Autism is characterized by numerous behavioral impairments, such as in communication, socialization and cognition. Recent studies have suggested that valproic acid (VPA), an anti-epileptic drug with teratogenic activity, is related to autism. In rodents, VPA exposure during pregnancy induces autistic-like effects. Exposure to VPA may alter zinc metabolism resulting in a transient deficiency of zinc. Therefore, we selected zinc as a prenatal treatment to prevent VPA-induced impairments in a rat model of autism. Wistar female rats received either saline solution or VPA (400 mg/kg, i.p) on gestational day (GD) 12.5. To test the zinc supplementation effect, after 1 h of treatment with saline or VPA, a dose of zinc (2 mg/kg, s.c.) was injected. The offspring were tested for abnormal communication behaviors with an ultrasound vocalization task on postnatal day (PND) 11, repetitive behaviors and cognitive ability with a T-maze task on PND 29, and social interaction with a play behavior task on PND 30. Tyrosine hydroxylase protein (TH) expression was evaluated in the striatum. Prenatal VPA decreased ultrasonic vocalization, induced repetitive/restricted behaviors and cognitive inflexibility, impaired socialization, and reduced striatal TH levels compared with control group. Zinc treatment reduced VPA-induced autistic-like behaviors. However, we found no evidence of an effect of zinc on the VPA-induced reduction in TH expression. The persistence of low TH expression in the VPA-Zn group suggests that Zn-induced behavioral improvement in autistic rats may not depend on TH activity.
The bidirectional relationship between the nervous system and the immune system is relevant for homeostatic organism maintenance. Studies from our laboratory showed that 14days of cohabitation with a sick partner (injected with Ehrlich tumor cells-TAE) produced behavioral, neurochemical, endocrinological and immunological changes. This study analyzes the effects of cohabitation with an Ehrlich tumor-bearing animal on ovalbumin (OVA)-induced lung inflammatory response in mice. Pairs of male mice were divided into three groups: naïve, control and experimental. Animals of the naïve group were kept undisturbed being used for the assessment of basal parameters. One animal of each experimental and control pair of mice was immunized with OVA. On ED(0), these OVA-immunized animals received an OVA booster. At this day (D(0)) the experimental mice that were kept undisturbed were inoculated with 5×10(6) Ehrlich tumor cells; their immunized cage-mates were then referred as to CSP ("companion of sick partner"). The undisturbed mice of each control pair were i.p. treated on D(0) with 0.9% NaCl; their sensitized cage-mates were subsequently referred as CHP ("companion of health partner"). The OVA challenge was performed on CSP and CHP mice on ED(12) and ED(13); blood and tissue collection were performed on ED(14). Fourteen days after cohabitation, in comparison to the CHP mice, the CSP mice displayed the following: (1) an increased number of eosinophils and neutrophils in the BAL, (2) a decreased bone marrow cell count, (3) increased levels of IL-4 and IL-5 and decreased levels of IL-10 and IFN-γ in the BAL supernatant, (5) increased levels of IgG1-OVA, decreased levels of IgG2a-OVA and no changes in OVA-specific IgE in the peripheral blood, (6) increased expression of L-selectin in the BAL granulocytes, (7) decreased tracheal reactivity to methacholine measured in vitro, (8) no changes in plasma corticosterone levels and (9) increased levels of plasmatic noradrenaline. These results suggest that allergic lung inflammatory response exacerbation in CSP mice is a consequence of the psychological stress induced by forced cohabitation with the sick partner. Strong involvement of the sympathetic nervous system (SNS) through adrenaline and noradrenaline release and a shift of the Th1/Th2 cytokine profile toward a Th2 response were considered to be the mechanisms underlying the cell recruitment to the animal's airways.
Mast cells, which are the main source of histamine, are significantly affected by sex steroids. The present study was undertaken to determine the effects of bilateral castration and testosterone replacement on peritoneal histamine concentration and lung histamine concentration in pubertal male rats (Wistar strain). Three groups of animals were used in this study: (1) untreated castrated animals, (2) castrated animals subjected to androgen replacement by injection of propionate of testosterone, and (3) intact males as a control group. Castration alone produced a dramatic reduction in peritoneal histamine concentration. In addition, androgen replacement was effective in restoring the histamine concentration to the normal value detected in the control males (P<0·05, Kruskal-Wallis test). On the other hand, there was no significant variation in the lung histamine concentration between control males, untreated castrated males and castrated males that received androgen replacement (P<0·05, Kruskal-Wallis test). These results demonstrate for the first time that castration markedly reduces the peritoneum histamine concentration in pubertal male rats, and testosterone replacement prevents the decrease. Further, these procedures do not affect lung histamine concentration, demonstrating that mast cells from different tissues may respond differently to the same biological factors.
Grooming behaviour has different functions on many species during development and can be observed and affected during periods of stress. By selecting male mice with high (HI) and low (LI) immobility traits in the tail suspension test, a screening for antidepressant drugs, we investigate how these phenotypes associated with grooming behaviour may be influenced by the effects of repeated restraint stress. For this we used the sucrose preference test and the splash test in a novel and a familiar cage performed before and after exposure to 2 days of restraint stress. Animals were submitted to an additional day of restraint stress before the hypothalamus, prefrontal cortex and midbrain extraction for dopamine activity analysis. Corticosterone analysis was made in three distinct moments: without stress (prior first restraint session), immediately after the last restrain, and 1 hr after the last restrain episode. Compared to LI group, HI animals exhibited an increased frequency and decreased time of grooming in the familiar cage. In the novel cage, stress increased frequency and time of grooming of HI animals compared to LI. Corticosterone levels were increased in HI animals after 3 days of stress. Lower hypothalamic dopaminergic activity without stress and decreased hypothalamic dopaminergic activity immediately after stress in HI group were observed. The HI group displayed decreased prefrontal cortex dopaminergic activity and increased activity in the mesolimbic area. We proposed that through the influence of stress the two phenotypes manifested as a resilient (LI) and a not resilient (HI) trait in response to restraint stress.
Heat stress has been related to the impairment of behavioral and immunological parameters in broiler chickens. However, the literature is not clear on the involvement of neuroimmune interactions in a heat stress situation associated with bacterial and parasitic infections. The present study evaluated the production of monoamines and their metabolites in brain regions (rostral pallium, hypothalamus, brain stem, and midbrain) in broiler chickens submitted to chronic heat stress and/or infection and co-infection with Eimeria spp. and Clostridium perfringens type A. The heat stress and avian necrotic enteritis (NE) modulated the neurochemical profile of monoamines in different areas of the central nervous system, in particular, those related to the activity of the hypothalamus-hypophysis-adrenal (HPA) axis that is responsible for sickness behavior. C. perfringens and/or Eimeria infection, heat stress increased 5-hydroxytryptamine (5-HT), 4,4 dihydroxyphenylacetic acid (DOPAC), and DOPAC/dopamine (DA) in the rostral pallium; 3-methoxy-4-hydroxyphenylethylene glycol (MHPG), homovanillic acid (HVA), HVA/DA, DOPAC/DA, and 5-hydroxyindoleacetic acid (5-HIAA)/5-HT in the hypothalamus; MHPG, 5-HIAA/5-HT, DOPAC/DA, and HVA/DA in the midbrain; and MHPG, DOPAC, HVA, HVA/DA, DOPAC/DA, and 5-HIAA/5-HT in the brainstem. Heat stress decreased noradrenaline + norepinephrine (NOR + AD) in all brain regions analyzed; 5-HT in the hypothalamus, midbrain, and brainstem; and DA in the midbrain. The results also showed the existence and activity of the brain-gut axis in broiler chickens. The brain neurochemical profile and corticosterone production are consistent with those observed in chronic stressed mammals, in animals with sickness behavior, and an overloading of the HPA axis.
This study reports that short-term social instability stress (SIS) in adolescence increases passive-coping in adulthood in male mice. Short-term SIS decreased the latency of immobility and increased the frequency and time of immobility in tail suspension test. These findings support the hypothesis that adolescent stress can induce a passive adaptation to stress in adulthood, even if it is a short period of stress.
We have shown that myocardial dysfunction induced by food restriction is related to calcium handling. Although cardiac function is depressed in food-restricted animals, there is limited information about the molecular mechanisms that lead to this abnormality. The present study evaluated the effects of food restriction on calcium cycling, focusing on sarcoplasmic Ca 2+ -ATPase (SERCA2), phospholamban (PLB), and ryanodine channel (RYR2) mRNA expressions in rat myocardium. Male Wistar-Kyoto rats, 60 days old, were submitted to ad libitum feeding (control rats) or 50% diet restriction for 90 days. The levels of left ventricle SERCA2, PLB, and RYR2 were measured using semi-quantitative RT-PCR. Body and ventricular weights were reduced in 50% food-restricted animals. RYR2 mRNA was significantly decreased in the left ventricle of the foodrestricted group (control = 5.92 ± 0.48 vs food-restricted group = 4.84 ± 0.33, P < 0.01). The levels of SERCA2 and PLB mRNA were similar between groups (control = 8.38 ± 0.44 vs food-restricted group = 7.96 ± 0.45, and control = 1.52 ± 0.06 vs food-restricted group = 1.53 ± 0.10, respectively). Down-regulation of RYR2 mRNA expressions suggests that chronic food restriction promotes abnormalities in sarcoplasmic reticulum Ca 2+ release. Key wordsFood restriction induces beneficial health effects such as increased longevity and retards or prevents a broad spectrum of agerelated pathophysiological changes such as loss of skeletal muscle mass, diabetes mellitus, hypertension, and cancer (1-3). Recent research from our laboratory has shown that 50% food restriction promotes left ventricular dysfunction and increases contraction and relaxation times in isolated papillary muscle of both young Wistar-Kyoto normotensive and spontaneously hypertensive rats (4-7). Sugizaki et al. (7) observed that myocardial dysfunction in food-restricted rats is related to calcium handling. However, these investigators were unable to identify calcium handling site abnormalities.Few studies have analyzed the molecular
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