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Biomedical subjects

B Siegfried

Publications and source records attributed to B Siegfried.

At least 37 records · Page 2Linked to original sources
PubMed1987

Effects of repeated as compared to single aggressive confrontation on nociception and defense behavior in C57BL/6 and DBA/2 mice.

Behavioral reactions (submissive postures, escape, immobility, activity, locomotion) in C57BL/6 and DBA/2 test mice were recorded during single (50 bites) or three repeated (3 X 50 bites, separated by 24 hr) aggressive confrontations, as well as during a nonaggressive confrontation 24 hr after the last aggressive confrontation with opponents of the opposite strain. Nociception (hot plate response latency) was measured 1 min after aggressive or nonaggressive confrontations. During repeated aggressive confrontation, DBA mice reacted with a stable pattern of escape and analgesia, whereas C57 mice failed to develop an analgesic response and changed their behavioral defense strategy during repeated aggressive confrontations (decrease of escape, increase of defensive upright). The conditioned display of submission and of escape behavior during nonaggressive confrontation did not change as a function of earlier repeated aggressive confrontations in DBA mice, while C57 mice showed a significant increase of defensive upright postures and immobility. Conditioned analgesia was not observed after nonaggressive confrontations. The results point toward a dissociation between attack-elicited behavior and antinociception and suggest that encounter-induced analgesia may influence the processing of aversive experience.

Aggression↗
PubMed1987

Analgesia induced by exposure to a novel environment in rats: effect of concurrent and post-training stressful stimulation.

Exposure of rats for 2 min to a new environment (a 50 X 25 X 25-cm box) induced a mild analgesia measured by the tail-flick method. Additional stressful stimuli (0.5 mA, 1.5-s footshocks, light flashes, or tones) presented during the 2-min exposure did not alter the analgesia. However, the postexposure presentation of light flashes or tones, for either 10 s or 2 min, while the animals were alone in a waiting cage, prevented the analgesic response. Similarly, placing the subjects with their conspecifics in the home cage for 2 min after the exposure prevented the analgesic response. The data suggest that the analgesia may represent a physiological correlate of novelty and that the response can be impaired by post-training treatments.

Animals↗
PubMed1987

Preexposure to a nonaggressive opponent prevents low-intensity, social-conflict analgesia in mice.

In a first experiment, exposure of DBA/2 mice to a small number of attack bites by a C57BL/6 mouse resulted in low-intensity analgesia as assessed by the tail-flick test. The analgesia dissipated within 10 min and was insensitive to naloxone (10 mg/kg, sc) but was antagonized by the irreversible opioid antagonist beta-chlornaltrexamine (5 mg/kg, sc). In a second experiment, preexposure to a nonaggressive C57BL/6 opponent prevented low-intensity analgesia induced by a small number of attack bites 24 hr later. The preexposure effect was abolished by naloxone (10 mg/kg, sc) given before the nonaggressive confrontation. This suggests that the release of endogenous opioids during preexposure interferes with the subsequent activation of endogenous opioid-mediated pain control mechanisms.

Aggression↗
PubMed1987

Exposure to novelty induces naltrexone-reversible analgesia in rats.

The exposure of rats for 2 min to an open field, to a small box, or to inhibitory avoidance training in the small box was followed by a mild analgesia measured by the tail-flick method. The analgesia was observed as soon as 10 s after the exposure and lasted between 10 and 30 min. It was not observed in animals previously made familiar with the test situation, and it was reversed by the administration of naltrexone (0.1 mg/kg). The data suggest that novelty per se is a sufficient stimulus to activate an opioid-mediated analgesic stimulus.

Animals↗
PubMed1987

Long-term analgesic reaction in attacked mice.

Four experiments were designed to characterize long-term analgesic (LTA) reaction in attacked mice. In Experiment 1 we showed that analgesic reaction in DBA mice, induced by the stress of being attacked (30 or 50 bites), is reinstated upon reexposure to seven bites 24 hr later. The magnitude of the LTA response depended on the level of analgesia on Day 1 and was smaller than the original response. In Experiment 2 we showed that LTA was prevented by naloxone or beta-chlornaltrexamine given before exposure (50 bites) on Day 1. Results of Experiment 3 revealed that naloxone or beta-chlornaltrexamine injected before reexposure to seven bites on Day 2 antagonized LTA measured 10 min, but not 1 min, after reexposure. In Experiment 4 we showed that morphine substituted for being attacked on Day 1 failed to produce LTA. We concluded that pain inhibitory mechanisms remain in a state of increased readiness for at least 24 hr after attack stress and that activation of opioid systems is necessary but not sufficient to produce LTA, a response that is only partly sensitive to opioid antagonists.

Aggression↗
PubMed1985

Hashish extract impairs retention of defeat-induced submissive behavior in mice.

The effects of hashish extract on adaptive behavior of male mice were studied in a paradigm which allows the investigation of learning mechanisms in a social context. Mice of the C3H strain, which were not submissive in a confrontation with a nonaggressive DBA mouse on day 1, were defeated on day 2 over 3 min by aggressive, isolated DBA mice, and showed conditioned submissive behavior upon mere contact with a nonaggressive DBA mouse on day 3. A hashish extract containing 38.6-39.4% delta 9-tetrahydrocannabinol (delta 9-THC), 11.6-12.0% cannabinol and 47.7-48.5% cannabidiol was administered orally in all experiments. Hashish extract given 90 min before defeat on day 2, in dosages corresponding to 1, 5, and 10 mg delta 9-THC/kg, impaired retention of defensive upright, defensive sideways and immobility on day 3 (experiment 1). Experiment 2 showed that the drug (5, and 10 mg delta 9-THC/kg) had no antinociceptive potency in mice and did not modify defeat-induced analgesia. Experiment 3, with drug (5 mg delta 9-THC/kg) or solvent administration on day 2 and day 3, showed that the retention deficit was neither due to state-dependent learning, nor to impaired retrieval. It is suggested that hashish extract administered before learning may interfere with memory processing.

Aggression↗
PubMed1985

Postaggression footshock inhibits aggressive behavior in dominant but not in isolated mice.

Aggressive behavior of dominant and isolated mice was assessed in intermale encounters with nonaggressive intruder mice. After an attack period of 90 s, the aggressor was exposed to a footshock punishment and retested the next day. The shock treatment, independent of the intensity and duration, failed to inhibit spontaneous aggression in isolated DBA/2 mice, while it significantly suppressed spontaneous aggression in dominant C57BL/6 mice. The different effects of post-trial shock punishment were not due to a different shock sensitivity and did not depend on the type of opponent used. Strain differences have been ruled out by the use of dominant and isolated ICR mice. Again, shock punishment was ineffective in isolates, while it reduced aggression in dominant animals. The findings were discussed with reference to the impaired learning performance reported for isolated animals, and suggest a difference between the aggression of isolated and that of dominant mice.

Aggression↗
PubMed1984

Vasopressin impairs or enhances retention of learned submissive behavior in mice depending on the time of application.

The effects of vasopressin on learning and memory were investigated in a paradigm using adaptive capabilities of interacting male mice. Test animals of the DBA/2 strain which were not submissive in a confrontation with a non-aggressive subordinate C57BL/6 mouse on day 1 (baseline), were defeated on day 2 (learning) by an aggressive dominant C57 mouse, and showed learned submissive behavior upon mere contact with a non-aggressive C57 mouse on day 3 (retest). Pretrial injections of lysine-vasopressin (0.01, 0.1 or 1.0 I.U., s.c.) 20 min before defeat on day 2 resulted in less submissive behavior on day 3 compared to controls, with 0.1 I.U. (equal to 370 ng) being the most effective dose. Post-trial injections of vasopressin (0.1 I.U.) immediately after defeat on day 2 significantly improved retention on day 3. Preretention injections of vasopressin (0.1 I.U.) 20 min before testing on day 3 significantly increased learned submissive behavior. The amnesic effect observed after pretrial injections of vasopressin was neither due to state dependency nor to an acquisition deficit, nor to antinociception. It is concluded that processing of the stressful experience of defeat is differently influenced by vasopressin given before or after training, resulting in an impaired or facilitated retention, respectively. Among the hypothetically discussed underlying mechanisms, one suggestion is that exogenous vasopressin interacts with an assumed discriminative stimulus function of endogenously released vasopressin. Another possibility might be that exogenous vasopressin interferes with the defeat-activated opioid peptide system.

Aggression↗
PubMed1984

Defeat, learned submissiveness, and analgesia in mice: effect of genotype.

Defeat-induced unconditioned and conditioned behaviors of C57BL/6 and DBA/2 mice were assessed in a social-learning paradigm. Upon bites, mice of the DBA strain reacted with significantly more escape reactions, while C57 mice showed more immobility, crouch, and defensive sideways and upright postures. Clear genotype-dependent patterns were also evident from the conditioned responses recorded 24 h after defeat. DBA mice displayed more escape and defensive sideways and upright postures upon contact with a nonaggressive partner mouse; in contrast, C57 mice reacted with more immobility and crouch. With an increasing number of bites the sum of learned responses increased in C57 mice while it decreased in mice of the DBA strain. This decrement was paralleled by an increase in the analgesic response measured on the hot plate in defeated DBA mice. The possible role of endogenous opioids in the genotype-dependent interaction of defeat-induced learned submissiveness and analgesia is discussed.

Aggression↗
PubMed1983

Inhibition of morphine-induced analgesia and locomotor activity in strains of mice: a comparison of long-acting opiate antagonists.

The long-acting opiate antagonistic potency of naloxazone (NXZ), beta-chlornaltrexamine (beta-CNA) and beta-funaltrexamine (beta-FNA) was compared using three inbred strains of mice, in which morphine induces either analgesia (DBA/2), locomotion (C57BL/6), or both responses (C3H/He). The antagonists were applied SC 24-120 hr before morphine (10 or 20 mg/kg, IP), followed by the tests after 30 min. The minimal dose which completely antagonized morphine-induced analgesia in DBA and locomotion in C57 mice during 24 hr were: for NXZ 50 and 100 mg/kg, for beta-CNA 0.8 and 6.2 mg/kg, for beta-FNA 1.6 and 12.5 mg/kg, respectively. beta-FNA and beta-CNA more potently blocked morphine-induced analgesia in DBA mice than the activity response in the C57 strain. In contrast, beta-FNA prevented morphine-induced locomotion at a lower dose (6.2 mg/kg) than analgesia (greater than 50 mg/kg) in C3H mice, while beta-CNA was equipotent (1.6 mg/kg). In general, beta-CNA turned out to be the most reactive compound, antagonizing morphine effects in low doses up to 120 hr. beta-FNA selectively antagonized either morphine-induced analgesia or locomotion, depending on the strain used. This suggests that a given morphine response might be caused by a genetically determined multiplicity of opiate receptor types and their mutual interactions.

Animals↗
PubMed1982

Strain differences in recovery from sensorimotor neglect after unilateral globus pallidus lesions in mice.

Recovery of somatosensory orientation after unilateral electrolytic lesions of globus pallidus was studied in two inbred strains of mice (C57BL/6, Sec 1/ReJ). During the first four post-lesion days mice of both strains did not react to tactile stimuli (von Frey hair of 2 g intensity) applied to the thorax area contralateral to the lesion. Successively, there was a gradual replacement by non-oriented activation and incomplete oriented responses, followed by normal precise orientation. Recovery of orientation proceeded at a significantly higher rate in C57 mice. After a period of four months C57 mice reached a recovery level of 91% in comparison to 56% of Sec mice. The genotype dependent differences of recovery mechanisms are discussed in terms of plasticity and dopaminergic systems.

Animals↗
PubMed1982

Lack of morphine-induced hyperactivity in C57BL/6 mice following striatal kainic acid lesions.

Bilateral injection of kainic acid (0.15 micrograms/0.3 microliters) into the striatum (caudatus/putamen) of C57BL/6 mice prevented stimulation of locomotor activity by morphine (20 mg/kg, i.p.). This effect was specific to morphine since mice with the same lesion did not show any impairment of amphetamine (2 mg/kg)-induced locomotor hyperactivity. Histological inspections showed neuron damage also in the nucleus accumbens, while hippocampus was not damaged by kainic acid. Moreover, mice with kainic acid lesions in the hippocampus were more stimulated by morphine, compared with the morphine-injected sham lesion group. The results, which suggest the existence of non-catecholaminergic mediations in the locomotor effects of morphine, are discussed in terms of opioid systems in the brain.

Amphetamine↗
PubMed1981

Effects of isolation on activity, reactivity, excitability and aggressive behavior in two inbred strains of mice.

In order to investigate mechanisms of isolation-induced aggressive behaviour, inbred mice of the C57BL/6 and DBA/2 strains were individually housed over a period of 8 weeks. In the DBA/2 strain only, isolation was followed by a clear increase in activity (Animex), reactivity (reactions upon tactile body stimulation), excitability (duration of EEG desynchronization elicited by tactile stimulation of the thorax area under urethane anesthesia) and intermale aggression (biting and fighting responses). The use of inbred strains of mice proved to be a useful tool for the examination of the relationship between various parameters. It is concluded that there are no clear correlations between activity, reactivity and aggressive behavior and that the resulting aggressive responses in the DBA/2 strain are likely due to the increase of excitability.

Aggression↗
PubMed1979

Conditioning compensates the neglect due to unilateral 6-OHDA lesions of substantia nigra in rats.

The degree of the contralateral sensory neglect in rats with unilateral 6-OHDA lesions of substantia nigra was assessed by a conditioning procedure, employing lateralized CS. In the first experiment visual neglect (revealed by failure of the visually elicited placing reaction contralateral to the lesion) was shown to be accompanied by slower acquisition of a brightness discrimination task. The impairment was due to ipsilateral turning tendency rather then to visual deficit, however, since monocular relearning yielded equal savings with the ipsilateral and contralateral eyes. The second experiment showed that rats anesthetized with urethane reacted to noxious skin stimulation contralateral to the lesion with shorter-lasting EEG arousal than to ipsilateral stimulation of the same intensity. The electrophysiological asymmetry could be compensated by classical conditioning, i.e. by pairing habituated tactile stimuli with noxious tail shock. The conditioned arousal reaction could be elicited with the same efficiency from the neglected and intact body surface. It is concluded that neglect is due neither to a sensory nor to a motor failure, but that 6-OHDA lesions of substantia nigra in one hemisphere reduce the arousing efficiency of unconditioned stimuli and interfere with sensorimotor integrating mechanisms on the side contralateral to the lesion. Compensation of the neglect by conditioning indicates that the role of the nigrostriatal system can be partly substituted by other circuits.

Animals↗
PubMed1979

Lateralized hunger: ipsilateral attenuation of cortical spreading depression-induced feeding after unilateral 6-OHDA injection into the substantia nigra.

Unilateral injections of 6-hydroxydopamine into the substantia nigra in the rat significantly attenuated cortical spreading depression (CSD)-induced eating from the hemisphere ipsilateral but not contralateral to the lesion. The lateralized decrease in elicited feeding was correlated with postlesion body weight loss, striatal catecholamine depletion (dopamine, 94%; norepinephrine, 52%) and amphetamine-induced ipsilateral turning, and can be characterized as an inability of the lesioned nigrostriatal system to maintain the CSD-elicited response rather than a failure to induce it. The interhemispheric control procedure allows us to exclude various general sensory and motor deficits to account for the decrement of feeding, and to attribute the feeding deficit to a reduced nigrostriatal transmission. It is suggested that CSD-induced feeding is due to an activation of integrative sensorimotor systems (especially the nigrostriatal dopamine system), rather than to homeostatic imbalances.

Amphetamine↗