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Biomedical subjects

B Bohus

Publications and source records attributed to B Bohus.

At least 73 records · Page 4Linked to original sources
PubMed1993

Cardiac, neuroendocrine, and behavioral effects of central amygdaloid vasopressinergic and oxytocinergic mechanisms under stress-free conditions in rats.

The central nucleus of the amygdala (CEA) is considered to play a major role in the expression of behavioral, autonomic, and neuroendocrine components of the stress response. The present study was designed to examine possible modulating effects of the neuropeptides arginine-8-vasopressin (AVP) and oxytocin (OXT) on functioning of the CEA in male Wistar rats. Heart rate, neuroendocrine parameters, and behavioral activity were repeatedly measured before, during, and after local administration of several doses of AVP and OXT under stress-free resting conditions. In comparison with control artificial-CSF infusion, AVP infusion in the lowest dose (20 pg) caused in a part of the animals a long-lasting decrease in heart rate, i.e., bradycardia, without affecting behavioral activity. In contrast, local infusion with high doses of AVP and OXT (2 ng) induced a transient cardioacceleration concomitant with an increase in behavioral activity. Moreover, these latter effects of AVP could effectively be blocked by pretreatment with a selective OXT receptor antagonist. These findings suggest that higher doses of AVP are effective via agonistic action on OXT receptors in the CEA. A strong correlation existed between the magnitudes of the tachycardiac response and behavioral activation. Thus, heart rate increase by OXT receptor stimulation is possibly due to somatic-autonomic coupling rather than genuine autonomic activation. Additionally, plasma corticosterone, but not epinephrine and norepinephrine, concentrations were elevated in response to AVP and OXT infusions. In conclusion, these results suggest that vasopressinergic influences on CEA function involve two receptor mechanisms possibly related to differential output systems.

Amygdala↗
PubMed1993

Social conflict situations in rats differentially affect the development of amygdala kindling.

Clinical studies revealed an association between the occurrence of convulsions and stress. However, the direction of such relations and their mechanisms are not quite clear. The present study investigated the influence of stress-inducing agonistic conflict situations on the progressive process of kindling epileptogenesis induced by daily tetanic stimulation of the amygdala. Whereas repeated exposure to defeat in an agonistic setting did not affect the development of amygdala kindling, repeated victory experiences resulted in a significant retardation of the kindling process. Moreover, the kindling process was retarded to a greater extent in rats that quickly displayed offensive behavior and won the confrontation. Possible underlying mechanisms and biological substrates are discussed in terms of the ability of the individual to control or cope with the nature of the stressor.

Amygdala↗
PubMed1993

Posttraining norepinephrine infusion into the central amygdala differentially enhances later retention in Roman high-avoidance and low-avoidance rats.

Memory-enhancement effects of norepinephrine (NE) were investigated by infusing NE into the central amygdala (CEA) of Roman high-avoidance (RHA) and low-avoidance (RLA) rats after training on active and passive behaviors in the defensive-burying paradigm. During acquisition, both lines spent comparable time in burying behavior. RLA rats, but not RHA rats, also displayed substantial immobility. During retention, the cerebrospinal-fluid-treated RLA rats mostly displayed immobility to the nonelectrified probe, whereas the RHA rats showed neither burying nor immobility. In the RLA rats, high-dose (200 ng), but not low-dose (20 ng), NE infusion enhanced the duration of the passive response (immobility) without affecting the active response. NE given into the CEA of RHA rats caused a selective dose-dependent appearance of the active behavioral component. The results suggest a phenotype-dependent effect of intra-amygdaloid NE on memory processes in the rat.

Amygdala↗
PubMed1993

Immunological responses to social stress: dependence on social environment and coping abilities.

Social interactions as a consequence of the social position represent stressful conditions for the individual. Manipulation of social conditions or forming long-term social hierarchies by colony aggregation allow to investigate the regulation of immune defense mechanisms under seminatural circumstances. The present paper describes the effects of dyadic social interaction in male rats with or without direct aggressive interactions on some indices of humoral and cellular immunity. In addition, for comparative and reference purposes, in one experiment the conventional stressor of inescapable footshock was used as well. Primary humoral immune response to sheep red blood cell antigen is suppressed by repeated experience of both defeat and inescapable footshock. At individual level the social stressor is as effective as the conventional stressor of inescapable footshock, less individual rats show suppression following the social than after the conventional stress. The social stressors, i.e. being exposed to a resident or intruder of the territory, facilitate lymphocyte proliferation in the spleen by the mitogen ConA and PHA independently of the presence or absence of direct aggressive interaction. Finally, the different social stressors have some impact on the lymphocyte subpopulation in the spleen. Social stimulation without aggressive interactions increases the relative number of T-helper cells, whereas defeat leads to an increase in the T-suppressor/cytotoxic subpopulation. The data suggest multiple and differential effects of social stress on immune system functioning in the rat. Individual characteristics of the coping with stress, the social environment, and the immune indices under investigation determine the magnitude and direction of the changes in immune functioning.

Adaptation, Psychological↗
PubMed1993

Reversed alterations of hippocampal parvalbumin and protein kinase C-gamma immunoreactivity after stroke in spontaneously hypertensive stroke-prone rats.

BACKGROUND AND PURPOSE: Aging spontaneously hypertensive stroke-prone rats (SHR-SP) were previously shown to develop neocortical strokes. Because the hippocampal CA1 is selectively vulnerable to abnormal brain perfusion, the neuropathological effects of spontaneous strokes were investigated on specific neurochemical alterations in two major cell types of the hippocampal CA1 in SHR-SP. METHODS: The immunoreactivity for the gamma-isoform of protein kinase C (in pyramidal cells) and parvalbumin (in interneurons) was determined in the hippocampal CA1 by applying monoclonal antibodies. Because chronic treatment with the calcium antagonist nimodipine prevents the development of strokes in SHR-SP, we compared SHR-SP (stroke) with age-matched nimodipine-treated rats (nonstroke). RESULTS: After stroke in control animals, we observed a strikingly enhanced immunoreactivity for protein kinase C-gamma in CA1 pyramidal cells compared with nimodipine-treated rats, which can be interpreted as the result of an increased activation of these cells. The pathological increase of protein kinase C-gamma immunoreactivity was accompanied by a reduced parvalbuminergic innervation of these pyramidal cells in symptomatic SHR-SP. CONCLUSIONS: Because parvalbumin is present in a subset of GABAergic inhibitory interneurons, these data suggest that increased activity of CA1 pyramidal cells after spontaneous stroke may partially be related to a decreased inhibitory input on these cells.

Aging↗
PubMed1992

Vasopressinergic modulation of stress responses in the central amygdala of the Roman high-avoidance and low-avoidance rat.

The central nucleus of the amygdala (CEA) is selectively involved in the passive component of the behavioral (immobility) and the accompanying parasympathetic response during conditioned, stressful environmental challenges. Vasopressinergic mechanisms in the brain seem to play a role in these stress responses. The effects of the neuropeptides arginine-8-vasopressin (AVP) and oxytocin (OXT) on modulating CEA activity during conditioned stress of inescapable footshock were studied in male Roman high-avoidance (RHA/Verh) and low-avoidance (RLA/Verh) rats, psychogenetically selected on the basis of shuttle-box acquisition behavior. In RLA/Verh rats, the cardiac and behavioral responses to the conditioned emotional stressor were bradycardia and immobility, suggesting an important role for the CEA in these rats. The RHA/Verh rats, however, failed to show any change in heart rate or immobility in response to a conditioned stress situation. The low dose of AVP (20 pg) in the CEA of conscious RLA/Verh rats caused an enhancement of the stress-induced bradycardiac and immobility response. However, the high dose of AVP (2 ng) and OXT (200 pg) attenuated the bradycardiac and immobility responses in the RLA/Verh rats. Infusion of AVP and OXT in the RHA/Verh rats failed to induce any change in heart rate or immobility. Binding studies revealed that the AVP receptor selectively binds AVP with high affinity. In contrast, the OXT receptor recognizes both AVP and OXT with a similar (but lower) affinity. This suggests that the behavioral and autonomic responses of the high dose of AVP may be caused by OXT receptor stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1992

Effect of different agonistic experiences on behavioural seizures in fully amygdala kindled rats.

Fully amygdala kindled rats were exposed to two different inter-male agonistic experiences in order to study the interaction between epilepsy and acute social stress. Victory experience did not influence the severity of seizure behaviour, whereas a single acute defeat modified both ictal and postictal seizure manifestations. Defeat resulted in less severe and shorter lasting motor seizures, and the accompanied postictal inhibition or behavioural depression was of shorter duration in comparison with pre-stress values. The ability of acute defeat to trigger anticonvulsant activity as implied by the weakened convulsive response is discussed.

Agonistic Behavior↗
PubMed1992

Amygdala kindling-induced seizures selectively impair spatial memory. 1. Behavioral characteristics and effects on hippocampal neuronal protein kinase C isoforms.

Protein kinase C (PKC) comprises a family of kinases consisting of nine subspecies that are differentially distributed in the central nervous system. This implies distinct functions. Its involvement is suggested in cellular and molecular mechanisms by which the hippocampus exerts influence on information processing. In this study, it was questioned whether abnormal activity in the neuronal substrate, particularly the hippocampal formation, induced by amygdala kindling indeed impairs spatial memory performance and correlated alpha, beta I/II, and gamma PKC subspecies expression. Rats were trained in a spatial discrimination task (SDT) and simultaneously kindled in the amygdala to induce abnormal, epileptiform activity. Control rats were only trained in the holeboard, a "free choice" maze, in which working (WM) and reference memory (RM) were simultaneously examined. Halfway through and at the end of the experiments the influence of kindling and SDT training on the immunoreactivity for PKC subspecies alpha, beta I/II, and gamma was evaluated in the hippocampal formation. Kindling resulted in a gradual increase in afterdischarge duration and motor seizure (MS) severity. Repeated SDT training ultimately resulted in an asymptotic level of WM and RM performance. As soon as generalized MSs developed, kindled rats failed to improve RM, whereas WM was not influenced. Compared to untrained rats, in trained controls PKC gamma but not PKC alpha beta I/II immunoreactivity was elevated in CA1 pyramidal and dentate gyrus granular cells. Generalized but not partial MSs abolished these alterations in PKC gamma immunoreactivity. The present data indicate that repeated training in a SDT affects the expression of PKC subspecies gamma but not of alpha or beta in the rat hippocampus. Generalized epileptiform activity impair both acquisition of new spatial RM information and PKC gamma expression. It is argued that PKC gamma plays a role in cellular mechanisms through which pathological brain activity impairs certain aspects of spatial memory.

Amygdala↗
PubMed1992

Amygdala kindling-induced seizures selectively impair spatial memory. 2. Effects on hippocampal neuronal and glial muscarinic acetylcholine receptor.

The muscarinic acetylcholine receptor is linked via hydrolysis of phosphoinositides to the protein kinase C pathway. In a preceding paper (Beldhuis, H. J. A., H. G. J. Everts, E. A. Vander Zee, P. G. M. Luiten, and B. Bohus (1992) Amygdala kindling-induced seizures selectively impair spatial memory. 1. Behavioral characteristics and effects on hippocampal neuronal protein kinase C isoforms. Hippocampus 2:397-410), the role of different isoforms of protein kinase C in neurobiological processes associated with plasticity was studied using both a spatial learning paradigm and amygdala kindling in the rat. This study extended the findings on protein kinase C activity to the level of the muscarinic acetylcholine receptor. Rats were trained in a spatial learning paradigm and kindled simultaneously in the amygdala to develop generalized motor convulsions. Control rats were trained only in the spatial learning paradigm to acquire stable working and reference memory performance. Alteration in the expression of the muscarinic acetylcholine receptor was investigated using a monoclonal antibody to muscarinic acetylcholine receptor proteins. Trained control rats that were exposed repeatedly to the spatial learning paradigm showed an increase in immunoreactivity for the muscarinic acetylcholine receptor located in the same hippocampal regions in which the protein kinase C activity was increased. In fully kindled rats, however, this increase located in principal neurons was absent, whereas expression of muscarinic acetylcholine receptor proteins was increased in hippocampal astrocytes. Moreover, fully kindled rats showed an impairment in reference memory performance as compared to trained control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1992

Behavioral and cardiac responses after intracerebroventricular corticotropin-releasing hormone (CRH) administration: role of adrenal cortical hormones.

Intracerebroventricularly (icv) administered corticotropin-releasing hormone (CRH) produces a dose-dependent increase in heart rate in association with behavioral activation. The present study was designed to investigate whether these CRH-induced responses are dependent on adrenal function. The effects of adrenalectomy (ADX) and subsequent corticosterone replacement were studied. Administration icv of 300 ng of CRH failed to produce behavioral activation and tachycardia in ADX rats. Corticosterone replacement restored the CRH-induced behavioral response to preoperative levels, whereas the CRH-induced tachycardia was partially restored. This latter result may be related to the fact that the baseline heart rate of ADX animals appeared to be significantly higher than that of corticosterone-treated ADX animals. It is concluded that circulating adrenal corticosterone in ADX rats is involved in the expression of the behavioral and cardiac effect of central CRH.

Adrenal Cortex Hormones↗
PubMed1992

Conditioned neuroendocrine and cardiovascular stress responsiveness accompanying behavioral passivity and activity in aged and in young rats.

Mean arterial pressure (MAP), heart rate (HR), plasma epinephrine (E), plasma norepinephrine (NE), and plasma corticosterone (CORT) were measured in 3-month- and 24-month-old male Wistar rats exposed to a conditioned emotional stress response (CER) paradigm and a conditioned defensive burying (CDB) paradigm. In the CER situation blood samples were taken during reexposure to the training environment one day after a single inescapable footshock (0.6 mA, AC for 3 s) had been administered. In the CER paradigm the young rats displayed passive behavior (immobility) accompanied by an increase in plasma levels of CORT and E, whereas both the control and conditioned animals showed increased NE responses. Previously shocked aged rats exhibited an attenuated plasma NE response, whereas levels of E remained elevated to a greater extent. Aged animals showed elevated basal levels of CORT one day after footshock administration. Stress-induced immobility was preserved in the aged rats. These animals had an increase in basal MAP values and a decrease in basal HR values compared to young ones. In the CDB paradigm, rats were exposed to a nonelectrified probe 1 day after the repeated shock (2 mA/contact) procedure. Young rats displayed defensive burying accompanied by increments in MAP, HR, CORT, and NE. The aged animals showed similar hormonal, autonomic, and behavioral stress responses. Thus, the age-related alterations in neuroendocrine and autonomic response patterns are apparent in stressed animals during behavioral passivity in absence of control (CER) rather than during active control (defensive burying).

Adaptation, Psychological↗
PubMed1992

Behavioral and cardiac responses to mild stress in young and aged rats: effects of amphetamine and vasopressin.

Young (3-month-old) male Wistar rats showed a relative decrease in heart rate to a sudden silence superimposed on low intensity background noise. This bradycardia was accompanied by immobility behavior. In 26-month-old rats the magnitude of the heart rate response was reduced while immobility behavior remained in the same order of magnitude as in young controls. In the aged rats a shift in autonomic regulation of heart rate in the direction of increased sympathetic influence was indicated by the results obtained by blocking the autonomic input with atropine methyl-nitrate (0.5 mg/kg) or atenolol (1 mg/kg) given subcutaneously (SC) 30 min prior to testing. Pretest (30 min) administration of amphetamine (0.5 mg/kg SC) reinstated the bradycardiac response in aged rats to a level seen in young ones. Arginine-vasopressin (AVP, 10 micrograms/kg SC), administered 60 min before the experiment, markedly facilitated the cardiac response in young animals but failed to restore cardiac responses in aged ones. The immobility behavior in the peptide-treated aged rats was also absent. The present findings suggest that a diminished central aminergic drive in aged rats is causing a reduction of the parasympathetic cardiac response to stress of sudden silence. The results also indicate an age-related vasopressinergic modulation of behavioral and cardiac responses to mild stress.

Aging↗
PubMed1992

Differential effects of neonatal testosterone treatment on aggression in two selection lines of mice.

Selection lines of mice, artificially selected for aggression based upon the attack latency score (ALS), were used. In order to determine the relative contribution of neonatal testosterone (T) in the development of aggression, we vary the plasma-T level in males of both selection lines on the day of birth. At 14 weeks the ALS was measured. Neonatal T treatment results in a reduction of aggression in the long attack latency (LAL) line, whereas aggressive behaviour of the short attack latency (SAL) line is not affected. Both selection lines show reduction in testicular weight, although the total amount of T-producing Leydig cells was not affected. Neonatal T may cause a permanent reduction in aggressive behaviour in in the LAL line only, probably due to differential appearance of critical periods. It is suggested that the difference in aggressive behaviour between SAL and LAL selection lines is due to a prenatally determined difference in neonatal T sensitivity of the brain.

Aggression↗
PubMed1992

Neuroendocrine and behavioral responses during conditioned active and passive behavior in the defensive burying/probe avoidance paradigm: effects of ipsapirone.

Plasma epinephrine (E), norepinephrine (NE), and corticosterone (CORT) concentrations were determined in the rat before, during, and after a 15-min exposure to a nonelectrified probe on day after receiving electric shock (1.5 mA) through a probe mounted on the wall of the home cage. Rats displayed burying (active coping) if sawdust was provided on the floor and immobility (passive coping) if bedding was absent both during training and testing. The conditioned burying was accompanied by high plasma NE but low E and CORT concentrations, whereas immobility was associated with high CORT and low NE levels. A forced switch from the active to passive coping (training with and testing without sawdust) led to the highest rise in E concentration. The 5-HT1A agonist ipsapirone, with anxiolytic properties, dose-dependently (0.5 and 2.5 mg/kg, IV) reduced defensive burying behavior and increased the amount of time spent on feeding behavior in the presence of bedding material. Both plasma E and CORT levels were further elevated by the higher dose of ipsapirone. In the absence of bedding material, ipsapirone failed to affect immobility behavior, but it dose-dependently elevated the stress-induced increase in E, NE, and CORT concentrations. Accordingly, the behavioral anxiolytic action of the 5-HT1A agonist ipsapirone was restricted to active coping, whereas neuroendocrine activation by the drug was present in all conditions. It is suggested that the effects of ipsapirone on behavioral coping and neuroendocrine regulation are produced by different populations of 5-HT1A receptors in the brain.

Animals↗
PubMed1992

Adrenal hormones in rats before and after stress-experience: effects of ipsapirone.

The present study was designed to investigate the effects of the anxiolytic 5-HT1A receptor agonist ipsapirone on the hormonal responses in rats under nonstress and stress conditions by means of repeated blood sampling through an intracardiac catheter. Ipsapirone was given in doses of 2.5, 5, 10, and 20 mg/kg (IP) under nonstress conditions in the home cages of the rats. Plasma corticosterone levels increased in a dose-dependent way in the dose range of 5 to 20 mg/kg, whereas the plasma catecholamines were only significantly increased with the highest dose of the drug. The effect of ipsapirone in control and in stressed rats was studied with the selected dose of 5 mg/kg. Conditioned fear of inescapable electric footshock (0.6 mA, AC for 3 s) given one day earlier was used as stressor. Surprisingly, ipsapirone potentiated the magnitude of the neuroendocrine responses. Rats receiving an inescapable footshock 1 day earlier showed a further elevated corticosterone response to the 5-HT1A receptor agonist ipsapirone even before exposing them to the conditioned stress situation. The present findings suggest that if an animal has no possibilities to escape or avoid a noxious event, functional hypersensitivity will develop in the serotonergic neuronal system, which is reflected in the increased responsiveness of the HPA axis to a 5-HT1A agonist challenge.

Adrenal Cortex Hormones↗
PubMed1992

Vasopressin prolongs behavioral and cardiac responses to mild stress in young but not in aged rats.

In young male Wistar rats sudden silence superimposed on low intensity background noise evokes a relative decrease in heart rate. This bradycardia is accompanied by immobility behavior. In the present study, involving young (3 month), late-adult (14 month), aged (20 month), and senescent (25 month) rats the magnitude of the stress-induced bradycardia shows an age-related reduction while the behavioral immobility response remained unchanged during the process of aging. Arginine-8-vasopressin (AVP, 6 micrograms/kg SC) administered 60 min prior to the experiment led to a prolonged behavioral and cardiac stress response in young and late-adult rats, but not in aged and senescent animals. The peripheral and central mechanisms possibly involved in the failure of systemically applied AVP to improve bradycardiac stress responses in aged rats are discussed.

Aging↗
PubMed1992

Mesencephalic cuneiform nucleus and its ascending and descending projections serve stress-related cardiovascular responses in the rat.

The aim of the present study was to explore the neuroanatomic network that underlies the cardiovascular responses of reticular formation origin in the region of the cuneiform nucleus (CNF). The study was performed in urethane anesthetized male Wistar rats. The left iliac artery was supplied with a catheter for the measurement of systemic blood pressure. Low intensity electrical stimulation of the mesencephalic reticular formation (MRF) in the vicinity of the CNF always resulted in pressor and bradycardiac responses, whereas stimulation in the parabrachial nucleus (PB) and Kölliker-Fuse nucleus (KF) led to a pressor response and a small tachycardiac response. The cuneiform area may be placed in the center of a circuit that serves a specific autonomic response pattern to stress: parallel activation of the sympathetic (pressor response) and parasympathetic limb (bradycardia). The efferent connections of the effective stimulation sites in the MRF and the CNF area, were investigated by anterograde tracing with the lectin Phaseolus vulgaris leucoagglutine (PHA-L). The CNF sends descending fibers to the gigantocellular reticular nuclei (GI), the motor nucleus of the vagus (DMNV) and nucleus tractus solitarius (NTS). These projections are probably involved in the bradycardiac response to stimulation. The descending pathway to the NTS/DMNV and GI may therefore be the parasympathetic limb of the circuit. Furthermore, the CNF sends ascending fibers to limbic forebrain areas and descending fibers to the PB-KF complex. The KF in its turn projects to the rostroventrolateral medullary nucleus (RVLM) and the intermediolateral cell column (IML). These latter projections are partly involved in producing the pressor response and thereby represent the sympathetic limb of the circuit. Accordingly, the transection of the descending fibers from the CNF to the PB-KF complex resulted in a decreased pressor and an increased bradycardiac response. This suggests that a baroreceptor reflex-induced bradycardia which results from blood pressure increase can be excluded as the origin of the stimulation-induced bradycardia, and that the pressor and bradycardiac responses are two independent moieties. It cannot be excluded that ascending fibers from the CNF are also involved in producing the pressor response. On the basis of the present physiological and neuroanatomical study, a brain circuit has been proposed in which the cuneiform nucleus has a central position. The described brain circuit may serve a passive coping strategy to novel, painful or threatening stimuli during which the animals show orientation/attention or freezing behavior accompanied by a bradycardiac and pressor response.

Adaptation, Psychological↗