Protective role of the ginsenoside Rg1 against methimazole-induced gestational hypothyroidism on reflexive behaviors, conditioned fear and cortical antioxidant levels in mice offspring.

Ginsenoside Rg1(Rg1), a monomer of a tetracyclic triterpenoid derivative, possesses diverse medicinal properties attributed to its unique chemical structure and may have beneficial effects on fetal development. This study aimed to investigate the protective effects of prenatal exposure to Rg1 against Methimazole-induced gestational hypothyroidism on reflexive behaviors, conditioned fear, and cortical antioxidant levels in mouse offspring.40 female virgin mice and 12 male NMRI mice were assigned to four groups: group 1 served as the control, group 2 received Methimazole(MMI) at a concentration of 0.02% in their drinking water, group 3 received Rg1(150 mg/kg), and group 4 received both MMI and Rg1.Groups of 2-4 were administered the substances from days 1-9 of gestation. After delivery, pups were selected, and reflexive motor behaviors and conditioned fear were assessed. Additionally, levels of brain tissue catalase(CAT), malondialdehyde(MDA), superoxide dismutase(SOD), and glutathione peroxidase(GPx) levels were measured. Furthermore, postpartum immobility time in the forced swimming test (FST), tail suspension test (TST), and the number of squares crossed in the open field test (OFT)were determined. The results demonstrated that maternal exposure to Rg1 improved ambulation score, hind-limb suspension score, grip strength, front-limb suspension, hind-limb foot angle, negative geotaxis, surface righting, and conditioned fear in hypothyroidism-induced offspring(P<0.05). Rg1 decreased immobility time in the FST, and TST, and increased the number of squares crossed in the OFT in postpartum hypothyroidism-induced mice(P<0.05). Moreover, Rg1 reduced brain tissue MDA levels and increased brain tissue CAT, SOD, and GPx levels in mice and their offspring(P<0.05). These findings indicate that Rg1 mitigated postpartum depression in mice and improved reflexive motor behaviors in their pups.

Role of the intracerebroventricular injection of the visfatin and its interaction with neuropeptide Y and nitric systems on food intake in neonatal chicken.

Visfatin play an essential role in the central regulation of appetite in birds. This study aimed to determine role of intracerebroventricular (ICV) injection of the visfatin on food intake and its possible interaction with neuropeptide Y (NPY) and nitric oxide system in neonatal broiler chicken. In experiment 1, neonatal chicken received ICV injection visfatin (1, 2 and 4 µg). In experiment 2, chicken received ICV injection of B5063 (NPY1 receptor antagonist 1.25 µg), visfatin (4 µg) and co-injection of the B5063 + Visfatin. In experiments 3-6, SF22 (NPY2 receptor antagonist 1.25 µg), SML0891 (NPY5 receptor antagonist 1.25 µg), L-NAME (nitric oxide synthase inhibitor, 100 nmol) and L-arginine (Precursor of nitric oxide, 200 nmol) were injected instead of B5063. Then the amount of cumulative food was measured at 30, 60 and 120 min after injection. Obtained data showed, injection visfatin (2 and 4 µg) increased food intake compared to control group (P < 0.05). Co-injection of the B5063 + Visfatin decreased visfatin-induced hyperphagia compared to control group (P < 0.05). Co-injection of the L-NAME + Visfatin amplified visfatin-induced hyperphagia compared to control group (P < 0.05). The result showed that visfatin has hyperphagic role and this effect mediates via NPY1 and nitric oxide system in neonatal chicken.

Effects of in ovo injection of the L-carnosine on physiological indexes of neonatal broiler chicken.

The objective of the present investigation was to ascertain the impact of in ovo administration of L-carnosine on physiological indicators in neonatal broiler chickens. A total of 280 viable broiler eggs were allocated to 7 distinct groups: control, Sham in ovo injection of sterile water on d 7 of incubation. Groups 3 and 4 were subjected to in ovo injections of L-carnosine (25 and 50 µg) on d 7 of incubation. Group 5, functioning as a sham in ovo, received an injection of sterile water on d 18 of incubation. Groups 6 and 7 were in ovo injected with L-carnosine (25 and 50 µg) on d 18 of incubation. All eggs were subjected to incubation, and the hatching rate and body weight were measured post-hatch. Subsequently, blood samples were collected, and the levels of biochemical constituents in the serum were determined. Based on the outcomes, the administration of L-carnosine (50 µg) on d 7 of incubation led to a significant increase in post-hatch body weight compared to the control group (P < 0.05). The in ovo injection of L-carnosine (25 and 50 µg) on d 7 and 18 of incubation resulted in a significant decrease in the levels of serum glucose, triglyceride (TG), low-density lipoprotein (LDL), phosphorus (P), alkaline phosphatase (ALP), aspartate aminotransferase (AST), and alanine transaminase (ALT) in the newly hatched chickens (P < 0.05). Furthermore, the in-ovo injection of L-carnosine (25 and 50 µg) on d 7 and 18 of incubation led to a significant increase in the levels of serum high-density lipoprotein (HDL), calcium, and total protein (TP) in the newly hatched chickens (P < 0.05). Nonetheless, L-carnosine did not have a significant effect on the levels of serum IgY and IgA in the newly hatched chickens (P > 0.05). These findings indicate that the in ovo administration of L-carnosine yielded favorable outcomes in neonatal broiler chickens.

Central effects of the serotoninergic, GABAergic, and cholecystokinin systems on neuropeptide VF (NPVF)-induced hypophagia and feeding behavior in neonatal broiler chicken.

The study was performed to evaluate the role of central serotoninergic, GABAergic, and cholecystokinin systems in neuropeptide VF (NPVF)-induced hypophagia in broiler chickens. In this study, 9 experiments were designed, each with one control and three treatment groups (n = 44 in each experiment). Control chicks of all groups were subjected to normal saline + Evans blue 0.1 % Intracerebroventricular (ICV) injection. In the first experiment, 3 groups of chicks received NPVF (4, 8, and 16 nmol). In experiment 2-9, one group of chicks received NPVF (16 nmol), another received 10 µg fluoxetine (serotonin reuptake inhibitor) (experiment 2), 1.25 µg PCPA (serotonin synthesis inhibitor) (experiment 3), 1.5 µg SB-242,084 (5-HT2C receptor antagonist) (experiment 4), 15.25 nmol 8-OH-DPAT (5-HT1A receptor antagonist) (experiment 5), 0.5 µg picrotoxin (GABAA receptor antagonist) (experiment 6), 20 ng CGP54626 (GABAB receptor antagonist) (experiment 7), 1 nmol devazepide (CCKA receptor antagonist) (experiment 8), and 1 nmol/L-365(-|-),260 (CCKB receptor antagonist) (experiment 9), and another final group received combination of specific neurotransmitter + NPVF Then, the cumulative food intake was measured until 120 min post-injection. ICV injection of NPVF (8 and 16 nmol) significantly decreased food intake (P < 0.05). Simultaneous injection of fluoxetine + NPVF and also picrotoxin + NPVF significantly increased hypophagia caused by NPVF (P < 0.05). However, co-administration of PCPA + NPVF and also SB242084 + NPVF significantly decreased NPVF-induced hypophagia (P < 0.05). Finally, 8-OH-DPAT, CGP54626, devazepide, and L-365,260 had no effect on the hypophagia brought on by NPVF (P > 0.05). Count-type behaviors were dose-dependent and decreased in groups that received NPVF compared to the control group (P < 0.05). Our finding recommended an interconnection between central NPVF and serotoninergic, GABAergic, and cholecystokinin systems in neonatal chickens.

Resveratrol plays neuroprotective role on ketamine-induced schizophrenia-like behaviors and oxidative damage in mice.

This study aimed to determine effects of the resveratrol on ketamine-induced schizophrenia-like behaviors and oxidative damage in mice. Twenty-four male mice were allocated into four experimental groups as control, ketamine (20 mg/kg), resveratrol (80 mg/kg) and co-administration of the ketamine (20 mg/kg) + resveratrol (80 mg/kg). Mice were received resveratrol for 30 days and ketamine was used for an animal model of schizophrenia and was injected from days 16 to 30 of the study. After the drug administration was finished, schizophrenia-like behaviors were evaluated using object recognition test, tail suspension test, forced swimming test and open field test and brain malondialdehyde, glutathione peroxidase, superoxide dismutase and catalase levels were determined. According to the results, ketamine treatment significantly decreased body weight and pretreatment with resveratrol elevated body weight compared to ketamine group (P < 0.05). Ketamine treatment significantly decreased number of the cross in open field test and pretreatment with resveratrol improved i (P < 0.05). Immobility time in tail suspension and forced swimming tests increased in mice treated with ketamine (P < 0.05). Pretreatment with resveratrol diminished immobility time compared to ketamine group (P < 0.05). Ketamine significantly decreased memory deficits while pretreatment with resveratrol significantly reduced the memory deficits induced by ketamine (P < 0.05). Brain MDA increased in both cortical and sub-cortical area in ketamine treated mice while pretreatment with resveratrol decreased ketamine-induced elevation in MDA (P < 0.05). Ketamine significantly decreased brain SOD, GPx and CAT levels while pretreatment with resveratrol improved SOD, GPx and CAT levels (P < 0.05). Findings suggested resveratrol has neuroprotective effects against ketamine-induced behavioral deficits and oxidative damages.

Maternal music exposure during pregnancy influences reflexive motor behaviors in mice offspring.

Evidence supports that music can modulate many physiological roles, exerting clear effects on the central nervous system. For this effect to be positive, music should be tuned at a frequency of 432 Hz. This study aims to determine the effects of prenatal exposure to music on reflexive motor behaviors in mice offspring. Six pregnant female NMRI mice (8-10 weeks old) were randomly and equally allocated into two groups. Group 1 as control was placed in a normal housing area (average room noise 35 dB), and Group 2 was exposed to music pitched at 432 Hz for 2 h a day played at constant volume (75/80 dB) during pregnancy. Following delivery, four pups from each pregnant mouse were selected, and reflexive motor behaviors including ambulation, hind-limb foot angle, surface righting, grip strength, front- and hind-limb suspension, and negative geotaxis were determined. Based on the findings, prenatal exposure to music significantly increased ambulation score, grip strength, and front- and hind-limb suspension compared to the control group (P < 0.05). Also, prenatal exposure to music significantly decreased hind-limb foot angle, negative geotaxis, and surface righting compared to the control group (P < 0.05). These results suggested that music exposure during pregnancy had a significant positive effect on all tested reflexive motor behaviors in mice offspring.

Maternal supplementation of L-carnosine improves reflexive motor behaviors in mice offspring.

This study aimed to investigate the effect of maternal supplementation of L-carnosine on improved reflexive motor behaviors in mice offspring. Forty pregnant female NMRI mice were allocated into four groups. In the control group, mice received water, while in groups 2-4, female mice received supplementation of the L-carnosine (0.001, 0.01, or 0.1 mg/kg) at gestation days (G.D.) 5, 8, 11, 14, and 17. Newborn male pups were selected, and reflexive motor behaviors were analyzed on days 5, 7, 10, and 10-15, respectively. Serum malondialdehyde(MDA), superoxide dismutase(SOD), glutathione peroxidase(GPx) and total antioxidant status(TAS) of was determined in offspring's. According to findings, prenatal supplementation of the L-carnosine significantly increased ambulation score, surface righting, hind-limb suspension score, grip strength, front-limb suspension time, and negative geotaxis in mice offspring (P < 0.05). Hind-limb foot angle decreased in mice offspring by maternal supplementation of the L-carnosine (P < 0.05). Prenatal supplementation of the L-carnosine significantly decreased the MDA and increased the SOD, GPx, and TAS levels in offspring (P < 0.05). These results suggested maternal supplementation of the L-carnosine improved reflexive motor behaviors and antioxidant status in mice offspring.

Effect of troxerutin consumption during gestation period on reflexive motor behavior in mice offspring.

This study aimed to determine the effects of troxerutin consumption during gestation on reflexive motor behavior in mice offspring. Forty pregnant female mice were allocated into four groups. In the control group, mice received water, while in groups 2-4, female mice p.o. administered troxerutin (50, 100, and 150 mg/kg) at 5, 8, 11, 14, and 17 days of gestation (GD). Following delivery, pups were selected based on their experimental group, and reflexive motor behaviors were determined. Also, serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and total antioxidant status (TAS) were determined. Based on the findings, maternal exposure to troxerutin (100 and 150 mg/kg) increased ambulation scores in offspring's compared with control group (P < 0.05). Also, prenatal exposure to troxerutin increased front- and hind-limb suspension scores in newborns compared with control group (P < 0.05). Maternal exposure to troxerutin increased grip strength and negative geotaxis in newborns in comparison with control mice (P < 0.05). Prenatal exposure to troxerutin (100 and 150 mg/kg) decreased hind-limb foot angle and surface righting in pups compared with control group (P < 0.05). Maternal exposure to troxerutin decreased MDA production and increased SOD, GPx, and TAS levels in offspring (P < 0.05). These results suggested that prenatal consumption of the troxerutin improves reflexive motor behaviors in mice pups.

Protective effect of crocin on cuprizone-induced model of multiple sclerosis in mice.

Crocin is the main bioactive components of the saffron which has positive role in the nervous system; however, its neuroprotective activity is not fully elicited. So, the aim of the current study was to determine effects of the crocin on reflexive motor and anti-depressive behaviors as well as serum and brain tissue antioxidant activities in cuprizone-induced (CPZ) model of multiple sclerosis (MS) mice. Forty male C57BL/6 mice were randomly assigned into 4 groups. Mice in the control group were received normal diet. In group 2, mice received normal diet and orally received crocin (100 mg/kg) 3 times per week for 5 weeks. In group 3, CPZ-induced demyelination was done by chew palate containing 0.2% (w/w) CPZ for 5 weeks. In group 4, mice feed CPZ containing diet and orally received crocin (100 mg/kg) three times per for 5 weeks. After determination of the MS signs, reflexive motor behavior and depressive tests were done. Also, serum and brain tissue antioxidant activity was determined. According to the data, CPZ had negative effects on hind-limb foot angle, hind- and front-limb suspension, surface righting, grip strength, and negative geotaxis while crocin improved it. Co-administration of the CPZ + crocin reversed effect of the CPZ on the reflexive motor behaviors. CPZ increased immobility time in the forced swimming test (FST) and tail suspension test (TST), while co-administration of the CPZ + crocin reversed effect of the CPZ on immobility time. CPZ decreased number of cross in open field test (OFT) and spending time on rotarod, while co-administration of the CPZ + crocin reversed effect of the CPZ. Malondialdehyde (MDA) production increased, and glutathione peroxidase (GPx), superoxide dismutase (SOD), and total antioxidant status (TAS) levels decreased in serum and brain tissue of the mice treated with CPZ. Pretreatment with crocin decreased adverse effect of the CPZ on serum and brain tissue antioxidants. These results suggested crocin has protective effect against CPZ-induced MS in mice.

Resveratrol exerts anxiolytic-like effects through anti-inflammatory and antioxidant activities in rats exposed to chronic social isolation.

Emerging evidence has confirmed resveratrol's (RES) antioxidant, anti-inflammatory, and antidepressant effects. The beneficial effects of RES were confirmed for several emotional and cognitive deficits. This research aimed to assess the impacts of RES on behavior and hippocampal levels of anti-inflammatory and pro-inflammatory factors in rats exposed to chronic social isolation (SI) stress, which is known to induce mental disorders such as depressive-like behavior. The animals were treated by RES (20, 40, or 80 mg/kg/intraperitoneally) for 28 days following a 28-day exposure to stress. Behavioral tests, including the forced swim test (FST), open-field test (OFT), tail suspension test (TST), and sucrose preference test (SPT), assessed depressive symptoms. Finally, the animals were sacrificed, and molecular studies (qPCR and ELISA) were performed. Exposure of animals to SI dramatically increased the immobility of animals in TST and FST, enhanced the time spent in the open-field peripheral zone of the OFT, and reduced the sucrose preference rate. In addition, SI increased serum levels of corticosterone and hippocampal content of MDA, whereas it reduced hippocampal SOD and CAT activities. Moreover, SI upregulated the expression of IL-10, IL-18, and IL-1ß and downregulated the expression of TGF-ß in the hippocampus. RES treatment (40 & 80 mg/kg) significantly improved the behavioral alterations through the modulation of neuroinflammation and oxidative stress. The 20 mg/kg RES dose was inefficient for treating SI-induced depressive-like behavior. These results indicated that RES attenuated depressive-like behavior in prolonged stressed animals. These properties might be associated with RES-mediated improvements in serum corticosterone and hippocampal inflammatory and oxidative stress biomarkers.

Study of fear and fear evoking stimuli in a population of domestic dogs in Iran: A questionnaire-based study.

General and social acceptance, condition, and rules for dog ownership in Iran are different from western countries. So, this phenomenon leads dissimilar fear and fear evoking stimuli in dogs. So, stress and fear­related factors and dog's behavioral problems is not fully studied in Iran. Thus, the aim of the current study was to measuring fear­related factors in dogs in Iran. In the first part of this study demographic information of the owners and dogs were collected using questionnaire from clinics and veterinary hospitals in Tehran. In the second part behavioral tests was done. Questionnaire data were recorded based on 4 items as neuroticism, fear caused by other dogs, fear caused by human and separation behavior. The social contact test was used to determine dog's experience for greeting, cooperation, and handling. According to the results, 69.3% of the dog owners were women and 30.7% men. 84.1% of the dogs were small breeds and 15.9% large­breed dogs. 63.6% of the owner's complained for impact of laws and prohibitions on their dogs' access to outdoor. The score for greeting, cooperation and handling were 1.76 ± ± 0.93, 3.06 ± 1.25 and 2.44 ± 1.21, respectively. Mean score for neuroticism, fear caused by other dogs, fear caused by human and separation behavior were 29.69 ± 9.24, 14.75 ± 5.38, 9.84 ± 4.05 and 6.57 ± 3.05, respectively. Principal component analysis (PCA) revealed fear using neuroticism, fear caused by other dogs and human were 1st fear related factor while separation­related behavior was the 2nd priority (P = 0.001). Small­breed dogs had more separation behavior and fear caused by other dogs compared to the large­breed dogs (P = 0.001). These findings suggested keeping the dogs indoor with limit access to a yard had negative impact on dog's behaviors. Legal restrictions have adverse effect on fear behavior in dogs. Determination of fear­related factors might prove useful for dog's behavioral intervention in Iran.

Possible interaction of central noradrenergic, serotoninergic and oxytocin systems with nesfatin-1 induced hypophagia and feeding behavior in newborn broiler.

There are some differences between mammals and birds in terms of central food intake regulation. In avian species, the hypophagic role of nesfatin-1 has not been investigated with other neurotransmitters. Therefore, this study aimed to determine the alteration of feeding behavior following intracerebroventricular (ICV) injection of nesfatin-1 and its possible interaction with central noradrenergic, serotoninergic, and oxytocin systems in newborn broiler chicks. In experiment 1, birds received ICV injection of phosphate-buffered saline (PBS), prazosin (α1 receptors antagonist, 10 nmol), nesfatin-1 (40 ng), and co-administration of prazosin and nesfatin-1. Experiments 2-10 were similar to experiment 1, except that yohimbine (α2 receptors antagonist, 13 nmol), metoprolol (ß1 receptors antagonist, 24 nmol), IC1118,551 (ß2 receptors antagonist for, 5nmol), SR59230R (ß3 receptors antagonist, 20 nmol), fluoxetine (serotonin reuptake inhibitor, 10 µg), PCPA (serotonin synthesis inhibitor, 1.5 µg), 8-OH-DPAT (5-HT1A receptors agonist, 15.25 nmol), SB242084 (5-HT2C receptors antagonist,1.5 µg) and tocinoic acid (oxytocin receptors antagonist, 2 µg) were injected instead of prazosin. Immediately after the injection, food consumption and behavioral traits were recorded. Nesfatin-1 decreased food consumption (P < 0.05). Nesfatin-1 along with ICI118551 decreased food consumption (P < 0.05). The nesfatin-1- induced hypophagia were reduced by the simultaneous injection of PCPA and nesfatin-1 (P < 0.05). Nesfatin-1induced hypophagia were decreased by the simultaneous injection of SB242084 (P < 0.05). The nesfatin-1 -induced hypophagia were abolished by the simultaneous injection of the tocinoic acid and nesfatin-1 (P < 0.05). ICV injection of the nesfatin-1 decreased the number of steps, jumps, exploratory food, and pecks (P < 0.05) with no effect on drink pecks (P > 0.05). Nesfatin-1 significantly decreased standing time and increased both sitting time and rest time (P < 0.05). Nesfatin-1 could play an important role in feeding behavior, and its hypophagic effects were mediated by ß2 adrenergic, 5-HT2C serotoninergic, and oxytocin receptors in neonatal chickens.

Parental exposure of Tadalafil has beneficial effect on reflexive motor behaviors in mice offspring.

Tadalafil has positive effects on neurodevelopment and antioxidant defense system, but there is no information for its possible role during gestation on reflexive motor behavior in offspring. So current study determined the effect of prenatal exposure to the Tadalafil on reflexive motor behaviors and antioxidant activity in mice offspring and antidepressive behaviors in postpartum dams. Forty pregnant female NMRI mice were allocated into four groups. In control group, mice received water while in Groups 2-4, female mice orally gavage with Tadalafil (0.4, 0.8, and 1.6 mg/kg) at gestation day (GD) 5, 8, 11, 14, and 17, respectively. Following delivery, pups were selected and reflexive motor behaviors determined using ambulation, hind-limb foot angle, surface righting, hind-limb strength, grip strength, front-limb suspension, and negative geotaxis tests. Also, serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and total antioxidant status (TAS) were determined in offspring. On Day 2 postpartum, antidepressant activity of Tadalafil was determined by open field test (OFT), rotarod, forced swimming test (FST), and tail suspension test (TST) in dams. Based on the findings, maternal exposure to Tadalafil improved ambulation score, hind-limb suspension score, grip strength, and front-limb suspension in offspring (P < 0.05). Prenatal exposure to Tadalafil decreased surface righting, hind-limb foot angle, and negative geotaxis in offspring (P < 0.05). Tadalafil decreased blood MDA and increased SOD and GPx levels in offspring (P < 0.05). Tadalafil significantly decreased immobility time in FST and TST and increased number of squares crossed in OFT and spending time on rotarod on postpartum mice (P < 0.05). These results suggested that parental exposure of Tadalafil has positive effect on reflexive motor and postpartum behaviors.

Effects of intracerebroventricular injection of spexin and its interaction with NPY, GalR2 and GalR3 receptors on the central food intake regulation and nutritional behavior in broiler chickens.

Food intake and appetite in birds can be adjusted by the complex homeostatic control mechanisms. There seem to be many similarities between mammalian and avian species in terms of the regulatory feeding systems. Therefore, the aim of this study was to investigate the effects of ICV injection of spexin and its interaction with GalR and NPY receptors on central food intake regulation and nutritional behavior in broiler chickens. In experiment 1, chicken received ICV injection of saline, spexin (2.5 nmol), spexin (5 nmol) and spexin (10 nmol). In experiment 2, birds received ICV injection of saline, B5063 (NPY1 receptor antagonist 1.25 µg), spexin (10 nmol) and B5063 + spexin. In experiments 3-6, SF22 (NPY2 receptor antagonist,1.25 µg), ML0891 (NPY5 receptor antagonist,1.25 µg), M871 (GalR2 receptor antagonist,10 nmol) and SNAP37889 (GalR3 receptor antagonist,10 nmol) were injected in chickens instead of B5063. Then food intake was measured until 120 min after the injection and nutritional behavior was monitored at 30 min after the injection. Based on the data, a dose-dependent hypophagia was observed by the injection of spexin (P < 0.05). Concomitant injection of B5063 + spexin enhanced spexin-induced hypophagia (P < 0.05). Co-injection of SNAP37889 + spexin (10 nmol) attenuated -induced hypophagia (P < 0.05). Spexin (5 and 10 nmol) decreased number of steps, jumps, the exploratory food and pecks at 15 min after the injection (P < 0.05). Spexin (5 and 10 nmol) decreased standing time while siting time and rest time increased at 10 min after injection (P < 0.05). Based on observations, spexin-induced hypophagia could be mediated by NPY1 and GalR3 receptors in neonatal broiler chickens.

Betaine Ameliorates Depressive-Like Behaviors in Zinc Oxide Nanoparticles Exposed Mice.

The aim of the current study was to determine protective effects of betaine on depressive-like behaviors in zinc oxide nanoparticles (ZnO NPs) exposed mice. Forty male mice randomly allocated into four experimental groups. Group 1 kept as control and groups 2-4 received oral administration of betaine (30 mg/kg), ZnO NPs (600 mg/kg), and ZnO NPs (600 mg/kg) 1 h after pre-administration of betaine (30 mg/kg) for 7 days, respectively. Then, forced swimming test (FST), tail suspension test (TST), open field test (OFT), and rotarod tests were done. Furthermore, serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and total antioxidant capacity (TAC) levels were determined. Hippocampal tissue samples were collected for histopathological assessment. According to the results, treatment with ZnO NPs significantly increased immobility time in the FST and TST (P<0.05). Betaine significantly decreased immobility time in the FST and TST (P<0.05). Pretreatment with betaine significantly decreased ZnO NPs-induced alterations in the FST and TST (P<0.05). The duration of staying on the rotarod and the numbers of crossings in the OFT significantly decreased in the mice that received ZnO NPs (P<0.05). These results were significantly improved in betaine+ZnO NPs treated mice as compared to the ZnO NPs group (P<0.05). Treatment with ZnO NPs significantly increased serum MDA level while decreased SOD and GPx compared to the control group (P<0.05). These changes were effectively ameliorated by pretreatment with betaine compared to the ZnO NPs group (P<0.05). No significant effect on serum TAC level was observed in all groups (P˃0.05). Administration of ZnO NPs decreased the thickness of hippocampus and pyramidal neurons in the hippocampal dentate gyrus (DG) and CA1 regions were sparsely arranged. Pretreatment with betaine caused an improvement in the histological features of the hippocampus when compared with ZnO NPs-treated mice. Taken together, these results suggest that betaine has protective role against ZnO NPs-induced toxicity in mice.

Prenatal exposure to α-pinine improves reflexive motor behaviours in mice offspring.

α-pinene is a well-known compound representative of the monoterpenes group with a wide range of pharmacological activities. This article aims to determine effects of the prenatal exposure to α-pinene on reflexive motor behaviours in mice offspring. Forty pregnant female NMRI mice (8-10 weeks old) were allocated into four groups. Group 1 served as control and groups 2-4 were intraperitoneally (i.p.) injected α-pinene (0.1, 0.5 and 1 mg/kg) on 5, 8, 11, 14 and 17 days of gestation (GD). The control group was injected with saline at the same days. Following delivery, 20 pups from each litter were selected and reflexive motor behaviours determined using ambulation, hindlimb foot angle, surface righting, hindlimb strength, grip strength, front-limb suspension and negative geotaxis tests. Based on the findings of the present study, maternal exposure to α-pinene increased ambulation score, hind-limb suspension score, grip strength, front-limb suspension compared with the control group (P < 0.05). Also, prenatal exposure to α-pinene decreased surface righting, hind-limb foot angle and negative geotaxis in mice offspring compared with the control group (P < 0.05). α-pinene (0.1, 0.5 and 1 mg/kg) decreased blood MDA and increased SOD and GPx levels in mice offspring (P < 0.05). These results suggested α-pinene exposure during pregnancy has positive effect on reflexive motor behaviours in mice offspring possibly due to its antioxidant properties.

Effects of the prenatal exposure to crocin in the expression of withdrawal syndrome on reflexive motor behaviors in mice offspring's.

The aim of the current study was to determine effects of the prenatal exposure to crocin in the expression of withdrawal syndrome on reflexive motor behaviors in mice offspring's. Fourteen male mice and 56 adult female mice were randomly divided into seven groups as: control group (morphine-abstinent male and female); group 2, drug-naïve female and morphine-abstinent male; group 3, drug-naïve male and morphine-abstinent females; group 4, drug-naïve male and female. Groups 5-7, were similar to groups 2-4, except crocin (5 mg/kg) were injected to drug-naïve subjects. Following delivery, 20 pups from each litter were selected and behavior and reflexive motor behaviors were determined. Also, blood samples were taken to determine serum antioxidant activity. According to the results, immobility time significantly increased in offspring of the paternal + maternal exposed to morphine swimming test and tail suspension tests (P < 0.05) and significantly decreased in offspring of paternal + maternal exposed to morphine + crocin group (P < 0.05). Ambulation, surface righting, hind-limb suspension, grip strength and front limb suspension significantly decreased in offspring of the mice exposed to morphine (P < 0.05) and significantly improved in offspring of paternal + maternal exposed to morphine + crocin group (P < 0.05). Hind-limb foot angle and negative geotaxis significantly increased in mice with morphine-exposed offspring's (P < 0.05) while improved in offspring of paternal + maternal exposed to morphine + crocin group (P < 0.05). Prenatal exposure to morphine increased Malondialdehyde while decreased Superoxide dismutase, Glutathione peroxidase and total antioxidant status in mice offspring's (P < 0.05) and these results reversed by prenatal exposure to crocin (P < 0.05). In all studied factors, paternal + maternal exposed to morphine + crocin group had better results compared to the other crocin-received drug-naïve groups (P < 0.05). These results suggested prenatal exposure to crocin decreased morphine-induced adverse effect which paternal and maternal exposed to morphine + crocin had the highest prevention against these effects in mice offspring's.

Mediatory role of the central NPY, melanocortine and corticotrophin systems on phoenixin-14 induced hyperphagia in neonatal chicken.

Animal research indicates the neuropeptide Y (NPY), corticotrophin and melanocortin systems have a mediatory role in reward, however, how these substances interact with phenytoin-14 (PNX-14) induced food intake in birds remains to be identified. Accordingly, in this research eight tests were carried out to investigate the potential interactions of the NPY, melanocortin, as well as corticotrophin systems with PNX-14 on food consumption in neonatal chickens. In the first experiment, chickens were intracerebroventricular (ICV) injected with phosphate-buffered saline (PBS) and PNX-14 (0.8, 0.16, and 3.2 nmol). In second experiment, PBS, the antagonist of CRF1/CRF2 receptors (astressin-B, 30 µg) and PNX-14 + astressin-B were injected. In the rest of the experiments chicken received astressin2-B (CRF2 receptor antagonist; 30 µg), SHU9119 (MCR3/MCR4 receptor antagonist, 0.5nomol), MCL0020 (MCR4 receptor agonist, 0.5 nmol), B5063 (NPY1 receptor antagonist, 1.25 µg), SF22 (NPY2 receptor antagonist, 1.25 µg) and SML0891 (NPY5 receptor antagonist, 1.25 µg) rather than astressin-B. Then, cumulative intake of food was recorded for 2 h. Based on the findings, PNX-14 (0.16 and 3.2 nmol) led to increment in food consumption compared with the control (P < 0.05). Co-administration of the PNX-14 and astressin-B promoted PNX-14-induced hyperphagia (P < 0.05). Co-injection of the PNX-14 + astressin2-B potentiated hyperphagia PNX-14 (P < 0.05). Co-injection of PNX-14 + B5063 inhibited the effects of the PNX-14 (P < 0.05). The co-administration of the PNX-14 and SML0891 potentiated hypophagic effects of the PNX-14 (P < 0.05). The results showed that PNX-14-induced hyperphagia mediates via NPY1, NPY5, and CRF1/CRF2 receptors in neonatal chickens.

Central and peripheral methylamine-induced hypophagia is mediated via nitric oxide and TAAR1 in neonatal layer-type chicken.

The aim of the current study was to determine effects of intracerebroventricular (ICV) and intraperitoneal (i.p.) administration of Methylamine (MET) and possible interactions with nitric oxide (NO) and TAAR1 pathways in 24-h fasted (FD24) and ad libitum layer-type chicken. In experiment 1, FD24 chicken ICV injected with MET (15, 30, 45, 60 and 75 µg). In experiment 2, ICV injection of MET (15, 30, 45, 60 and 75 µg) was injected in the ad libitum birds. Experiments 3-4 were similar to experiments 1-2, except chicken i.p. injected with MET (15, 30, 45, 60 and 75 mg/kg). In experiment 5, FD24 birds ICV injected with l-NAME (NO synthesis inhibitor, 100 nmol), MET (75 µg) and co-injection of l-NAME + MET. Experiment 6 was similar to experiment 5, except, ad libitum birds received injections. In experiment 7, FD24 chicken i.p. injected with l-NAME (100 mg/kg), MET (75 mg/kg) and co-injection of l-NAME + MET. In experiment 8, FD24 birds ICV injected with RO5256390 (selective TAAR1 agonist, 10, 20 and 40 µg). In experiment 9, ad libitum birds ICV injected with RO5256390 (10, 20 and 40 µg). In experiment 10, FD24 birds ICV injected with RO5256390 (10 µg), MET (75 µg) and their co-injection. Experiment 11 was similar to experiment 10, except, ad libitum birds received ICV injections. In experiment 12, FD24 chicken i.p. injected with RO5256390 (2.5, 5 and 10 mg/kg). In experiment 13, FD24 chicken i.p. injected with RO5256390 (2.5 mg/kg), MET (75 mg/kg) and RO5256390 + MET. Then cumulative food intake was determined until 120 min after injection. According to the results, ICV injection of MET decreased food intake in FD24 and ad libitum chicken (P < 0.05). MET (i.p.) diminished food consumption in fasted (P < 0.05) but not in ad libitum chicken (P> 0.05). Co-injection of the l-NAME + MET significantly decreased MET-induced hypophagia in FD24 and ad libitum chicken (P < 0.05). MET-induced hypophagia (i.p.) weakened by l-NAME in FD24 chicken (P < 0.05). RO5256390 decreased food intake in FD24 and ad libitum chicken (P < 0.05). Co-injection of RO5256390 + MET increased MET-induced hypophagia in FD24 and ad libitum chicken (P < 0.05). RO5256390 decreased food intake in FD24 chicken (P < 0.05). Co-injection of the RO5256390 + MET amplified MET-induced hypophagia in FD24 chicken (P < 0.05). Based on the findings, MET-induced hypophagia is mediated via NO and TAAR1 pathways on food intake in layer chicken.

Prenatal exposure to hesperidin improves reflexive motor behaviors in mice offspring.

Prenatal exposure during the embryonic period has positive or adverse effect on newborn brain development. Neuroprotective activity of the hesperidin is well documented but there is no evidence for maternal exposure to hesperidin on offspring reflexive motor behaviors. So, the aim of the current study was to determine the prenatal exposure to hesperidin on reflexive motor behaviors in mice offspring. Forty pregnant female NMRI mice (8-10 weeks old) were allocated into four groups. Group 1 kept as control and groups 2-4 intraperitoneal (i.p) injected with hesperidin (0.1, 0.5, and 1 mg/kg) on days of 5, 8, 11, 14, and 17 of pregnancy. The control group injected with saline at the same days. Following delivery, 20 pups from each litter were selected and reflexive motor behaviors determined using ambulation, hind-limb foot angle, surface righting, hind-limb strength, grip strength, front-limb suspension, and negative geotaxis tests. At the end of the study serum Malondialdehyde (MDA), Superoxide dismutase (SOD), Glutathione peroxidase (GPx), and total antioxidant status (TAS) levels were determined. According to the results, maternal exposure to hesperidin (0.1, 0.5, and 1 mg/kg) increased ambulation score, front-limb suspension time, and hind-limb suspension score in mice offspring compared to the control group (p < .05). Hesperidin (0.1, 0.5, and 1 mg/kg) decreased hind-limb foot angle in mice offspring compared to the control group (p < .05). Prenatal exposure to hesperidin (0.5 and 1 mg/kg) significantly increased the surface righting and grip strength in comparison to the control group (p < .05). Hesperidin (0.1, 0.5, and 1 mg/kg) decreased MDA and increased SOD and GPx levels in mice offspring (p < .05). These results suggested hesperidin exposure during pregnancy has positive effect on reflexive motor behaviors in mice offspring may be due to its antioxidant activity.