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Biomedical subjects

B Bohus

Publications and source records attributed to B Bohus.

At least 127 records · Page 7Linked to original sources
PubMed1983

Reduction of a centrally induced pressor response by neurohypophyseal peptides: the involvement of lower brainstem mechanisms.

Pressor and bradycardiac responses induced by electrical stimulation of the mesencephalic reticular formation in urethane-anesthetized rats were used as model of neurogenic hypertension. Oxytocin (OXT) and prolyl-leucyl-glycinamide (OXT-(7-9] administered into the fourth cerebral ventricle markedly attenuated the magnitude of the pressor response. OXT-(7-9) was somewhat more potent than OXT and its effect was dose-dependent. Microinjection of OXT-(7-9) into the dorsal raphe nucleus reduced the pressor response as well. [Arg8]vasopressin (AVP) did not affect the pressor response when administered via this route, while prolyl-arginyl-glycinamide (AVP-(7-9] had an action that was similar to that of OXT-(7-9). None of these peptides affected the magnitude of the bradycardiac response. It is suggested that OXT and related fragments modulate neurogenic hypertensive responses through lower brainstem mechanisms.

Animals↗
PubMed1983

Naltrexone-sensitive behavioral actions of the ACTH 4-9 analog (Org 2766).

The effects of the ACTH 4-9 analog (Org 2766) and the COOH-terminal tripeptide of Org 2766 (Phe-D-Lys-Phe; PDLP) on retrieval of one-trial learning passive avoidance behavior were compared with those of beta-endorphin, [Met5]-enkephalin, [D-Ala2,Met5]-enkephalin, des-Tyr1-[Met5]-enkephalin and des-enkephalin-gamma-endorphin (DE gamma E). Amounts of intracerebroventricularly administered Org 2766, PDLP, [Met5]-enkephalin, [D-Ala2,Met5]-enkephalin and DE gamma E, which induced a comparable attenuation of passive avoidance behavior were determined. Pretreatment with the opiate antagonist naltrexone prevented the attenuating effect of these peptides on passive avoidance behavior except that of DE gamma E. The attenuating effect of Org 2766 and of [Met5]-enkephalin was reversed to facilitation of passive avoidance behavior in the presence of naltrexone. Subcutaneous treatment with Org 2766 and [D-Phe7]-ACTH 4-10 decreased electrical self-stimulation behavior elicited from the medial septal area. Naltrexone prevented the inhibitory effect of Org 2766 on this behavior, but not that of [D-Phe7]-ACTH 4-10. Although the attenuating effect of PDLP on passive avoidance behavior was not reduced by pretreatment with [Met5]-enkephalin- or beta-endorphin-antiserum, and PDLP induced neither analgesia nor excessive grooming, the data suggest that the inhibitory effect of Org 2766 and PDLP on passive avoidance behavior and electrical self-stimulation are mediated by endorphin systems in the brain.

Adrenocorticotropic Hormone↗
PubMed1983

Prolactin-enhanced grooming behavior: interaction with ACTH.

The interaction between prolactin (PRL) and ACTH in enhancing grooming behavior after intracerebroventricular (i.c.v.) administration was investigated in intact and endogenously hyperprolactinaemic rats. In intact rats, 4 h after the i.c.v. injection of rat PRL or ACTH, a subsequent administration of ACTH or rat PRL did induce similar excessive grooming as observed after the first injections. In hyperprolactinaemic rats, which displayed excessive grooming 12 days after homografting adenopituitaries under the kidney capsule, i.c.v. injection of rat PRL failed to enhance further the grooming activity while this behavior was substantially enhanced by i.c.v. injection of ACTH1-24. Twenty-six days after surgery, when the grooming activity of hyperprolactinaemic rats was at the same level as control animals, the i.c.v. injection of rat PRL was effective in inducing excessive grooming in control but not in hyperprolactinaemic animals. In contrast, at this time the i.c.v. injection of ACTH1-24 induced again excessive grooming in both hyperprolactinaemic and control rats. Accordingly, there was no cross-tolerance between PRL and ACTH in inducing excessive grooming, but hyperprolactinaemic rats became hyposensitive to exogenous PRL. It is suggested that although PRL and ACTH may affect common neurotransmitter systems in the brain, the two hormones probably act on independent neural mechanisms in inducing excessive grooming in the rat.

Adrenocorticotropic Hormone↗
PubMed1983

Pituitary stalk section transiently impairs the acquisition of shuttle box avoidance behavior.

Three days after stalk section, rats displayed a marked deficit in acquiring a shuttle box avoidance response. The performance of stalk sectioned rats was similar to that of 3-day hypophysectomized rats. At eighteen days after stalk section acquisition of the avoidance response was, however, not different from that of sham-operated controls. Stalk sectioned rats that showed poor performance at three days and that were tested again at eighteen days displayed similar avoidance behavior at eighteen days as their sham-operated controls. The results suggest that pituitary stalk section impairs performance of an active avoidance response. The transient nature of this effect may be due to disruption and subsequent regeneration of vascular contact between pituitary and brain.

Animals↗
PubMed1983

Sites of behavioral and neurochemical action of ACTH-like peptides and neurohypophyseal hormones.

In order to localize the site of action of neuropeptides in relation to their effects on behavior and memory various approaches have been used. As a result of studies using rats bearing lesions in different areas of the limbic system as well as of studies in which neuropeptides were locally applied into various areas of the brain it appeared that the limbic system (amygdala, hippocampus, septum and some thalamic areas) plays an essential role in the effect of vasopressin and ACTH and their derivatives on behavior and memory. Neurochemical studies generally indicate that changes occur in catecholamine utilization in these various limbic regions upon administration of these neuropeptides. It can be concluded that the effects of vasopressin in the terminal regions of the coeruleo-telencephalic noradrenalin system correlate with its effects on consolidation of memory. It is likely that the effects of vasopressin on other transmitter systems (e.g. dopamine in the amygdala and serotonin in the hippocampus) correspond with the effect of this neuropeptide on retrieval processes. In addition, regional differences in biotransformation of the neurohypophyseal hormones suggest that different patterns of behaviorally active fragments of these peptides may be present locally in the brain.

Adrenocorticotropic Hormone↗
PubMed1983

Effects of beta-endorphin and its fragments on inhibitory avoidance behavior in rats.

The effects on retrieval of a one-trial learning inhibitory avoidance response of beta-endorphin, alpha-endorphin, and gamma-endorphin, given prior to test have been studied in rats. beta-Endorphin (beta-LPH 61-91) in a relatively low dose (1.56 micrograms sc. or 50 ng icv.) facilitated inhibitory avoidance behavior, while a higher dose (10 micrograms sc. or 100 ng icv.) caused bimodal changes (facilitation in 50% of the animals and attenuation in another 40%. Peripheral injection of gamma-endorphin attenuated inhibitory avoidance behaviour in a dose-dependent manner. The C-terminus of beta-endorphin (beta-LPH 78-91) was ineffective. alpha-Endorphin facilitated inhibitory avoidance behavior in a dose dependent manner. Naltrexone pretreatment antagonized the bimodal effect of beta-endorphin: following pretreatment with the opiate antagonist the low latency component disappeared, but the facilitatory effect of the neuropeptide remained the same. It is suggested that beta-endorphin carries more than one bit of behavioral information. Inherent activities either related or unrelated to naltrexone-sensitive opiate as well as biotransformation into alpha- and gamma-endorphin may contribute to the multiple behavioral effects of this neuropeptide.

Animals↗
PubMed1983

The modulation of the dorsal immobility response in the adult male Wistar rat: the opposite effects of ACTH4-10 and [D-Phe7]ACTH4-10.

A series of experiments were conducted to determine the behavioral effect of ACTH4-10 and [D-Phe7]ACTH4-10 on the dorsal immobility response (DIR) in adult male Wistar rats. Both peripheral and central injections of ACTH4-10 attenuated the duration of DIR, whereas, peripherally injected [D-Phe7]ACTH4-10 resulted in the potentiation of this response. The effect of peripherally administered ACTH4-10 was dose dependent in the range of 0.2 to 20 micrograms. These results, in part, extend the prior findings on the modulation of various learned and species-typical behaviors by ACTH-related peptides to a complex state of behavioral inhibition and immobility.

Adrenocorticotropic Hormone↗
PubMed1983

Inhibitory avoidance deficit following short-term adrenalectomy in the rat: the role of adrenal catecholamines.

Impaired retention of an inhibitory avoidance response was observed in rats subjected to adrenalectomy (ADX) up to 120 hr before the single learning trial. Corticosterone substitution failed to normalize this behavioral deficit. Rats ADX 240 hr prior to the learning trial showed a normalized behavior. Adrenomedullectomy (ADXM) 48 or 240 hr before learning caused a similar impairment as in short-term ADX rats. The 240-hr ADX rats subjected to corticosterone substitution showed the same behavioral deficit as short-term ADX rats or ADXM ones. Immediate postlearning subcutaneous injection of adrenaline in a dose range of 0.005-5.0 micrograms/kg or of noradrenaline (0.005-0.5 microgram/kg) to 48-hr ADX rats resulted in a dose-related improvement of later retention behavior. Higher doses of catecholamines were less or ineffective. Postlearning treatment of 48-hr ADXM rats with adrenaline (0.5-500 micrograms/kg) caused a similar pattern of behavioral changes. It is concluded that adrenal catecholamines play an important role in the modulation of consolidation of memory. In addition, the high circulating ACTH levels that follow long-term ADX may correct for the behaviorial deficit induced by the absence of adrenomedullary catecholamines.

Adrenal Glands↗
PubMed1983

Comparative effects of ACTH-related peptides on acquisition of shuttle-box avoidance behavior of hypophysectomized rats.

Hypophysectomy resulted in a marked impaired acquisition of shuttle-box avoidance learning, when lower shock intensity (0.05 mA) was used as the unconditioned stimulus, but not when shock intensity was increased to 0.12 mA. Daily subcutaneous treatment with ACTH4-10 (6 micrograms/day), ACTH4-7 (6 micrograms/day), [Met(O2)4]ACTH4-7 (2 micrograms/day), ACTH4-9 analog (Org 2766) (60 ng/day), and an ACTH4-16 analog (HP 953 A) (60 ng/day) for 7 days normalized avoidance acquisition of hypophysectomized rats during the treatment period. The beneficial effect of the peptides was of a short-term nature, since it disappeared after discontinuation of the treatment. Microgram amounts of Org 2766 did not influence acquisition of hypophysectomized rats. [D-Phe7]ACTH4-10 (60 micrograms/day) further reduced the already deficient acquisition of avoidance behavior of hypophysectomized rats. This latter effect may be due to an antagonistic effect towards brain-borne ACTH-related peptides. ACTH1-16 -NH2 antiserum administered intracerebroventricularly 30 min prior to a massed-trial shuttle-box acquisition session reduced avoidance acquisition in hypophysectomized rats. This suggests that in addition to ACTH and related peptides from the pituitary, brain-borne ACTH-like peptides are involved in avoidance learning.

Adrenocorticotropic Hormone↗
PubMed1983

The effects of endorphins on cardiac responses during an emotional stress.

Male rats were punished (0.6 mA/2 sec) for entering the shock compartment of a passive avoidance chamber. Twenty four hours later they were returned to the apparatus and confined to the grid floor of the shock compartment for 5 min (forced exposure). The bradycardic response found in control rats during forced exposure was not altered by either alpha-endorphin (beta-LPH 61-76) or (des-tyrl)-alpha-endorphin (beta-LPH 62-76) (1.5 micrograms/rat) injected subcutaneously 60 min prior to forced exposure. In contrast (des-tyrl)-gamma-endorphin (beta-LPH 62-77) (1.5 micrograms/rat/SC) enhanced the bradycardic response of shocked rats during forced exposure without altering heart rate in non-shocked rats. (Des-tyrl)-gamma-endorphin did not affect the rats' bradycardic response to a sudden reduction in background noise. The results conform to a pattern whereby C-terminal beta-LPH fragments may be distinguished in a number of behavioural tests and show that (des-tyrl)-gamma-endorphin treatment facilitates the rat's cardiac response to aversive but not novel experiences.

Animals↗
PubMed1982

Decreased serotonin turnover in the dorsal hippocampus of rat brain shortly after adrenalectomy: selective normalization after corticosterone substitution.

Pargyline-induced accumulation of serotonin (5-HT) was used as an index of 5-HT turnover rate in the dorsal hippocampus. One hour after bilateral removal of the adrenals, 5-HT turnover was significantly reduced when compared to that of the sham-operated controls. A low dose of corticosterone given immediately after adrenalectomy restored the 5-HT response, while the same dose of dexamethasone was ineffective. Pretreatment with dexamethasone blocked the 5-HT response to corticosterone in the acutely adrenalectomized rat. The specificity of the 5-HT response in the hippocampus corresponds to the properties of the glucocorticoid receptor system in rat hippocampal neurons.

Adrenal Glands↗
PubMed1982

Behavioral responses of long-term hyperprolactinaemic rats.

Rats with long-term endogenous hyperprolactinaemia induced by pituitary homografts under the kidney capsule displayed an enhancement of amphetamine- and apomorphine-induced stereotypy, a facilitated acquisition of active avoidance behavior and a decreased responsiveness to electrical footshock. However, no difference between homografted and sham-operated rats was observed with respect to grooming behavior. It is concluded that at least two processes occur during prolonged hyperprolactinaemia, i.e. development of tolerance to prolactin with respect to enhanced grooming activity and of supersensitivity of postsynaptic dopaminergic receptor systems. These two processes may be dependent or independent from each other.

Adrenal Glands↗
PubMed1982

Effect of des-Tyr1-gamma-endorphin and des-Tyr1-alpha-endorphin on alpha-MPT-induced catecholamine disappearance in rat brain nuclei: a dose--response study.

The effect of des-Tyr1-gamma-endorphin (beta-LPH62-77, DT gamma E) and des-Tyr1-alpha-endorphin (beta-LPH62-76, DT alpha E), administered intracerebroventricularly (icv) in doses of 0.01, 0.1, 1 and 10 micrograms, was studied on the alpha-methyl-p-tyrosine-(alpha-MPT) induced disappearance of catecholamines in a number of microdissected rat brain regions, which were selected on the basis of the neuroanatomy of the dopamine systems in the brain and of previous observations. A dose-dependent increase in the disappearance of dopamine in alpha-MPT-pretreated rats was observed following icv administration of DT gamma E in the nucleus interstitialis striae terminalis, the paraventricular nucleus, the anterior hypothalamic nucleus and the zona incerta. In these same brain regions a decrease in the alpha-MPT-induced disappearance of dopamine was found following the administration of DT alpha E, but only after doses of 0.01, 0.1 and 1 microgram. In none of these regions were effects observed after 10 micrograms of DT alpha E. No effects were seen on dopamine utilization in the nucleus accumbens, caudate nucleus and median eminence after any of the doses of DT gamma E or DT alpha E. The alpha-MPT-induced disappearance of noradrenaline was significantly enhanced in the anterior hypothalamic nucleus of rats treated with DT gamma E. It is concluded that DT gamma E and DT alpha E induce opposite changes in the utilization of dopamine selectively in brain regions which are predominantly innervated by neurons belonging to the intradiencephalic dopamine systems.

Animals↗
PubMed1982

Comparative effects of the ACTH 4-9 analogue (ORG 2766), ACTH 4-10 and [D-Phe7] ACTH 4-10 on medial septal self-stimulation behaviour in rats.

Experiments were performed to examine the effects of various analogues of ACTH on electrical self-stimulation behaviour elicited from the medial septal area using an ascending or descending sequence of stimulus intensities within a session. When an ascending sequence of threshold multiples was used ACTH 4-10 and the ACTH 4-9 analogue (ORG 2766) enhanced level pressing for low intensity stimulation but attenuated self-stimulation at greater current intensities. The analogue ORG 2766 appeared to be a thousand times more potent than ACTH 4-10; [D-Phe7] ACTH 4-10 inhibited the response rate at threshold level but was inactive at greater current intensities. The same effect was found following administration of ORG 2766 in a dose which was 20 times greater (1 microgram/rat) than that used in the first experiments. Lever pressing was not affected by treatment with ACTH 4-10 or ORG 2766 when a descending sequence of stimulus intensities was used within a session. Thus, ACTH-related peptides may affect motivational processes involved in self-stimulation rather than the reward of the stimulation per se. It is suggested that although ORG 2766 mimicked the action of ACTH 4-10 this synthetic peptide may have additional behavioural properties.

Adrenocorticotropic Hormone↗
PubMed1982

Inhibition of centrally-evoked pressor responses by neurohypophyseal peptides and their fragments.

Intracerebroventricular administration of fragments of [arginine8]-vasopressin (AVP) such as AVP1-6 and AVP7-9 attenuated the pressor response evoked by electrical stimulation of the mesencephalic reticular formation in urethane-anaesthetized rats. Oxytocin (OXT) and the fragment OXT7-9 were also active, although OXT1-6 did not affect the pressor response. These peptides did not influence the bradycardia accompanying the rise in blood pressure, nor the basal blood pressure. The inhibition of the pressor response was shown for OXT7-9 to be dose-dependent up to 25 ng. These data suggest that oxytocin, vasopressin and some neuropeptide fragments have an inhibitory role in the regulation of blood pressure. Both the covalent pressinoic ring structure and the C-terminal linear portion of vasopressin contain active sites, while the activity of oxytocin appears to be present in the C-terminal tripeptide Pro-Leu-Gly.

Animals↗