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Biomedical subjects

B Bohus

Publications and source records attributed to B Bohus.

At least 163 records · Page 9Linked to original sources
PubMed1979

Effect of oxytocin and vasopressin on memory consolidation: sites of action and catecholaminergic correlates after local microinjection into limbic-midbrain structures.

The effects of local postlearning microinjections of arginine-vasopressin (AVP) and oxytocin (OXT) on one-trial learning passive avoidance behavior and the influence of AVP on alpha-MPT-induced disappearance of norepinephrine (NE) and dopamine (DA) in discrete brain regions have been studied in the rat. OXT injected bilaterally in the hippocampal dentate gyrus (25-25 pg) or in the midbrain dorsal raphe nucleus (50 pg) significantly attenuated passive avoidance behavior. Facilitation of passive avoidance behavior was observed when the peptide was injected into the dorsal septal nucleus. AVP facilitated passive avoidance behavior when administered into the hippocampal dentate gyrus, dorsal raphe nucleus or dorsal septal nucleus. Injection of either neuropeptides into the central amygdaloid nucleus appeared to be ineffective. One week after the behavioral experiments a repeated injection of AVP into the hippocampal dentate gyrus increased the disappearance of NE in the dentate gyrus and in the nucleus ruber. An injection into the dorsal septal nuclei decreased the NE disappearance in the dorsal septal nucleus itself and increased it in the nucleus ruber. Injection in the dorsal raphe nucleus led to an increase in the disappearance of DA in the locus coeruleus and in the nucleus ruber. It is concluded that memory consolidation can be oppositely influenced by local application of minute amounts of either OXT or AVP into certain limbic-midbrain structures, suggesting an involvement of these brain regions in the memory effects of these peptides. Modulation of catecholamine turnover in specific brain areas after AVP administration may be related to this behavioral effect.

Animals↗
PubMed1979

Facilitation of memory consolidation by vasopressin: mediation by terminals of the dorsal noradrenergic bundle?

Administration of arginine-vasopressin (AVP, 5 micrograms, s.c.) immediately after the learning trial results in a long-term facilitation of a one-trial learning passive avoidance response. This effect of AVP is absent in animals with prior destruction of the ascending dorsal noradrenergic bundle by bilateral microinjection of 6-hydroxydopamine (6-OHDA). Postlearning local microinjection of a minute amount of AVP via chronically implanted cannulae into the locus coeruleus did not influence passive avoidance behavior. Upon injection into the midbrain dorsal raphe nucleus, however AVP facilitated passive avoidance behavior. This effect, however, was absent in rats receiving previous microinjection of 5,6-dihydroxytryptamine (5,6-DHT) or of 6-OHDA into the dorsal raphe nucleus. Bilateral 6-OHDA-induced lesions of the nucleus accumbens or 5,6-DHT-induced destruction of the dorsal raphe nucleus did not prevent the effect of AVP administered subcutaneously. The data suggest that vasopressin facilitates memory consolidation processes by modulating noradrenergic neurotransmission in terminals of the dorsal noradrenergic bundle. The serotoninergic neuronal network originating from the dorsal raphe nucleus has a secondary--norepinephrine-mediated--influence upon these processes.

5,6-Dihydroxytryptamine↗
PubMed1979

Hippocampal function and putative corticosterone receptors. Effect of septal lesions.

In order to investigate the relation between septohippocampal function and hippocampal corticosterone (B) receptors, discrete septal areas were destroyed by electrolytic lesions; the effects of the lesions on cytosol receptor binding of B in the hippocampus were determined 10 or 30 days after lesioning in male rats adrenalectomized 12 h prior to sacrifice. The septal lesions were also characterized functionally by endocrine, neurophysiological and behavioral parameters in the same group of animals. Hippocampal B receptor activity was increased 30 days after lesioning the lateral septal area. The same lesions impaired the acquisition of a conditioned avoidance response. The increase was not due to a behavioral deficiency per se as lesions in the parafascicular nucleus did impair acquisition behavior without affecting B receptors. There was no change in B receptor activity 30 days after destruction of the medial septal nucleus, although such a lesion completely abolished the hippocampal theta activity measured at 10 days. In another group of animals hippocampal B receptors were not affected at 10 days after any of the lesions, while a transient increase in basal plasma levels of B was noted at that time. It appears that the hippocampal receptor activity for B depends on the integrity of the efferents from the hippocampus and/or the dorsolateral septal B receptor system rather than on the septal afferents to the hippocampus.

Adrenalectomy↗
PubMed1979

Effects of ACTH-like neuropeptides on animal behavior and man.

In this review the behavioral effects of neuropeptides related to ACTH have been considered and evidence concerning their mechanism of action in animal and man are briefly presented. Psychoactive properties of these neuropeptides manifest themselves in enhancing motivation, attention, learning and memory processes. The application of these peptides in the mentally ill awaits further exploration.

Adrenocorticotropic Hormone↗
PubMed1978

Behavioral and electrophysiological effects of peptides related to lipotropin (beta-LPH).

Both C-terminal fragments of lipotropin (beta-LPH) (endorphins) and N-terminal fragments (e.g., ACTH 4-10) delayed extinction of pole-jumping avoidance behavior in rats. After subcutaneous injection Met5-enkephalin appeared to be as active as ACTH 4-10 whereas beta-LPH 61-69, alpha- and beta-endorphin were more potent in delaying extinction of pole-jumping avoidance behavior (approximate ED50 of alpha-endorphin 4 x 10(-11) M rat.) However, the potency of beta-LPH 61-69 and alpha-endorphin appeared to be approximately the same whereas that of beta-endorphin was less than that of ACTH 4-10 after intraventricular administration (approximate ED50 of alpha-endorphin 0.2 x 10(-11) M rat). alpha-Endorphin and ACTH 4-10, administered subcutaneously in a dose which markedly delayed extinction of pole-jumping avoidance behavior, had only slight effects on open field behavior and on responsiveness to electric footshock. A 5 times higher dose of both peptides facilitated passive avoidance behavior. Morphine in two doses significantly delayed extinction of pole-jumping avoidance behavior but the effect was not dose dependent. The specific opiate antagonist naltrexone, however, markedly facilitated extinction of the avoidance response. ACTH 4-10, alpha- and beta-endorphin and a behaviorally potent ACTH 4-9 analog (Org 2766) restored pole-jumping avoidance behavior of rats pretreated with naltrexone. Treatment with a similar dose of naltrexone blocked beta-endorphin-induced analgesia. These results suggest that the influence of peptides related to C-terminal and N-terminal fragments of lipotropin on extinction of avoidance behavior may be dissociated from those exerted on opiate receptor sites. Subcutaneously injected beta-LPH 61-69 or intraventricularly administered beta-endorphin induced a shift from lower to higher frequencies of hippocampal theta rhythm during paradoxical sleep in the same way as that found after ACTH 4-10. This effect is interpreted as indicating an increased arousal state in certain midbrain limbic structures. This may, as has been postulated for ACTH 4-10, alter the motivational value of environmental stimuli (e.g., aversive stimulation).

Adrenocorticotropic Hormone↗