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J I Koenig

Publications and source records attributed to J I Koenig.

65 records · Page 4Linked to original sources
PubMed1985

Altered responses to serotonergic agents in Fawn-Hooded rats.

The incidence of "wet dog" shakes elicited by quipazine, the hyperthermic response induced by 5-methoxy-N,N-dimethyltryptamine (5MeODMT) and the hypothermic response to 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were compared in rats of the Fawn-Hooded (FH) and Sprague-Dawley (SD) strains. The behavioral responses of FH rats to quipazine and 5MeODMT were significantly greater than those of SD rats. On the other hand, the hypothermic effect of 8-OH-DPAT in FH rats was significantly less than that elicited in SD animals. The present results are supportive of the view that the responsiveness of serotonergic mechanisms in the CNS of FH rats differs markedly from those in SD animals.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1985

Possible delta receptor mediation of the effect of beta-endorphin on luteinizing hormone (LH) release, but not on prolactin (PRL) release, in the ovariectomized rat.

Administration of opioid receptor antagonists was utilized to determine the opioid receptor type involved in the suppression of LH release by beta-endorphin (beta-END). Long-term (three to four weeks) ovariectomized rats with chronic third ventricular cannulae were fitted with jugular catheters and received treatment with vehicle or one of three opioid antagonists. The delta antagonist ICI 154, 129, but not the mu1 or mu antagonists naloxazone or beta-funaltrexamine, respectively, blocked the suppressive effect of beta-END on plasma LH levels and transiently but significantly increased LH levels above preinfusion value. None of the antagonists significantly reduced the beta-END-induced release of PRL. These results provide evidence that the inhibitory effect of beta-END on LH release may be mediated by delta receptors.

Animals↗
PubMed1984

Differential role of the opioid mu and delta receptors in the activation of prolactin (PRL) and growth hormone (GH) secretion by morphine in the male rat.

Administration of naloxazone (50 mg/kg i.v.), an irreversible, selective and long acting antagonist of the mu 1 subclass of the opioid receptors, strongly reduced stimulation of PRL secretion by morphine (5.0 mg/kg i.v.) injected 24 hours later into conscious, unrestrained rats. In contrast, the effect of morphine on PRL release was unimpaired in rats treated 24 hours beforehand with either the reversible opioid antagonist naloxone (50 mg/kg i.v.), or the vehicle for naloxazone. A complete suppression of the PRL response to morphine (3.0 mg/kg i.v.) was observed in animals given intraventricular (IVT) injection of beta- funaltrexamine (beta-FNA, 2.5 micrograms), another selective, irreversible and long acting antagonist of the mu receptors, 24 hours beforehand. Neither naloxazone nor beta-FNA had any effect on the activation of GH secretion by morphine, which, however, was conspicuously reduced by ICI 154, 129, a preferential delta receptor antagonist, injected IVT (50 micrograms) 5 minutes before morphine. ICI 154, 129 had no effect on the PRL response to morphine. It is concluded that the PRL stimulating effect of morphine is mediated by the mu receptors, whereas activation of GH probably involves the delta sites.

Animals↗
PubMed1984

Site of action for beta-endorphin-induced changes in plasma luteinizing hormone and prolactin in the ovariectomized rat.

A number of sites have been hypothesized as loci at which opioid substances act to alter the secretion of luteinizing hormone (LH) and prolactin (PRL) (1-8). The aim of the present study was to determine the site(s) at which the opioid peptide beta-endorphin (beta-END) acts to influence plasma LH and PRL levels in the ovariectomized (OVX) rat. beta-END, administered into the third ventricle of conscious OVX rats fitted with jugular catheters, significantly decreased plasma LH in doses greater than or equal to 50 ng and increased PRL levels at all doses administered (10, 50, 100 and 250 ng) in a dose dependent fashion. To identify possible central nervous system sites of action, 250 ng beta-END was unilaterally infused into various brain sites. Plasma LH was significantly decreased and plasma PRL significantly increased by infusions into the ventromedial hypothalamic area, the anterior hypothalamic area, and the preoptic-septal area. There was no significant effect of beta-END infusions into the lateral hypothalamic area, amygdala, midbrain central gray, or caudate nucleus. When hemipituitaries of OVX rats were incubated in vitro with beta-END (10(-7)M to 10(-5)M), there was no suppression of basal or LHRH-induced LH release, nor was there any alteration of basal PRL release. It is concluded that beta-END acts at a medial hypothalamic and/or preoptic-septal site and not the pituitary, to alter secretion of LH and PRL.

Animals↗
PubMed1982

The morphology and distribution of peptide-containing neurons in the adult and developing visual cortex of the rat. I. Somatostatin.

Using conventional immunocytochemical techniques, we have examined the morphology and distribution of somatostatin-like immunoreactive neurons in the visual cortex of albino rats between the first postnatal day and maturity. In the adult, somatostatin-immunoreactive neurons were observed in layers II to VI but were concentrated in layers II and III. These cells displayed morphological features characteristic of the multipolar and bitufted varieties of cortical non-pyramidal neurons as described in Golgi preparations of rat visual cortex. On the first postnatal day and in the subsequent few days, immunoreactivity was confined to immature bipolar and multipolar neurons concentrated in layers V and VI. Labelled cells first appeared in the more superficial layers at the beginning of the second postnatal week and attained a distribution similar to that observed in adult animals at the end of this week. At this time they closely resembled their adult counterparts from which they appeared indistinguishable by the end of the third postnatal week. The late appearance of labelled cells in the superficial layers, where they are predominantly located in adult animals, suggests that the somatostatin immunoreactivity exhibited by most of these neurons develops several days after they have completed their migration and assumed their positions in the visual cortex.

Aging↗
PubMed1982

On the prolactin-inhibiting effect of neurotensin. The role of dopamine.

Neurotensin (NT) when injected in a dose of 5 micrograms into the third cerebral ventricle of conscious, unrestrained male rats, outfitted with chronic third ventricle and jugular cannulae, decreased the resting prolactin (PRL) levels. NT (5 micrograms) also markedly inhibited the PRL-releasing effect of activation of central serotonin receptors by 5-hydroxytryptophan (5HTP, 15 mg/kg) in animals pretreated with fluoxetine (4 mg/kg). however, interruption of dopamine (DA) neurotransmission by either alpha-methyl-p-tyrosine (alpha MT, 250 mg/kg) or spiroperidol (0.3 mg/kg) led to a blockade of the PRL-inhibiting effect of NT. Treatment of animal with alpha MT prior to the injection of fluoxetine and 5HTP also blocked the PRL-inhibiting effect of NT. These results suggest that the central dopaminergic system mediates the PRL-inhibitory effect of NT.

Animals↗
PubMedDate not supplied

Tissue-specific sex differences in galanin-like immunoreactivity and galanin mRNA during development in the rat.

Galanin-like immunoreactivity (Gal-LI), as determined by radioimmunoassay, was detectable in the brain and gastrointestinal tract by day 15 of gestation. Concentrations of Gal-LI increased after birth in the hypothalamus but decreased in the stomach and duodenum. A sex difference in Gal-LI concentrations appeared during puberty in the median eminence, neurointermediate lobe, and the anterior pituitary (AP), where females had higher Gal-LI concentrations compared to males. This difference was most pronounced in the AP; adult females had up to 4-fold greater Gal-LI concentrations and 5-fold more abundant rGal-specific mRNA compared to males.

Aging↗