, ir-α-NEO, ir-β-E) were measured in the brain, pituitary and gut of rats subjected to a variety of manipulations. Water deprivation caused an increase in the ir-DYN and ir-α-NEO content in the hypothalamus and a decrease in the neurointermediate (NI) lobe of the pituitary. The ir-β-E level decreased in the hypothalamus and anterior lobe of the pituitary, while it increased in the Nl-pituitary. Food deprivation, as well as chronic fenfluramine (10–20 mg/kg) treatment increased, while acute muscimol (0.5 µg/10 µl) treatment decreased the ir-β-E, but not ir-DYN or ir-α-NEO content in the hypothalamus. The anterior pituitary content of ir-β-E was increased after food deprivation and decreased after chronic fenfluramine treatment. However, the ir-DYN and ir-α-NEO contents in the duodenum were markedly increased after food deprivation, while chronic fenfluramine treatment led to a dramatic decrease in the ir-DYN content. These results suggest that the levels of opioid peptides in the brain, pituitary and gut may be differentially and independently affected by alteration of the inges

ISSN:0028-3835    

DOI:10.1159/000124450

出版商:S. Karger AG    

年代:1986

数据来源: Karger