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This study deals with the controlling of self-injurious behaviour in a profoundly retarded girl. The main therapeutic tool, social isolation, was carried out under normal ward conditions and was statistically evaluated in an intra-subject design without reversal conditions. The procedure reduced the self-injurious behaviour to a near-zero level.
The present study examined the effectiveness of a group language training procedure for directly increasing and generalizing the rate of verbal interaction among four elderly, socially isolated, moderately mentally retarded men. A withdrawal of treatment design was used to examine the effect of the procedure that used verbal prompts. behavioral rehearsal, and contingent social praise. Changes in behavior were examined in two generalization settings, one similar to the training environment (Generalization I) and the other arranged as part of the subjects' daily routine (Generalization II). Baseline data indicated no verbal interaction among the subjects. During treatment the training procedure increased the rate of subjects' verbal interactions not only in the training situation, but also in the two generalization settings. An analysis of the data obtained during the Generalization II situation indicated that subjects' verbal interaction increased not only among themselves, but with nonsubject peers present in this setting. Follow-up data showed that increases in rates of verbal interaction were maintained four months after the cessation of training. The implications of the results for program generalization and work with the language deficient individual is discussed.
1. These experiments determined whether the housing conditions of rats influenced the effects of nicotine in two animal tests of anxiety, social interaction and elevated plus-maze tests. 2. In animals housed singly for 7 days, (-)nicotine (0.025 mg kg(-1) s.c.) was ineffective, but 0.05, 0.1 and 0.25 mg kg(-1) (s.c.) significantly increased the time spent in social interaction, without changing locomotor activity, thus indicating anxiolytic actions. (-)Nicotine (0.45 mg kg(-1) s.c.) significantly reduced social interaction, indicating an anxiogenic effect. 3. However, in group-housed animals, (-)nicotine (0.025 mg kg(-1) s.c.) had a significant anxiolytic effect in the social interaction test, but 0.01, 0.05, 0.1, 0.25 and 0.45 mg kg(-1) were ineffective. (-)Nicotine (1 mg kg(-1)) reduced motor activity and social interaction in the group-housed animals. 4. In the elevated plus-maze, the time-course and the dose-response curve to nicotine were investigated. In both singly- and group-housed rats, (-) nicotine (0.1 - 0.45 mg kg(-1) s.c.) decreased the per cent entries into, and per cent time spent on, the open arms, indicating anxiogenic effects. 5. The housing condition influenced the time course, with significant effects at 5 and 30 min after injection in group-housed rats, and significant effects at 30 and 60 min in singly-housed rats. 6. In the social interaction test there was no difference in the scores of the first and last rats removed from group cages, whereas the order of removal from the cages did affect the scores in the elevated plus-maze. 7. These results provide further evidence that the two animal tests model distinct states of anxiety, and show how social isolation powerfully modifies both anxiolytic and anxiogenic effects of nicotine.
1. The aim of this study was to investigate the cardiovascular responses to repetitive alerting stimuli in rats subjected to intermittent social isolation, in comparison with animals housed in pairs. 2. Ten male Wistar rats were implanted with a blood pressure (BP) telemetric system and enrolled in a randomized cross-over study design. Rats were either isolated or housed in pairs for an 8 day period. At the end of each period, the animals were exposed to five acoustic stimuli (110 dB at 15 kHz, 80 ms after the impact, duration 700 ms) at 60 s intervals. For each stimulus, maximal BP and heart rate (HR) responses were calculated. BP variability was analysed in the frequency domain before the first stimulation using power spectral analysis. 3. Isolated animals showed more faster breathing (1.71 vs 1.42 Hz in the paired condition). The 0.4 Hz zone of the systolic BP spectral power was not significantly affected by isolation (1.11 vs 0.85 mmHg2). BP and HR resting levels of isolated rats (121 mmHg for the systolic BP and 290 b.p.m.) were similar to those of animals housed in pairs (119 mmHg for the systolic BP and 279 b.p.m.). 4. The first acoustic stimulus caused a brief rise in BP of a comparable amplitude in both conditions (24 +/- 2 mmHg). A biphasic HR response was also observed, but the delayed bradycardia was more marked during isolation (37 vs 6 b.p.m. decrease). BP and HR levels were restored within 20 s. 5. Interestingly, BP responses were progressively attenuated to become negligible at the fifth presentation (1 mmHg) in the isolated state, while during the paired state a substantial pressor response (13 mmHg) after each successive stimulus was maintained. Paired rats exhibited a constant HR profile across the trials, consisting in a slight HR increase (< 5 b.p.m.), concomitant with the BP elevation, followed by a delayed bradycardia (around 15 b.p.m.). HR profiles in the isolated condition differed markedly: HR rises increased in magnitude with the trial number, reaching 30 b.p.m. after the 5th trial. 6. Spontaneous BP and HR increases, as observed throughout the experiment were quantitatively small (6 mmHg and < 10 b.p.m.) in the two conditions. 7. These data indicate that isolation markedly affects the BP habituation profile to repetitive alerting stimuli. The BP response attenuation might unmask a tachycardic response. Alternatively, the amplified tachycardia following the latter stimuli might express sensitization to the conditioned fear resulting from isolation.
This study examined the interaction of dietary tryptophan (TRP) and differential housing on territorial-induced aggression, locomotor activity, and monoamine neurochemistry in mice. Groups of male CF-1 mice were singly-housed or group-housed and administered a semisynthetic basal diet supplemented with TRP (0.25-1.0%). Behavioral measures were taken at various intervals up to 2 weeks after dietary administration was instituted. Separate groups of mice were given the same experimental treatment and sacrificed for whole brain determination of the monoamines and their metabolites. Isolated mice were consistently more aggressive than grouped animals, suggesting that territorial-induced aggression is synergistic with intermale aggression based on social isolation. The combination of isolation and 0.50% TRP was particularly effective in producing increases in aggression that reached maximal levels after 10 days of diet administration. However, motor activity of singly-housed mice was unaffected by TRP, while that of grouped mice was decreased after 5 days of 0.50% TRP. By day 14 of administration behavioral changes tended to return to baseline levels. Neurochemical measures indicated increased DA and 5-HT turnover in isolated mice, with the 5-HT system most affected by dietary TRP. Because housing conditions were a prominent factor in the aggression and neurochemistry, the results suggest the involvement of both transmitter systems in this behavior. However, there were no changes in monoamine turnover that could account for the development of behavioral tolerance.
The staggerer murine mutation induces olfactory deficits. Mutant males do not prefer oestrous odours to anoestrous ones. A period of social isolation after weaning induces such a preference in mutants.
This paper outlines two pathways through which social support can influence the prevention or progression of cardiovascular disease: health behaviors and neuroendocrine mechanisms. Its primary focus is on neuroendocrine pathways, reviewing data which suggest that lack of social support is etiologically related to coronary artery lesion development through two mechanisms: sympathetic-adrenomedullary influences on platelet function, heart rate and blood pressure in the initial endothelial injury; and pituitary-adrenal cortical factors involved in smooth muscle cell proliferation during progression of the lesion after injury has taken place. It hypothesizes that the buffering effect of social support on the cardiovascular system is mediated primarily through mechanisms associated with the release of oxytocin.
Doses (0.1--0.7 mg/kg body weight) d-amphetamine were administered to three independent groups of green vervet monkeys (Cerecopithecus aethiops). Each group formed a triad with one male and two females. Amphetamine changed both the individual and the social behavior patterns significantly. Stereotypy and social isolation (withdrawal) were characteristic features of the amphetaminized animals. Also stereotyped social grooming was observed. The results are discussed in relation to behavior changes seen in amphetamine psychoses and in naturally occurring endogenous psychoses. It is emphasized that the study of patterns of behavior is an important object of research and relevant line in future investigations on psychopathology.
Three experiments were conducted to control for the effects of housing conditions during play deprivation on subsequent play rebound in periadolescent rats. To address play deprivation without the confound of social isolation, in Experiment 1, pairs of subjects were housed either in cages divided by wire mesh that allowed for olfactory, visual, auditory, and tactile interactions with a same-sex age-mate but prevented rough and tumble play or in standard cages. Running wheels were provided to similarly housed subjects in Experiment 2 to control for the ability to engage in physical activity. In Experiment 3, standard and brooder cages were used to control for the effects of housing area. Play-deprived subjects in all conditions showed a greatly increased number of play responses immediately following deprivation. The results from these experiments more clearly indicate that the absence of play is the crucial feature that brings about play rebound following deprivation.
A single social defeat in male rats has long lasting physiological and behavioural consequences, which are similar to those seen in depressive patients. In addition, the housing conditions after social defeat appear to be crucial for the development of depression-like symptoms. Because the dopaminergic system is thought to be altered in depressive illness, we investigated the impact of individual and group housing on the temporal development of changes of dopamine transporter (DAT) binding in male rats after a single social defeat. The number of striatal DAT binding sites was reduced in animals that remained isolated after being defeated. The isolation length after social defeat amplified this effect, indicating a temporal development of the changes on the striatal DAT. In animals which returned to the familiar group after social defeat the density of striatal DAT binding sites was not affected. We conclude that social isolation after a single defeat reduces the number of DAT binding sites. In contrast, a familiar environment after a single social defeat appears to prevent the stress-induced alterations on the dopaminergic system. This finding suggests that housing conditions are critical when investigating the central nervous effects of social defeat in male rats.
The role of cholecystokinin (CCK) receptors in the development of anxiety caused by social isolation of rats was studied using the elevated plus-maze and receptor binding techniques. The isolation of male Wistar rats significantly reduced their exploratory activity in the elevated plus-maze compared with that of rats kept in groups of four. Caerulein (0.1-5 micrograms/kg s.c.), an agonist at CCK receptors, only at the highest dose (5 micrograms/kg) significantly decreased the exploratory behaviour of rats housed in groups, but not in the isolated rats. By contrast, small doses of caerulein (0.1-0.5 microgram/kg) even tended to increase the behavioural activity of isolated rats in the plus-maze test. In parallel to the behavioural changes, isolation of the rats increased the number of [3H]pCCK-8 binding sites in the frontal cortex, but not in the other forebrain structures (the mesolimbic area, striatum and hippocampus). Isolation did not affect the density of benzodiazepine receptors in the frontal cortex. In conclusion, the isolation of rats for 7 days produced anxiogenic-like effect on the behaviour of rats and increased the number of CCK receptors in the frontal cortex without affecting benzodiazepine receptors.
This paper tested the hypothesis that social isolation of children brings about a reduced pattern of habitual physical activity, influences body composition during growth, and hampers development of physical performance capacity. Two cohorts of children were studied, one living at or close to the center, the other living in the periphery of the community of Lom in Southern Norway. The two cohorts of children differed in their patterns of physical behavior, but were otherwise similar in genetic traits, nutrition, and environmental conditions. During a 4-year period the two cohorts of children were tested annually. The center children were leaner, and their maximal oxygen uptake and forced expiratory volume were greater in all years of growth when related to body size.
Aging is a risk factor of human depression. Middle-aged or older men are vulnerable to adverse life events and an absence of social contact and easily become depressed. In the present study, we investigated the influence of aging on responses to life events in socially isolated conditions. We applied isolation-rearing (4 W) to two age groups, older (18 M) and younger (11 W), of male F344 rats that had been reared in a group and then examined responses to novelty stress (20 min). Changes in brain monoamines and their metabolites such as dopamine (DA), serotonin (5-HT), dihydroxyphenylacetic acid (DOPAC), homovanilic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA) were measured in six regions: the prefrontal cortex, nucleus accumbens, hippocampus, amygdala, midbrain, and raphe nuclei. MANOVA was carried out for rearing condition, age, and novelty stress. Isolation significantly changed monoamines and their metabolites, except in amygdala and raphe nuclei. Aging significantly altered them in all regions, although novelty stress did not. In the amygdala and midbrain, isolation significantly changed monoamine biosynthesis, with monoamine turnover remaining unchanged. In the prefrontal cortex and nucleus accumbens, aging significantly altered turnover, while biosynthesis remained unchanged. Novelty stress significantly varied only the turnover in the prefrontal cortex. The interaction between isolation and aging indicated that aging influences changes in turnover and biosynthesis elicited by isolation primarily at the center of the mesolymbic DA system, the midbrain, and in raphe nuclei of the 5-HT system. In peripheral regions of the mesolymbic system, aging primarily affects changes in turnover induced by isolation.
A quantitative Golgi study was carried out in order to detect changes in the number of dendritic spines in neurones of the strial part of the medial preoptic area during a long-term (10 months) social isolation in prematurely weaned rats. An increase has been found in these postsynaptic structures for the isolated animals. Such an increase can indicate that a greater synaptic connectivity exists in this area. In this paper our results are compared with data reported by other authors showing an increased unit activity in this area under stress conditions.
The hypothesis that early social isolation results in long-term alterations in dopamine receptor sensitivity was tested using older adult rhesus monkeys. Isolated and control monkeys were challenged with apomorphine (0.1 and 0.3 mg/kg), and the drug effects on spontaneous blink rate, stereotyped behavior, and self-injurious behavior were quantified using observational measures. Monoamine metabolites were quantified from cisternal CSF by HPLC-EC, prior to pharmacological challenge. Isolated and control monkeys did not differ in CSF concentrations of HVA, 5-HIAA, or MHPG. At the higher dose, apomorphine significantly increased the rate of blinking, the occurrence of whole-body stereotypies, and the intensity of stereotyped behavior (as measured by observer ratings) in isolated monkeys. The frequency of occurrence of self-injurious behavior was too low to allow for meaningful comparisons. These significant differences in response to apomorphine challenge support the hypothesis that long-term or permanent alterations in dopamine receptor sensitivity, as assessed by drug challenge, are a consequence of early social deprivation.
Ultrastructural changes in the central nucleus of the amygdalar body, field CA I of the hippocampus, piriform cortex, field 17 and field 7 have been studied in dogs, bred under conditions of social isolation. The changes are more numerous in emotiogenic structures. Similar ultrastructural rearrangements are revealed in the amygdalar body, hippocampus and in both fields of the neocortex. They are: neurons with different degree of chromatolysis, reactive changes in some organelles, terminals with agglutinated vesicles, or with their reduced number, increasing amount of synapses with a short active zone. At the same time, in the piriform gyrus vacuoles, membrane-like and osmiophilic inclusions, terminals with granular vesicles of various size are found more often.
This study investigated the effects of isolation rearing from weaning in rats on extracellular noradrenaline in the dorsal hippocampus in vivo, measured using microdialysis. Male Lister hooded rats were obtained at weaning and reared in social isolation or in groups for six to eight weeks. Basal noradrenaline efflux did not differ between isolation- and group-reared rats. Local K+ stimulation (50 and 100 mM) increased noradrenaline efflux in the hippocampus of both groups of rats; however, this effect was greater in group-reared rats (50 mM K+). The alpha 2-adrenoceptor agonist, clonidine (0.3 mg/kg, i.p.), reduced noradrenaline efflux in both groups of rats, but this decrease was greater in isolates. Systemic (1.0 mg/kg, i.p.) and local (via the probe; 100 microM) administration of the alpha 2-adrenoceptor antagonist, idazoxan, increased noradrenaline efflux, but these responses were also greater in isolation-reared rats. The magnitudes of the idazoxan-induced increases in noradrenaline efflux were similar for both systemic and local administration, indicating that presynaptic terminal alpha 2-adrenoceptors were predominantly involved. Furthermore, although tail pinch increased noradrenaline efflux in both isolation- and group-reared rats, there was a significant/attenuation in the response in the isolation- compared to group-reared rats. Taken together with previous findings, the present results provide evidence in favour of an isolation-induced enhancement in the function of the presynaptic terminal alpha 2-autoreceptor in the dorsal hippocampus in vivo, resulting in decreased functional responsiveness of hippocampal noradrenergic nerve terminals.
Isolating a sexually mature Aplysia fasciata for either 1 or 24 hr immediately after training that a food is inedible blocks the subsequent expression of memory measured 24 hr later. Isolation that is delayed for 1 hr after training, but not for 12 hr after training, is also effective in blocking memory. Isolation affects memory because of a specific effect caused by the absence of pheromones secreted by conspecifics rather than by a nonspecific change in the chemical environment, because transferring animals to a novel environment (120% seawater) that contains a conspecific does not affect memory. Isolation also does not affect memory in sexually immature Aplysia, even though immature animals are able to sense one another's presence. Isolation may affect memory because social (and sexual) isolation is a form of stress in mature A. fasciata, and stress after training affects retention in many animals.