Cold Water Swim Stress Research Articles

Comparative Study on the Effect of Bacopa monniera and Omega3 Fatty Acids on the Cortisol Hormone Level in Cold Stress Induced Wistar Albino Rats

In recent years, researchers have identified several natural compounds that could potentially help to retard mental stress. Extracts of Bacopa monniera (BM), a traditional ayurvedic medicine and omega3 faffy acids (OFA) have been reported to enhance effects mental functions by combating the stress. However, there is still an lacunae studies on which of those two drugs has better results on cortisol hormonal changes due to stress. The current study aimed to compare the effects of BM and omega3 fatty acids on cold stress induced Wistar rats. We divided the animals into seven groups. Group I was control in which rats were kept under ideal laboratory conditions, Group II was given cold water swim stress for a period of one month after which the rats were sacrificed for hormonal assay, Group III in which cold water swim stress given for a month followed by oral administration of normal saline as vehicle for a month, Group IV and V in which cold water swim stress given for a month followed by oral administration of BM extracts 40mg/kg and 80mg/kg respectively as treatment for a month. Group VI and VII includes cold stress followed by oral gavages of OFA 60mg/Kg of Docosahexaenoic acid (DHA) and Eicosapentaenoic acid (EPA) for 2 weeks (short-term model) and 4 weeks (long term model) respectively. After the treatment period blood was collected and cortisol assay was done. The data were compared with those of control rats. The results showed an increase in the cortisol level in the stressed group of rats when compared to the treatment group. These results indicate that oral administration of high dose of BM and long-term administration of OFA improves the cortisol level and helps in controlling the stress in rats.

Effect of Bacopa monniera on the Level of Cortisol Hormone in Forced Cold Water Swim Stress Induced Wistar Albino Rats

The human brain remains a mystery even after years of research into the biological processes underlying its specific actions. In recent years, researchers have identified several natural compounds that could potentially help to retard mental deterioration. Extracts of Bacopa monniera, a traditional ayurvedic medicine, have been reported to have memory-enhancing effects in animals. However, there are no studies on bp in cold stress induced neuronal changes in hippocampus have been explored. The current study examined the effects of standardized extract of Bacopa monniera, on Wistar rats. We divided the animals into 4 groups. Group I was control in which rats were kept under ideal laboratory conditions, Group II was given cold water swim stress for a period of one month after which the rats were sacrificed for histological studies to study the changes in the hippocampus caused by cold stress, Group III in which cold water swim stress given for a month followed by oral administration of normal saline as vehicle for a month, Group IV in which cold water swim stress given for a month followed by oral administration of Bacopa monniera, extracts 40mg/kg treatment for a month. Group V in which cold water swim stress given for a month followed by oral administration of Bacopa monniera, extracts 80mg/kg treatment for a month. After the treatment period blood was collected and cortisol assay was done. The data were compared with those of control rats. The results showed an increase in the cortisol level in the stressed group of rats when compared to the treatment group. These results indicate that oral administration of Bacopa monniera, extract improves the cortisol level and helps in controlling the stress in rats.

Effects of Semax in the Models of Acute Stress

Acute stress exposure causes a cascade of neurochemical reactions, leading, in particular, to a change in behavior and increased tolerance to pain in humans and animals. ACTH/MSH-like peptides play an important role in regulating the body’s response to stressful exposures. The aim of the present study was to assess the effects of the ACTH4–10 analogue heptapeptide Semax in various models of acute stress. The effect of intraperitoneal Semax administration at doses of 0.05 and 0.5 mg/kg on changes in behavior and pain sensitivity of Wistar rats in models of inescapable intermittent foot shock stress and forced cold-water swim stress was investigated. To assess the involvement of the endogenous opioid system in the effects of stress, an impact of pretreatment with opioid receptor antagonist naloxone (1 mg/kg) was studied. The stressors used led to an increase in the pain threshold in the paw-pressure test, which indicates the development of stress-induced analgesia (SIA). In addition, rats exposed to stress had an decrease in exploratory behavior and an increase in the anxiety-like behavior in the hole board test. Both Semax and naloxone attenuated SIA in the model of inescapable foot shock stress, but did not affect the value of the pain threshold in the model of forced cold swim stress. Both studied drugs did not affect the behavior of rats in the models of acute stress used. It can be concluded that Semax blocks the opioid form of stress-induced analgesia, but does not affect the behavioral alterations in rats exposed to acute stress.

Effect of vestibular stimulation on cold water stress-induced neurological changes in Wistar rats

The current study was undertaken to see the effects of cold-water stress on the brain and to evaluate the beneficial effect of vestibular stimulation on stress-induced brain changes. Healthy, male, Wistar rats, weighing 180 to 250 gm with 3-6 months of age, were used for the study. Stress was induced by making the animals swim in cold water maintained at 100C for 30 min a day, for 14 days. Following cold water swimming stress, bilateral hot water caloric vestibular stimulation was given to the animals using 410C temperature water for 15 days. Rats were sacrificed and histopathological brain changes were studied by Hematoxylin & Eosin staining. Serum corticosterone level has increased significantly after cold water swimming stress (p<0.01). Corticosterone was less in animals that received caloric vestibular stimulation in comparison with the animals which did not receive caloric vestibular stimulation (p<0.05). Coldwater swimming stress had induced focal neuronal atrophy, nuclear pyknosis with congested blood vessels and infiltration of mononuclear inflammatory cells in the hippocampus and hypothalamus. Stressed animals that received caloric vestibular stimulation recovered well and showed the cerebral cortex with the normal neuroglial arrangement. Hypothalamus showed normal morphology and the hippocampus showed a pyramidal layer with a normal thickness in comparison to the animals which did not receive caloric vestibular stimulation. We conclude Caloric vestibular stimulation was effective in reversing the cold-water stress-induced serum corticosterone and histopathological changes in the brain.

The changes of nociception and the signal molecules expression in the dorsal root ganglia and the spinal cord after cold water swimming stress in mice.

Several studies have previously reported that exposure to stress provokes behavioral changes, including antinociception, in rodents. In the present study, we studied the effect of acute cold-water (4°C) swimming stress (CWSS) on nociception and the possible changes in several signal molecules in male ICR mice. Here, we show that 3 min of CWSS was sufficient to produce antinociception in tail-flick, hot-plate, von-Frey, writhing, and formalin-induced pain models. Significantly, CWSS strongly reduced nociceptive behavior in the first phase, but not in the second phase, of the formalin-induced pain model. We further examined some signal molecules' expressions in the dorsal root ganglia (DRG) and spinal cord to delineate the possible molecular mechanism involved in the antinociceptive effect under CWSS. CWSS reduced p-ERK, p-AMPKα1, p-AMPKα2, p-Tyk2, and p-STAT3 expression both in the spinal cord and DRG. However, the phosphorylation of mTOR was activated after CWSS in the spinal cord and DRG. Moreover, p-JNK and p-CREB activation were significantly increased by CWSS in the spinal cord, whereas CWSS alleviated JNK and CREB phosphorylation levels in DRG. Our results suggest that the antinociception induced by CWSS may be mediated by several molecules, such as ERK, JNK, CREB, AMPKα1, AMPKα2, mTOR, Tyk2, and STAT3 located in the spinal cord and DRG.

Modulation of corticosterone and changes of signal molecules in the HPA axis after cold water swimming stress

ABSTRACT In the present study, we examined the effect of cold-water swimming stress (CWSS) on plasma corticosterone levels. Mice were exposed to stress in 4°C for 3 mins. Plasma corticosterone (CORT) level was measured at 0, 15, and 30 min after stress stimulation. The plasma CORT level was gradually increased up to 30 min. Then we further examined the changes of several signaling molecules expression levels, such as p-ERK, p-JNK, p-P38, p-AMPKα1, p-AMPKα2, and p-mTOR, in the HPA axis. We observed that those signaling molecules were altered after stress in the HPA axis. p-ERK, p-JNK, p-P38, and p-mTOR proteins expression were reduced by CWSS in the HPA axis. However, the phosphorylation of AMPKα1 and AMPKα2 were activated after CWSS in the HPA axis. Our results suggest that the upregulation of plasma CORT level induced by CWSS may be modulated by the those signaling molecules.

Constitutive activation of kappa opioid receptors at ventral tegmental area inhibitory synapses following acute stress.

Stressful experiences potently activate kappa opioid receptors (κORs). κORs in the ventral tegmental area regulate multiple aspects of dopaminergic and non-dopaminergic cell function. Here we show that at GABAergic synapses on rat VTA dopamine neurons, a single exposure to a brief cold-water swim stress induces prolonged activation of κORs. This is mediated by activation of the receptor during the stressor followed by a persistent, ligand-independent constitutive activation of the κOR itself. This lasting change in function is not seen at κORs at neighboring excitatory synapses, suggesting distinct time courses and mechanisms of regulation of different subsets of κORs. We also provide evidence that constitutive activity of κORs governs the prolonged reinstatement to cocaine-seeking observed after cold water swim stress. Together, our studies indicate that stress-induced constitutive activation is a novel mechanism of κOR regulation that plays a critical role in reinstatement of drug seeking.

Effect of pertussis toxin pretreated centrally on blood glucose level induced by stress.

In the present study, we examined the effect of pertussis toxin (PTX) administered centrally in a variety of stress-induced blood glucose level. Mice were exposed to stress after the pretreatment of PTX (0.05 or 0.1 µg) i.c.v. or i.t. once for 6 days. Blood glucose level was measured at 0, 30, 60 and 120 min after stress stimulation. The blood glucose level was increased in all stress groups. The blood glucose level reached at maximum level after 30 min of stress stimulation and returned to a normal level after 2 h of stress stimulation in restraint stress, physical, and emotional stress groups. The blood glucose level induced by cold-water swimming stress was gradually increased up to 1 h and returned to the normal level. The intracerebroventricular (i.c.v.) or intrathecal (i.t.) pretreatment with PTX, a Gi inhibitor, alone produced a hypoglycemia and almost abolished the elevation of the blood level induced by stress stimulation. The central pretreatment with PTX caused a reduction of plasma insulin level, whereas plasma corticosterone level was further up-regulated in all stress models. Our results suggest that the hyperglycemia produced by physical stress, emotional stress, restraint stress, and the cold-water swimming stress appear to be mediated by activation of centrally located PTX-sensitive G proteins. The reduction of blood glucose level by PTX appears to due to the reduction of plasma insulin level. The reduction of blood glucose level by PTX was accompanied by the reduction of plasma insulin level. Plasma corticosterone level up-regulation by PTX in stress models may be due to a blood glucose homeostatic mechanism.

Protective effect of Vitis vinifera and Cichorium intybus on adrenocortical activity in stress induced albino rats

Effects of Vitis vinifera and Cichorium intybus in stress induced albino rats was evaluated by determining their adaptogenic effect on adrenocortical activity. The ethanolic extracts of Vitis vinifera seed and Cichorium intybus roots, at the doses of 250 and 500mg/kg body weight for both the extracts were tested. Cold water swimming stress induced effect on adrenocortical activity in Wistar albino rats was evaluated by measuring their levels of plasma corticosterone and adrenal gland weight. In this study cold water swimming stress of rats exhibited elevation in the plasma corticosterone and adrenal gland weight. Pre-treatment with Vitis vinifera seed and Cichorium intybus roots extracts have significantly prevented elevation in plasma corticosterone level and adrenal gland weight at the tested dose. On the basis of results, it was concluded that Vitis vinifera and Chicorium intybus possess potential antistress activity. The observed antistress effect of Vitis vinifera and Cichorium intybus extracts was found to be through hypothalamic pituitary adrenal axis.

The critical role of spinal 5-HT7 receptors in opioid and non-opioid type stress-induced analgesia

The opioid and non-opioid types of stress-induced analgesia have been well defined. One of the non-opioid type involve the endocannabinoid system. We previously reported that the spinal serotonin 7 receptor (5-HT7) blockers inhibit both morphine and cannabinoid-induced analgesia, thus we hypothesized that descending serotonergic pathways-spinal 5-HT7 receptor loop might contribute to stress-induced analgesia.Stress-induced analgesia was induced with warm (32°C) or cold (20°C) water swim stress in male Balb-C mice. The effects of intrathecal injection of a selective 5-HT7 receptor antagonist, SB 269970, of the denervation of serotonergic neurons by intrathecal administration of 5,7-dihydroxytryptamine (5,7-DHT) and of lesions of the dorsolateral funiculus on opioid and non-opioid type stress-induced analgesia were evaluated with the tail-flick and hot plate tests. The expression of 5-HT7 receptors mRNA in the dorsal lumbar region of spinal cord were analyzed by RT-PCR following spinal serotonin depletion or dorsolateral funiculus lesion. The effects of the selective 5-HT7 receptor agonists LP 44 and AS 19 were tested on nociception.Intrathecal SB 269970 blocked both opioid and non-opioid type stress-induced analgesia. Dorsolateral funiculus lesion or denervation of the spinal serotonergic neurons resulted in a marked decrease in 5-HT7 receptor expression in the dorsal lumbar spinal cord, accompanied by inhibition of opioid and non-opioid type stress-induced analgesia. However, the systemic or intrathecal LP 44 and AS 19 alone did not produce analgesia in unstressed mice.These results indicate that descending serotonergic pathways and the spinal 5-HT7 receptor loop play a crucial role in mediating both opioid and non-opioid type stress-induced analgesia.

Effect of bacopa monniera on cold stress induced neurodegeneration in hippocampus of wistar rats: a histomorphometric study.

Bacopa monniera/ Brahmi,is used over centuries in Ayurvedic medicine for memory development, learning, concentration and other mental illnesses such as nervousness and poor cognition. The present study aims to evaluate the effect of Bacopa monniera (Brahmi, BM) on cold stress induced histological changes in hippocampus of Wistar rats. Total 24 male rats divided into four groups were used (n=6) for this study. Group I was control in which rats were kept under ideal laboratory conditions, Group II was given 40 mg/kg of BM extract, Group III was cold water swim stress in which rats were forced to swim in the cold water maintained at 18±2(o)C till it started to sink for a period of one month and Group IV in which cold water swim stress given for a month followed by oral administration of BM extracts 40mg/kg treatment for a month. The whole study was carried out for a period of 60 d. The animals were sacrificed next day and their brains dissected out for histomorphometric analysis. The diameter, packing density and total number of neurons were calculated from stained histological section by using micrometry in the CA-1 region of the hippocampus. The analysis and plotting of graphs were carried out using Sigma Plot 12 (Systat Software Inc., USA). Values are expressed as Mean ± SEM (n = 6). One way analysis of variance followed by Student-Newman-Keul's multiple comparisons test was used for the comparison of means. A probability of 0.05 and less was taken as statistically significant. The results showed that there is no significant difference in the diameter of the cells between the groups but total number of the cells in Group II was statistically significant when compared with the others groups. Student-Newman-Keuls method showed that Group II and Group IV are statistically significant when compared to Group III (p<0.05). RESULTS indicates that when BM extracts administered orally produce neuroprotective effect in cold stress induced hippocampal neurodegeneration of rats. Hence, the herb BM can possibly be used as an adjuvant to improve memory to combat stress in our day to day life.

How Does Stress-Induced Activation of the Kappa Opioid System Increase Addiction Risk?

How Does Stress-Induced Activation of the Kappa Opioid System Increase Addiction Risk?

Poststress Block of Kappa Opioid Receptors Rescues Long-Term Potentiation of Inhibitory Synapses and Prevents Reinstatement of Cocaine Seeking

Dopaminergic neurons in the ventral tegmental area of the brain are an important site of convergence of drugs and stress. We previously identified a form of long-term potentiation of gamma-aminobutyric acid (GABA)ergic synapses on these neurons (LTPGABA). Our studies have shown that exposure to acute stress blocks this LTP and that reversal of the block of LTPGABA is correlated with prevention of stress-induced reinstatement of cocaine-seeking behavior. Sprague-Dawley rats were subjected to cold-water swim stress. Midbrain slices were prepared following stress, and whole-cell patch clamp recordings of inhibitory postsynaptic currents were performed from ventral tegmental area dopamine neurons. Antagonists of glucocorticoid receptors and kappa opioid receptors (κORs) were administered at varying time points after stress. Additionally, the ability of a kappa antagonist administered following stress to block forced swim stress-induced reinstatement of cocaine self-administration was tested. We found that an acute stressor blocks LTPGABA for 5 days after stress through a transient activation of glucocorticoid receptors and more lasting contribution of κORs. Even pharmacological block of κORs beginning 4 days after stress has occurred reversed the block of LTPGABA. Administration of a κORs antagonist following stress prevents reinstatement of cocaine-seeking behavior. A brief stressor produces changes in the reward circuitry lasting several days. Our findings reveal roles for glucocorticoid receptors and κORs as mediators of the lasting effects of stress on synaptic plasticity. κORs antagonists reverse the neuroadaptations underlying stress-induced drug-seeking behavior and may be useful in the treatment of cocaine addiction.

Therapeutic effect of bone marrow mesenchymal stem cells on cold stress induced changes in the hippocampus of rats.

The present study aims to evaluate the effect of bone marrow mesenchymal stem cells on cold stress induced neuronal changes in hippocampal CA1 region of Wistar rats. Bone marrow mesenchymal stem cells were isolated from a 6-week-old Wistar rat. Bone marrow from adult femora and tibia was collected and mesenchymal stem cells were cultured in minimal essential medium containing 10% heat-inactivated fetal bovine serum and were sub-cultured. Passage 3 cells were analyzed by flow cytometry for positive expression of CD44 and CD90 and negative expression of CD45. Once CD44 and CD90 positive expression was achieved, the cells were cultured again to 90% confluence for later experiments. Twenty-four rats aged 8 weeks old were randomly and evenly divided into normal control, cold water swim stress (cold stress), cold stress + PBS (intravenous infusion), and cold stress + bone marrow mesenchymal stem cells (1 × 106; intravenous infusion) groups. The total period of study was 60 days which included 1 month stress period followed by 1 month treatment. Behavioral functional test was performed during the entire study period. After treatment, rats were sacrificed for histological studies. Treatment with bone marrow mesenchymal stem cells significantly increased the number of neuronal cells in hippocampal CA1 region. Adult bone marrow mesenchymal stem cells injected by intravenous administration show potential therapeutic effects in cognitive decline associated with stress-related lesions.

Intermittent swim stress causes Morris water maze performance deficits in a massed-learning trial procedure that are exacerbated by reboxetine

Various animal models of depression have been used to seek a greater understanding of stress-related disorders. However, there is still a great need for research in this area, as many unanswered questions remain. Therefore, we sought to employ a novel animal model of depression known as intermittent swim stress (ISS). In this model, the animal experiences 100 trials of cold water swim stress. ISS has already shown subsequent immobility in the forced swim test (FST), deficits in instrumental and spatial (spaced-trial procedure), and responsiveness to norepinephrine. We are now examining how this will translate in the Morris water maze for rats in a massed-learning trial procedure, and further assessing ISS sensitivity toward norepinephrine selective anti-depressant drugs. The results indicated no difference in cued learning when the platform was visible in the water maze, but a hidden platform task revealed poorer spatial learning for ISS-exposed rats versus controls. In terms of spatial memory, there was a notable ISS-induced deficit 1h after the learning trials, regardless of performance on the previous platform task. Interestingly, the administration of reboxetine interfered with the spatial learning and memory trials for both ISS and CC groups. As a result, ISS exposure compromised spatial learning and memory in the Morris water maze, and norepinephrine does not appear to be a mediator of this deficit. The results demonstrate a key difference in the effects of reboxetine in a massed- vs. spaced-learning trial procedure in the Morris water maze following ISS exposure.

Prior cold water swim stress alters immobility in the forced swim test and associated activation of serotonergic neurons in the rat dorsal raphe nucleus

Prior adverse experience alters behavioral responses to subsequent stressors. For example, exposure to a brief swim increases immobility in a subsequent swim test 24h later. In order to determine if qualitative differences (e.g. 19°C versus 25°C) in an initial stressor (15-min swim) impact behavioral, physiological, and associated neural responses in a 5-min, 25°C swim test 24h later, rats were surgically implanted with biotelemetry devices 1week prior to experimentation then randomly assigned to one of six conditions (Day 1 (15min)/Day 2 (5min)): (1) home cage (HC)/HC, (2) HC/25°C swim, (3) 19°C swim/HC, (4) 19°C swim/25°C swim, (5) 25°C swim/HC, (6) 25°C swim/25°C swim. Core body temperature (Tb) was measured on Days 1 and 2 using biotelemetry; behavior was measured on Day 2. Rats were transcardially perfused with fixative 2h following the onset of the swim on Day 2 for analysis of c-Fos expression in midbrain serotonergic neurons. Cold water (19°C) swim on Day 1 reduced Tb, compared to both 25°C swim and HC groups on Day 1, and, relative to rats exposed to HC conditions on Day 1, reduced the hypothermic response to the 25°C swim on Day 2. The 19°C swim on Day 1, relative to HC exposure on Day 1, increased immobility during the 5-min swim on Day 2. Also, 19°C swim, relative to HC conditions, on Day 1 reduced swim (25°C)-induced increases in c-Fos expression in serotonergic neurons within the dorsal and interfascicular parts of the dorsal raphe nucleus. These results suggest that exposure to a 5-min 19°C cold water swim, but not exposure to a 5-min 25°C swim alters physiological, behavioral and serotonergic responses to a subsequent stressor.

Sex differences associated with intermittent swim stress

Various animal models of depression have been used to seek a greater understanding of stress-related disorders. However, there is still a great need for novel research in this area, as many individuals suffering from depression are resistant to current treatment methods. Women have a higher rate of depression, highlighting the need to investigate mechanisms of sex differences. Therefore, we employed a new animal model to assess symptoms of depression, known as intermittent swim stress (ISS). In this model, the animal experiences 100 trials of cold water swim stress. ISS has already been shown to cause signs of behavioral depression in males, but has yet to be assessed in females. Following ISS exposure, we looked at sex differences in the Morris water maze and forced swim test. The results indicated a spatial learning effect only in the hidden platform task between male and female controls, and stressed and control males. A consistent spatial memory effect was only seen for males exposed to ISS. In the forced swim test, both sexes exposed to ISS exhibited greater immobility, and the same males and females also showed attenuated climbing and swimming, respectively. The sex differences could be due to different neural substrates for males and females. The goal of this study was to provide the first behavioral examination of sex differences following ISS exposure, so the stage of estrous cycle was not assessed for the females. This is a necessary future direction for subsequent experiments. The current article highlights the importance of sex differences in response to stress.

Physical Exercise Prevents Stress-Induced Activation of Granule Neurons and Enhances Local Inhibitory Mechanisms in the Dentate Gyrus

Physical exercise is known to reduce anxiety. The ventral hippocampus has been linked to anxiety regulation but the effects of running on this subregion of the hippocampus have been incompletely explored. Here, we investigated the effects of cold water stress on the hippocampus of sedentary and runner mice and found that while stress increases expression of the protein products of the immediate early genes c-fos and arc in new and mature granule neurons in sedentary mice, it has no such effect in runners. We further showed that running enhances local inhibitory mechanisms in the hippocampus, including increases in stress-induced activation of hippocampal interneurons, expression of vesicular GABA transporter (vGAT), and extracellular GABA release during cold water swim stress. Finally, blocking GABAA receptors in the ventral hippocampus, but not the dorsal hippocampus, with the antagonist bicuculline, reverses the anxiolytic effect of running. Together, these results suggest that running improves anxiety regulation by engaging local inhibitory mechanisms in the ventral hippocampus.

The longitudinal study of rat hippocampus influenced by stress: Early adverse experience enhances hippocampal vulnerability and working memory deficit in adult rats

Epidemiologic studies indicate that early adverse experience is related to learning disabilities in adults, but the neurobiological mechanisms have not yet been identified. We used longitudinal animal experiments to test the hypothesis that early life stress enhances hippocampal vulnerability and working memory deficit in adult rats. The expression of Synaptophysin (SYN) and apoptosis (Apo) in hippocampal CA3 and dentate gyrus (DG) regions were examined to evaluate the effects of environmental factors on the hippocampus. The working memory errors via radial 8-arm maze were studied to evaluate the long-term effect of early stress on rats’ spatial learning ability. Our results indicated that chronic restraint stress in early life and forced cold water swimming stress in adulthood reduced SYN expression and increased Apo levels in rat hippocampus, but the hippocampal damage tended to recover when rats returned to a non-stress environment. In addition, when the rats were exposed to forced cold water swimming stress during adulthood, SYN expression (CA3 and DG regions) and Apo levels (CA3 region) in rat hippocampus showed statistical difference between early restraint stress group and non-early restraint stress group (rats exposed to stress in adulthood only). One month after the two groups of rats returned to non-stress environment, this difference of SYN expression (CA3 and DG regions) and working memory deficit between the two groups was still statistically significant. Our study findings suggested that early adverse experience enhances hippocampal vulnerability and working memory deficit in adult rats, and reduces structural plasticity of hippocampus.

Oxytocin stimulates adult neurogenesis even under conditions of stress and elevated glucocorticoids

Oxytocin has been linked to social behavior, including social recognition, pair bonding and parenting, but its potential role in promoting neuronal growth has not been investigated. We show here that oxytocin, but not vasopressin, stimulates both cell proliferation and adult neurogenesis in the hippocampus of rats. Oxytocin is also capable of stimulating adult neurogenesis in rats subjected to glucocorticoid administration or cold water swim stress. These findings suggest that oxytocin stimulates neuronal growth and may protect against the suppressive effects of stress hormones on hippocampal plasticity.