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PubMed1981

Pyridostigmine administration in newborn rats prevents permanent mental ill-effects produced by maternal deprivation.

Maternal deprivation from Day 3 to Day 14 of life, i.e., separation of the pups from their mother animals during this developmental period for 16 hours each day, gave rise to highly significantly decreased learning capability and memory capacity in adulthood associated with significantly decreased acetylcholinesterase activity in the brain. These permanent ill-effects of the brain, produced by maternal deprivation of newborn rats, could be prevented by the acetylcholinesterase inhibitor pyridostigmine when administered from Day 1 to Day 14 of life. In view of these findings, teratogenic mental ill-effects, produced by psychosocial and/or nutritional deprivation during brain development, appear to be preventable by correcting abnormal neurotransmitter concentrations during this critical period of brain organization.

Acetylcholinesterase↗
PubMed2001

Differential and age-dependent effects of maternal deprivation on the hypothalamic-pituitary-adrenal axis of brown norway rats from youth to senescence.

In this study, the hypothesis was tested that infants deprived from maternal care show persistent changes in hypothalamic-pituitary-adrenal activity. For this purpose, we studied the effect of maternal deprivation in one cohort of the healthy ageing Brown Norway rat strain showing still more than 80% survival rate at 32 months of age. Three-day-old male Brown Norway rats were either maternally deprived for 24 h or remained with the dam. In 3, 12 and 30-32 months (young, adult, senescent) deprived rats and their nondeprived littermates (controls), we determined basal resting and stress-induced plasma adrenocorticotropic hormone (ACTH) and corticosterone as well as corticotropin releasing hormone (CRH) mRNA expression in the paraventricular nucleus (PVN) of the hypothalamus. Mineralocorticoid (MR) and glucocorticoid receptors (GR) in hippocampus and PVN were also assessed using in vitro cytosol binding and in situ hybridization. The effect of ageing per se showed that in the control nondeprived Brown Norway rats, basal corticosterone and ACTH concentrations did not change during life. However, with age, the corticosterone response to novelty stress became progressively attenuated, but prolonged, while there was an age-related increase in the ACTH response. CRH mRNA expression in PVN decreased with age. Hippocampal MR binding and MR mRNA expression in the dentate gyrus were reduced at senescence, as were the GR binding capacities in hippocampus and hypothalamus. Maternal deprivation did not affect survival rate, body weight, nor adrenal weight of the ageing Brown Norway rats. Basal corticosterone and ACTH levels were not affected by deprivation, except for a rise in basal corticosterone concentrations at 3 months. At this age, the corticosterone output in response to novelty was attenuated in the deprived rats. In contrast, a striking surge in novelty stress-induced corticosterone output occurred at midlife while, at senescence, the corticosterone and ACTH responses were attenuated again in the deprived animals, particularly after the more severe restraint stressor. CRH mRNA expression was reduced only during adulthood in the deprived animals. After maternal deprivation, the MR mRNA in dentate gyrus showed a transient midlife rise. GR binding in hypothalamus and hippocampus GR binding was reduced in young rats while, in the senescent deprived animals, a reduced GRmRNA expression was observed in PVN and hippocampal CA1. In conclusion, in the Brown Norway rat, ageing causes a progressive decline in corticosterone output after stress, which is paralleled at senescence by decreased MR and GR mRNA expression in hippocampus and hypothalamus. The long-term effects of maternal deprivation become manifest differently at different ages and depend on test conditions. The deprivation effect culminates in a midlife corticosterone surge and results at senescence in a strongly reduced corticosterone output.

Adrenocorticotropic Hormone↗
PubMed2004

The role of the anterodorsal thalami nuclei in the regulation of adrenal medullary function, beta-adrenergic cardiac receptors and anxiety responses in maternally deprived rats under stressful conditions.

Maternal separation can interfere with growth and development of the brain and represents a significant risk factor for adult psychopathology. In rodents, prolonged separation from the mother affects the behavioral and endocrine responses to stress for the lifetime of the animal. Limbic structures such as the anterodorsal thalamic nuclei (ADTN) play an important role in the control of neuroendocrine and sympathetic-adrenal function. In view of these findings we hypothesized that the function of the ADTN may be affected in an animal model of maternal deprivation. To test this hypothesis female rats were isolated 4.5 h daily, during the first 3 weeks of life and tested as adults. We evaluated plasma epinephrine (E) and norepinephrine (NE), cardiac adrenoreceptors and anxiety responses after maternal deprivation and variable chronic stress (VCS) in ADTN-lesioned rats. Thirty days after ADTN lesion, in non-maternally deprived rats basal plasma NE concentration was greater and cardiac beta-adrenoreceptor density was lower than that in the sham-lesioned group. Maternal deprivation induced a significant increase in basal plasma NE concentration, which was greater in lesioned rats, and cardiac beta-adrenoreceptor density was decreased in lesioned rats. After VCS plasma catecholamine concentration was much greater in non-maternally deprived rats than in maternally-deprived rats; cardiac beta-adrenoreceptor density was decreased by VCS in both maternally-deprived and non-deprived rats, but more so in non-deprived rats, and further decreased by the ADTN lesion. In the plus maze test, the number of open arm entries was greater in the maternally deprived and in the stressed rats. Thus, sympathetic-adrenal medullary activation produced by VCS was much greater in non-deprived rats, and was linked to a down regulation of myocardial beta-adrenoceptors. The ADTN are not responsible for the reduced catecholamine responses to stress in maternally-deprived rats. Maternal deprivation or chronic stress also induced a long term anxiolytic effect, which was also not affected by ADTN lesion.

Adrenal Medulla↗
PubMed1978

Selective depression of serum growth hormone during maternal deprivation in rat pups.

Maternal deprivation was associated with a decline in immunoreactive growth hormone in the serum of rat pups. Pups that were returned to the mother showed a rapid reversal in this deprivation-induced decrease. The change in growth hormone concentration was not accompanied by changes in the concentrations of prolactin, thyrotropin, or corticosterone in the serum, but were correlated with alteration in the activity of ornithine decarboxylase in the brain. Treatment of neonatal rat pups with cyprohepatadine, a serotonin antagonist that suppresses growth hormone secretion, resulted in a significant decline in both serum growth hormone concentration and brain ornithine decarboxylase activity. These findings suggest that maternal deprivation elicits a specific suppression of growth hormone release which mediates the decrease in ornithine decarboxylase activity. The study is consistent with clinical findings of impaired growth hormone "responsitivity" in human maternal deprivation syndrome.

Animals↗
PubMed1980

Effects of reserpine and amphetamine on the development of hyperactivity in maternally deprived rat pups.

Maternal deprivation for 24 hr is known to produce hyperactivity in 2-week-old infant rats kept at nest temperature. Pretreatment with reserpine (0.5 mg/kg), at the time of separation, prevented the development of hyperactivity over the ensuing 24-hr, whereas the same dose in mothered littermates had no residual effects on behavior the next day. d-Amphetamine (0.25 and 2.0 mg/kg) produced dose-dependent increases in locomotion and rearing and decreases in self-grooming behavior, which were of comparable magnitude whether the pups were separated and kept warm, normally mothered, or separated at room temperature, a condition known to produce decreased activity levels. Cardiac rates were not affected by either drug; reserpine lowered respiratory rates slightly, amphetamine increased body temperature following behavior testing. Altered accumulation of catecholamines at presynaptic terminals is discussed as a possible neurochemical mechanism for behavior changes following maternal separation in this model system.

Animals↗
PubMed1988

Modification of hypothalamic content of growth hormone regulatory peptides in maternally deprived neonatal rats.

The possibility that maternal deprivation (MD) modifies growth hormone releasing hormone (GHRH) and/or growth hormone release inhibiting hormone (GHRIH) in 10-day-old rat pups was investigated by quantifying the total hypothalamic content of these two hormones which regulate the release of growth hormone (GH), since MD has previously been shown to suppress circulating GH levels. At 10 days of age, rat pups were maternally deprived for either 1 or 6 hours (control pups remained with their mother while littermates were deprived). At the end of the time period, hypothalami were dissected free, homogenized, frozen, and then lyophilized. Reconstituted extracts were later subjected to radioimmunoassay for GHRH and GHRIH. Tests for differences in the brain content of the hormones were performed by analysis of variance; multiple comparison of the means was performed using Tukey's test. A significant increase in the GHRIH content was observed in the hypothalami of maternally deprived rats as compared to control animals (P = 0.026). Small differences in the mean GHRIH content between the different experimental groups suggested a trend toward elevation of GHRIH after either 1 or 6 hours of MD and a trend toward higher levels in males as compared to females (P = 0.0636). No differences in hypothalamic GHRH content were found between maternally deprived and control pups (175.8 pg/hypothalamus vs. 171.5 pg/hypothalamus). The modification of GHRIH hypothalamic content during MD of neonatal rats demonstrated in the present study may be related to the suppression of GH that is known to result from MD.

Animals↗
PubMed2002

Maternal deprivation stress exacerbates cognitive deficits in immature rats with recurrent seizures.

PURPOSE: Maternal deprivation is stressful for the neonate. The aim of this study was to investigate the short- and long-term effects of maternal separation on recurrent seizures in the developing brain. METHODS: Rats were divided into four groups according to whether the rat pups were treated with maternal deprivation from postnatal day 2 (P2) to P9 or neonatal seizures induced by intraperitoneal (i.p.) injection of pentylenetetrazol (PTZ) from P10 to P14. Rats in the control group received saline i.p. injection from P10 to P14; rats in the isolation group underwent daily separation from their dams from P2 to P9; rats in the PTZ-treated group were subjected to PTZ-induced recurrent seizures from P10 to P14; rats in the isolation plus PTZ-treated group were subjected to maternal deprivation from P2 to P7 followed by serial seizures from P10 to P14. In addition, subsets of rats at P15 were killed and the brains assessed for acute neuronal degeneration. Visual-spatial memory test using the Morris water maze task was performed at P80. After testing, the hippocampus was evaluated for histologic lesions and cyclic adenosine monophosphate (cAMP)-responsive element-binding protein phosphorylation at serine-133 (pCREBSer-133), an important transcription factor underlying learning and memory. RESULTS: All rats given PTZ developed recurrent seizures. After PTZ administration, rats with a history of maternal deprivation had more intense impairment than did rats with maternal deprivation and neonatal seizures than those without deprivation. Neuronal degeneration was most prominent in the rats exposed to maternal deprivation plus recurrent seizures. Rats receiving maternal deprivation or PTZ-induced recurrent seizures exhibited only spatial deficits, but no morphologic changes in the hippocampus. However, rats with maternal deprivation plus PTZ-induced recurrent seizures exhibited worse visual-spatial learning compared with rats with either isolation or PTZ-induced recurrent seizures alone. The levels of pCREBSer-133 may play a role in the decrease in the hippocampus from the rats subjected to maternal deprivation and/or PTZ-induced recurrent seizures, as compared with rats exposed to vehicle-control saline. These results indicate that repeated maternal deprivation can exacerbate long-term cognitive deficits resulting from neonatal seizures. In addition, impaired phosphorylation of CREBSer-133. CONCLUSIONS: Repeated maternal deprivation stress has synergistic effects with recurrent seizures in inducing neurologic damage in the developing brain.

Animals↗
PubMed2002

Early maternal deprivation and prepulse inhibition: the role of the postdeprivation environment.

Early postnatal maternal deprivation leads to a variety of biochemical and behavioural alterations in the offspring, some of which do not develop until adulthood, like deficits in prepulse inhibition. Since a number of these deficits are similar to abnormalities observed in schizophrenic patients, maternal deprivation has been proposed as an interesting model for schizophrenia. However, little is still known about the processes that determine these long-term consequences. Previous experiments showed that the strain of rats and the deprivation procedure are important factors. In the present set of experiments, we focussed on the postdeprivation period. We showed that rearing normal Wistar rats in social isolation from weaning disrupts prepulse inhibition. However, if maternally deprived Wistar rats were reared in social isolation, the prepulse inhibition was normal. We further showed that if only half of the litters were maternally deprived at postnatal day 9, the animals had only a small disruption in prepulse inhibition compared to animals that came from litters where all the animals were deprived. In a final experiment, we crossfostered maternally deprived mothers to nondeprived pups and vice versa. This experiment showed that both the nondeprived pups raised by a deprived mother and the deprived pups raised by a nondeprived mother had small deficits in prepulse inhibition. Taken together, these data clearly show that the postdeprivation period is of crucial importance for the development of prepulse inhibition deficits in maternally deprived rats. We present a working model in order to explain the long-term behavioural consequences of maternal deprivation.

Animals↗
PubMed2000

Maternal deprivation affects behaviour from youth to senescence: amplification of individual differences in spatial learning and memory in senescent Brown Norway rats.

Previous studies have shown that deprivation of the infant rat from maternal care has pronounced effects on the stress system during ontogeny. Here we test the hypothesis that 24 h of maternal deprivation at postnatal day 3 will cause persistent changes in behaviour. Spatial learning and memory of male Brown Norway rats deprived as infants were observed in the Morris water maze at 3, 12, 24 and 30-32 months of age (young, adult, aged, senescent). Their nondeprived mother-reared littermates served as controls. (i) With increasing age, water maze performance declined in deprived and nondeprived groups. However, once the task was learned the animals maintained their good performance during retest at later ages. (ii) Maternal deprivation delayed acquisition until adulthood and caused at every age a higher degree of persistent behaviour as judged from the performance of deprived rats' free swim trials and reversal trials. (iii) At senescence the mean performance in the water maze did not differ between the groups. Instead, the individual performance was strikingly different within each group. Senescent deprived rats were either nonimpaired or impaired with only a few animals showing an intermediate performance. Thus, a large group of animals ( approximately 40%) ages successfully as they are resistant to the effect of maternal deprivation. In contrast, the majority of the control animals displayed intermediate performance. Taken together, maternal deprivation has life-long consequences for behaviour and culminates at senescence in amplification of individual differences in learning ability rather than in a generalized deterioration of cognitive functions.

Aging↗
PubMed1997

Persistent, but Paradoxical, Effects on HPA Regulation of Infants Maternally Deprived at Different Ages.

Twenty-four hours of maternal deprivation have been shown to have immediate and long-term effects on the hypothalamic-pituitary-adrenal (HPA) axis. In the first experiment the influence of such a maternal deprivation period (pnd 11-12) on basal and stress-induced ACTH and CORT levels 4 and 8 days following reunion was investigated. The results revealed a suppression of the ACTH response in the previously deprived animals which was not reflected in the CORT response. In the second experiment these persistent effects were studied in animals deprived during different stages of development. Deprivation early in development (pnd 3-4) produced an animal with a hyperreactive ACTH response whereas deprivation later (pnd 7-8, pnd 11-12) resulted in a hyporeactive ACTH response to stress at pnd 20. To study further the possible mechanisms leading to these different ACTH responses, we used in situ hybridization to investigate hippocampal mineralocorticoid (MR) and glucocorticoid receptor (GR) gene expression and corticotropin-releasing hormone (CRH) and GR mRNA levels in the paraventricular nucleus of the hypothalamus (PVN) of these 20-day old animals. Permanent changes in hippocampal GR mRNA were seen only in the later deprived pups, whereas GR mRNA was reduced in the PVN in all deprived pups. In conclusion, maternal deprivation during the neonatal period produces alterations in the ACTH response to a mild stress and sustained changes in GR transcript levels. The direction and magnitude of these effects are dependent upon the age at which maternal deprivation is experienced.

Journal Article↗
PubMed2004

Differences in modification of stress mechanisms in rat pups exposed to continuous and intermittent maternal deprivation.

During antenatal short-term intermittent maternal deprivation the content of epinephrine increased by 123% in the cortex and by 135% in the hypothalamus of 15-day-old rat pups, which is higher than during physiological development, while dopamine content, instead of increasing, decreased by 24% in the cortex and by 35% in the hypothalamus on day 15 of life. Shifts in norepinephrine and dopamine concentrations in the cortex were less pronounced in rat pups exposed to permanent maternal deprivation compared to intermittent deprivation, while the shifts in the hypothalamus were even more pronounced. Presumably, discoordination of the dopaminergic and sympathoadrenal systems in the course of development of the nervous system underlies behavioral disorders in rat pups under conditions of maternal deprivation.

Animals↗
PubMed2002

Maternal deprivation of rat pups increases clinical symptoms of experimental autoimmune encephalomyelitis at adult age.

Maternal deprivation of neonatal animals has been shown to induce long-lasting changes in the reactivity of the neuroendocrine system. The aim of the present study was to investigate whether maternal deprivation also affects susceptibility to immune-mediated diseases such as experimental autoimmune encephalomyelitis (EAE) in adult life. To this end, 9-day-old rat pups were subjected to a short-lasting maternal deprivation for a period of 24 h. At the age of 8 weeks, we induced EAE in these rats by immunization with myelin basic protein (MBP) in complete Freund's adjuvant. Our data demonstrate that short-lasting maternal deprivation induces a marked increase in the severity of EAE in the animals in later life. The histopathological evaluation of spinal cord and cerebellum corresponded with the observed differences in clinical symptoms of EAE. Moreover, neonatal maternal deprivation affects macrophage functioning at adult age. In contrast, no differences were observed in in vitro mitogen- and MBP-induced cytokine production by splenocytes. LPS-induced corticosterone release did not differ either between maternally deprived and control animals. We conclude that short-lasting neonatal maternal deprivation of rat pups has long-lasting consequences for macrophage activity and for susceptibility to the inflammatory autoimmune disease EAE.

Aging↗
PubMed2006

Maternal deprivation, acute respiratory infections and immune regulation.

OBJECTIVE: The study was designed to investigate the acute respiratory disease incidence (DI) in deprived infants and test the hypothesis if maternal deprivation effects the processes of immunoregulation in infants. METHODS: The prospective study during 1 year in Tbilisi Infant's House was performed. Cohort of 136 infants at age from 1 to 24 months without any congenital abnormalities formed the basic group. The cohort of 136 healthy infants at age 1 to 24 months of the same population living under the maternal care in three shelters of Tbilisi region was randomized as a control. The study included: DI, age of first attack, duration of illness, outcome, plasma immune parameters. RESULTS: The data have demonstrated that maternal deprivation induces a marked increase in the severity of acute respiratory disease among infants. DI was twice as much in deprived children as in control group. Moreover, there was diagnosed the disruption of normal correlations between plasma CD3, CD4 and CD8 in infants under maternal deprivation. CONCLUSION: Maternal deprivation induces changes in processes of immunoregulation in infants resulted in elevation of acute respiratory DI among them.

Acute Disease↗
PubMed2002

Postnatally induced differences in adult pain sensitivity depend on genetics, gender and specific experiences: reversal of maternal deprivation effects by additional postnatal tactile stimulation or chronic imipramine treatment.

Postnatal endotoxin exposure, handling or maternal deprivation produce long-lasting individual differences in various neuroendocrine and behavioural responses. However, the impact of postnatal experiences on adult pain sensitivity and its reversibility by postnatal additional tactile stimulation or antidepressants in adulthood is not well understood. Therefore, postnatal endotoxin application as a model for infection, maternal deprivation as a model for depression, and postnatal handling as a model for stimulation were compared with respect to the effects on pain sensitivity in adult Fischer 344 (F344) and Lewis (LEW) rats. Handling increased hot plate latencies in adult F344 and LEW rats, while maternal deprivation shortened hot plate latencies only in LEW rats. Prophylactic treatment strategies, such as tactile stimulation of the dorsal neck region of pups directly after maternal deprivation, or chronic treatment of adult maternally deprived rats using imipramine, successfully provide protection against the maternal deprivation-induced shortening of hot plate latencies. Thus, there is considerable specificity of certain postnatal experiences in modulating adult pain sensitivity and the maternal deprivation-induced hyperalgesia is reversible by different interventional regimes. These findings may explain some of the individual differences in pain sensitivity of humans and the differential efficacy of antidepressants in pain syndromes.

Animals↗
PubMed2002

Neonatal maternal deprivation modifies feeding in response to pharmacological and behavioural factors in adult rats.

Neonatal maternal deprivation permanently modifies the hypothalamo-pituitary-adrenal (HPA) axis and other neurobiological and behavioural parameters in rats. The HPA axis plays a central role in the control of feeding, and participates in the anorexigenic action of dexfenfluramine and restraint stress, and in the orexigenic action of a cafeteria diet. Therefore, we investigated whether maternal deprivation modifies feeding responses to these factors. Experimental pups were separated for 24h from the mother 5 or 14 days after birth. The anorexigenic response to both dexfenfluramine and restraint stress was increased, and body weight as well as subcutaneous adipose tissue gain induced by cafeteria diet was higher in early deprived adult rats. However, these effects were dependent on the time of maternal deprivation. According to our predictions, the feeding response of maternally deprived rats to anorexigenic and orexigenic agents was altered, which is probably partly due to an altered HPA function, but the participation of the serotonergic, the opioid and/or the dopaminergic system cannot be ruled out. Additional studies are needed to detail precisely the neurobiological substrates of modified feeding behaviour of maternally deprived animals. This early stress paradigm altering feeding behaviour could become an interesting model for research into human eating disorders.

Age Factors↗
PubMed1991

Further evidence for the hypothesis that beta-endorphin mediates maternal deprivation effects.

Lung DNA synthesis was examined in 9-day-old rat pups following a 2-hour separation from their mothers (maternal deprivation), and compared to that of pups placed with a nipple ligated dam (food deprivation) or a lactating dam (control). Maternally deprived pups consistently showed a significant reduction in lung DNA synthesis which was not attributable to food deprivation. Central administration of naloxone prevented the decrease in DNA synthesis observed after maternal deprivation but did not inhibit the reductions in lung DNA synthesis seen two hours after sc administration of isoproterenol, suggesting that DNA response to maternal deprivation is a specific opioid receptor mediated event. These results are consistent with previous reports from our laboratory indicating that CNS beta-endorphin may mediate many of the biological alterations observed following maternal deprivation in neonatal rats.

Animals↗
PubMed2001

Intergenerational effects of complete maternal deprivation and replacement stimulation on maternal behavior and emotionality in female rats.

The present study investigated the effects of early rearing experiences on the development of maternal behavior in Sprague-Dawley female rats. Pups from individual litters were assigned to four different groups on Day 3 of life. From days 4 to 20 of life, these were reared artificially, without mother and receiving minimal "licking-like" tactile stimulation (AR-MIN), or maximal stimulation (AR-MAX) or were reared with their mothers (MR-CONTROL and MR-SHAM). At 70-100 days all AR and MR animals were mated and then observed with their own offspring, culled to eight pups. After maternal testing open-field tests were conducted. The female offspring in these litters (all raised by their MR and AR mothers) were reared to adulthood and then observed interacting with their offspring. Results show that in adulthood AR mothers engaged in significantly fewer pup-retrievals and less pup-licking (genital and body), and crouching, but significantly more non-maternal tail-chasing, digging, and hanging/climbing. As well, they were more active in the open field. Comparisons between the two AR groups and the MR groups, showed that most of the differences were between the AR-MIN and MR groups, with the AR-MAX animals showing levels of behavior between the two, and differing from neither. Analyses of covariance indicated that early experience and adult emotional behavior both influence adult maternal behavior, but their effects are independent of one another. A cross-generational effect of artificial rearing was also found. Daughters of AR and MR mothers that were observed after the birth of their own litters in adulthood showed a pattern of behavior that mimicked the pattern shown by their mothers. These results are discussed in terms of the variety of possible behavioral, endocrine, and neurochemical mechanisms that mediate the effects of early experiences on adult maternal behavior.

Analysis of Variance↗