Maze Behavior Research Articles

Time-restricted feeding does not prevent adverse effects of palatable cafeteria diet on adiposity, cognition and gut microbiota in rats

Time-restricted feeding (TRF) is a popular dietary strategy whereby daily food intake is limited to a <12h window. As little is known about the effects of TRF on cognitive and behavioral measures, the present study examined the effects of time-restricted (8h/day; zeitgeber time [ZT]12–20) or continuous access to a high-fat, high-sugar cafeteria-style diet (Caf; Caf and Caf-TRF groups; n=12 adult male Sprague-Dawley rats) or standard chow (Chow and Chow-TRF groups) on short-term memory, anxiety-like behavior, adiposity and gut microbiota composition over 13-weeks with daily food intake measures. TRF significantly reduced daily energy intake in Caf- but not chow-fed groups. In Caf-fed groups, TRF reduced the proportion of energy derived from sugar while increasing that derived from protein. Caf diet significantly increased weight gain, adiposity and fasting glucose within 4 weeks; TRF partially reduced these effects. Caf diet increased anxiety-like behavior in the Elevated Plus Maze in week 3 but not week 12, and impaired hippocampal-dependent place recognition memory in week 11; neither measure was affected by TRF. Global microbiota composition differed markedly between chow and Caf groups, with a small effect of TRF in rats fed chow. In both chow and Caf diet groups, TRF reduced microbiota alpha diversity measures of Shannon diversity and evenness relative to continuous access. Results indicate only limited benefits of TRF access to an obesogenic diet under these conditions, suggesting that more severe time restriction may be required to offset adverse metabolic and cognitive effects when using highly palatable diets.

The Impact of Hydroxytyrosol on the Metallomic-Profile in an Animal Model of Alzheimer's Disease.

It is undeniable that as people get older, they become progressively more susceptible to neurodegenerative illnesses such as Alzheimer's disease (AD). Memory loss is a prominent symptom of this condition and can be exacerbated by uneven levels of certain metals. This study used inductively coupled plasma mass spectrometry (ICP-MS) to examine the levels of metals in the blood plasma, frontal cortex, and hippocampus of Wistar rats with AD induced by streptozotocin (STZ). It also tested the effects of the antioxidant hydroxytyrosol (HT) on metal levels. The Barnes maze behavior test was used, and the STZ group showed less certainty and greater distance when exploring the Barnes maze than the control group. The results also indicated that the control group and the STZ + HT group exhibited enhanced learning curves during the Barnes maze training as compared to the STZ group. The ICP-MS analysis showed that the STZ group had lower levels of cobalt in their blood plasma than the control group, while the calcium levels in the frontal cortex of the STZ + HT group were higher than in the control group. The most important finding was that copper levels in the frontal cortex from STZ-treated animals were higher than in the control group, and that the STZ + HT group returned to equivalent levels to the control group. The antioxidant HT can restore copper levels to their basal physiological state. This finding may help explain HT's potential beneficial effect in AD-patients.

Caffeic Acid, a Polyphenolic Micronutrient Rescues Mice Brains against Aβ-Induced Neurodegeneration and Memory Impairment.

Oxidative stress plays an important role in cognitive dysfunctions and is seen in neurodegeneration and Alzheimer's disease (AD). It has been reported that the polyphenolic compound caffeic acid possesses strong neuroprotective and antioxidant effects. The current study was conducted to investigate the therapeutic potential of caffeic acid against amyloid beta (Aβ1-42)-induced oxidative stress and memory impairments. Aβ1-42 (5 μL/5 min/mouse) was administered intracerebroventricularly (ICV) into wild-type adult mice to induce AD-like pathological changes. Caffeic acid was administered orally at 50 mg/kg/day for two weeks to AD mice. Y-maze and Morris water maze (MWM) behavior tests were conducted to assess memory and cognitive abilities. Western blot and immunofluorescence analyses were used for the biochemical analyses. The behavioral results indicated that caffeic acid administration improved spatial learning, memory, and cognitive abilities in AD mice. Reactive oxygen species (ROS) and lipid peroxidation (LPO) assays were performed and showed that the levels of ROS and LPO were markedly reduced in the caffeic acid-treated mice, as compared to Aβ-induced AD mice brains. Moreover, the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were regulated with the administration of caffeic acid, compared to the Aβ-injected mice. Next, we checked the expression of ionized calcium-binding adaptor molecule 1 (Iba-1), glial fibrillary acidic proteins (GFAP), and other inflammatory markers in the experimental mice, which suggested enhanced expression of these markers in AD mice brains, and were reduced with caffeic acid treatment. Furthermore, caffeic acid enhanced synaptic markers in the AD mice model. Additionally, caffeic acid treatment also decreased Aβ and BACE-1 expression in the Aβ-induced AD mice model.

Neuro-glial underpinning mechanisms in myelin plasticity for memory enhancement

Background and aim: Learning continually shapes our neuronal circuits to form new memories. Neural plasticity was considered as the principal mechanism for learning many decades ago. Although myelin was considered for a long time as static inert insulator, recent studies showed that myelination is dynamically changed to enhance neuronal activity under neural plasticity umbrella in terms of myelin plasticity, so our study aims to figure out the underlying mechanisms of myelin plasticity associated with learning and memory. Hypothesis: We hypothesized that many mechanisms promote memory consolidation by enhancing myelination and that glial cells have a crucial role in this myelin plasticity effect. Methods: The study was conducted on 24 rats, divided into 3 groups, with 8 rats in each; Group I (control); rats remained in their home cage, Group II (control untrained); rats were allowed to move and explore the maze for equal time but there was no active platform location learning, and Group III (trained); rats were trained using Barnez maze behavior test including three days of acquisition trials (AT), followed by two probe trials (PT). The gene expression analysis for SOX10, MYRF, NRG, EDGF, SERPINE2 and MBP was evaluated by qRT-PCR in hippocampus tissues, in addition, histopathological assessment was done with immunohistochemistry for Myelin Basic Protein (MBP), Glial Fibrillary Acidic Protein (GFAP), and Gallyas-Braak Silver staining. Furthermore, Pearson correlation was done comparing all genes with MBP expression. Results and data: The present study showed improved spatial memory with increased myelination in the trained group compared to all other groups (P&lt;0.001), in addition to increase of SOX10, and MYRF expression in the trained group indicating more OPC differentiation into mature oligodendrocytes (P&lt;0.001). NRG and EDGF were highly expressed in the trained group compared to other groups, in addition to the marked increase of number of the neuronal cells with more dendrites formation. SERPINE 2 and GFAP as markers of astrocytes showed high expression in the trained group in comparison with other groups (P&lt;0.001) with strong positive correlation between SEPRINE 2 and MBP (r= 0.76, P=0.02). Conclusion: Myelin plasticity as one of the crucial learning mechanisms, was influenced by different neural and environmental signals. Although role of glial cells was almost apparent in oligodendrocytes differentiation and proliferation, there was a significant role of astrocytes in promoting such myelination effect. There were no external funding sources for this study, it is self-funding This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

No detectable changes in anxiety-related and locomotor behaviors in adult ovariectomized female rats exposed to estradiol, the ERβ agonist DPN or the ERα agonist PPT

The sex steroid hormone 17β-estradiol (estradiol) and its Estrogen Receptors (ERs) have been linked to modulation of anxiety-related and locomotor behaviors in female rodents. Research suggests that estradiol mitigates anxiety-related behaviors through activating Estrogen Receptor (ER)β and increases locomotor behaviors through ERα. The influence of ERs on these behaviors cannot always be detected. Here we discuss two experiments in which we tested the hypothesis that anxiety-related behaviors would decrease after ERβ activation and locomotor behaviors would increase after ERα activation, and also assessed the persistence of these behavioral effects by varying the timing of behavioral testing. Two cohorts of adult female ovariectomized rats were exposed to estradiol, the ERβ agonist DPN, the ERα agonist PPT, or oil for four consecutive days. Body mass was assessed throughout as a positive control. In both cohorts, open field behaviors were assessed on the first day of exposure. In one cohort (Experiment 1), open field, light/dark box, and elevated plus maze behaviors were assessed on the final day of injections. In the second cohort (Experiment 2), these behaviors were assessed 24 h after the final exposure. As expected, significant differences in body mass were detected in response to estradiol and PPT exposure, validating the estradiol and ER manipulation. No significant differences were observed in anxiety-related or locomotor behaviors across treatment groups, indicating that the efficacy of these agonists as therapeutic agents may be limited. We review these results in the context of previous literature, emphasizing relevant variables that may obscure ER-related actions on behavior.

The protective role of Nrf2 on cognitive impairment in chronic intermittent hypoxia and sleep fragmentation mice

ObjectiveObstructive Sleep Apnea Hypopnea Syndrome (OSAHS) is a sleep respiratory disease associated with cognitive impairment, The nuclear factor erythroid 2 related factor 2 (Nrf2) plays a neuroprotective role. This study was designed to investigate the mechanism of Nrf2 protecting neural cells from endoplasmic reticulum stress (ERS), induced by chronic intermittent hypoxia (CIH) and sleep fragmentation (SF) which caused cognitive impairment in mice. MethodsEstablishment of CIH and SF mice to simulate OSAHS mouse model. An eight-arm maze behavior test measured the cognitive function of mice, and Nissl staining and TUNEL staining were used to detect pathological changes in hippocampal neurons. The expression of ERS and Nrf2 and its downstream related mRNAs and proteins were detected by qRT-PCR and Western blotting. ResultsCIH and SF lead to cognitive impairment in mice, and Sulforaphane (SFN, Nrf2 agonist) plays a protective role, while Nrf2-KO aggravates the cognitive impairment. CIH and SF reduced the number of Nissl bodies in neurons and induced apoptosis. The mRNA levels of BiP, CHOP, Nrf2, GCLC and Prdx1 in CIH, SF and CIH + SF groups were increased (p = 0.001), whereas the mRNA levels of BiP and CHOP in the CIH + SF + SFN group were decreased (p = 0.02) while those of Nrf2 and Prdx1 were increased (p = 0.005). The CIH + SF + Nrf2-KO group, the mRNA levels of CHOP were increased (p = 0.001) while Nrf2, GCLC and Prdx1 were decreased (p = 0.001). The protein levels of CHOP and active Caspase-12 in CIH, SF, CIH + SF and CIH + SF + Nrf2-KO groups were increased (p = 0.03), while those of Prdx1 and Nrf2 were increased (p = 0.03) in the CIH + SF + SFN group, while decreased (p = 0.02) in the Nrf2-KO group. ConclusionsChronic intermittent hypoxia(CIH) and sleep fragmentation(SF) could aggravate the inflammatory response of nerve cells through endoplasmic reticulum stress, leading to apoptosis of nerve cells, and causing cognitive impairment in mice.Nrf2 alleviates cognitive impairment induced by chronic intermittent hypoxia and sleep fragmentation by modulating endoplasmic reticulum stress. Activation of Nrf2 protects cognitive impairment through the Nrf2-Prdx1 signaling pathway.

Liposaccharide-induced sustained mild inflammation fragments social behavior and alters basolateral amygdala activity.

Conditions with sustained low-grade inflammation have high comorbidity with depression and anxiety and are associated with social withdrawal. The basolateral amygdala (BLA) is critical for affective and social behaviors and is sensitive to inflammatory challenges. Large systemic doses of lipopolysaccharide (LPS) initiate peripheral inflammation, increase BLA neuronal activity, and disrupt social and affective measures in rodents. However, LPS doses commonly used in behavioral studies are high enough to evoke sickness syndrome, which can confound interpretation of amygdala-associated behaviors. The objectives of this study were to find a LPS dose that triggers mild peripheral inflammation but not observable sickness syndrome in adult male rats, to test the effects of sustained mild inflammation on BLA and social behaviors. To accomplish this, we administered single doses of LPS (0-100μg/kg, intraperitoneally) and measured open field behavior, or repeated LPS (5μg/kg, 3 consecutive days), and measured BLA neuronal firing, social interaction, and elevated plus maze behavior. Repeated low-dose LPS decreased BLA neuron firing rate but increased the total number of active BLA neurons. Repeated low-dose LPS also caused early disengagement during social bouts and less anogenital investigation and an overall pattern of heightened social caution associated with reduced gain of social familiarity over the course of a social session. These results provide evidence for parallel shifts in social interaction and amygdala activity caused by prolonged mild inflammation. This effect of inflammation may contribute to social symptoms associated with comorbid depression and chronic inflammatory conditions.

Activation of IGF-1/GLP-1 Signalling via 4-Hydroxyisoleucine Prevents Motor Neuron Impairments in Experimental ALS-Rats Exposed to Methylmercury-Induced Neurotoxicity.

Amyotrophic lateral sclerosis (ALS) is a severe adult motor neuron disease that causes progressive neuromuscular atrophy, muscle wasting, weakness, and depressive-like symptoms. Our previous research suggests that mercury levels are directly associated with ALS progression. MeHg+-induced ALS is characterised by oligodendrocyte destruction, myelin basic protein (MBP) depletion, and white matter degeneration, leading to demyelination and motor neuron death. The selection of MeHg+ as a potential neurotoxicant is based on our evidence that it has been connected to the development of ALS-like characteristics. It causes glutamate-mediated excitotoxicity, calcium-dependent neurotoxicity, and an ALS-like phenotype. Dysregulation of IGF-1/GLP-1 signalling has been associated with ALS progression. The bioactive amino acid 4-hydroxyisoleucine (HI) from Trigonella foenum graecum acts as an insulin mimic in rodents and increases insulin sensitivity. This study examined the neuroprotective effects of 4-HI on MeHg+-treated adult Wistar rats with ALS-like symptoms, emphasising brain IGF1/GLP-1 activation. Furthermore, we investigated the effect of 4-HI on MBP levels in rat brain homogenate, cerebrospinal fluid (CSF), blood plasma, and cell death indicators such as caspase-3, Bax, and Bcl-2. Rats were assessed for muscular strength, locomotor deficits, depressed behaviour, and spatial learning in the Morris water maze (MWM) to measure neurobehavioral abnormalities. Doses of 4-HI were given orally for 42 days in the MeHg+ rat model at 50 mg/kg or 100 mg/kg to ameliorate ALS-like neurological dysfunctions. Additionally, neurotransmitters and oxidative stress markers were examined in rat brain homogenates. Our findings suggest that 4-HI has neuroprotective benefits in reducing MeHg+-induced behavioural, neurochemical, and histopathological abnormalities in ALS-like rats exposed to methylmercury.

Reduced microvascular expression of ADAM17 contributes to cognitive impairment in Alzheimer's disease model, APP/PS1 mice

The disintegrin and metalloproteinase 17 (ADAM17), abundantly expressed in cerebrovascular endothelial cells, is one of the important α‐secretases involved in the cleavage amyloid precursor protein‐α (APP). We hypothesized that abnormal function of vascular ADAM17 contributes to the cognitive impairment in Alzheimer’s disease (AD). We used 8‐10 months old male and female wild type and APP/PS1 mice containing human transgenes for both APP bearing the Swedish mutation and PSEN1 containing an L166P mutation. We found that the ADAM17 expression in brain microvessels is significantly reduced in the APP/PS1 mice, compared to wild type controls. Using the Morris Water Maze (MWM) behavior test the APP/PS1 mice showed longer latency to reach the hidden platform during the learning phase and spent significantly less time in the target quadrant during the memory probe test. ADAM17 was then overexpressed in APP/PS1 mice via tail vein systemic delivery of ADAM17‐AAV9. After 4 weeks, the ADAM17 overexpressed APP/PS1 mice spend less time to reach the platform and spend more time in the target quadrant during the MWM test compared to the control, eGFP overexpressed APP/PS1 mice. Thus, we propose that down‐regulation of cerebrovascular ADAM17 contributes to the development of cognitive dysfunction in APP/PS1 mice, which can be improved by AAV9 delivery of ADAM17.

The Effects of Melatonin on Cognition and Αβ load in an Alzheimer’s Disease Mouse Model

AbstractBackgroundThe neurohormone melatonin is released from the pineal gland and is an endogenous antioxidant and free radical scavenger that regulates sleep/wake cycle and circadian rhythm. Decline of nocturnal melatonin secretion with severe sleep disturbance has been consistently reported in Alzheimer’s Disease (AD), a neurodegenerative disease characterized by cognitive deficits and neuronal loss. However, exogenous melatonin supplementation can reduce Αβ neurotoxicity and formation while improving cognitive performance and sleep quality.MethodIn this study, the long‐term influence of melatonin on behavioral and neuropathological changes were evaluated in the 5xFAD mouse model, when treatment was started in adolescence. After ∼20 weeks of orally administered melatonin (10 mg/kg), Morris water maze behaviour was assessed in 54 mice, followed by Aβ42 quantification in hippocampal tissue.ResultOverall, transgenic mice showed impaired learning, and a significant increase in Aβ42 plaque load, replicating previous results with this strain. Melatonin marginally improved learning by decreasing distance travelled in the Morris water maze and slightly decreasing Aβ42 concentration in the hippocampus. These results support the hypothesis that long‐term melatonin supplementation may be beneficial at early stages of the disease process and should be explored more fully.ConclusionAbnormal accumulation of neurotoxic forms of Αβ occur in brain regions involved in the regulation of sleep in AD patients and the disturbed regulation of sleep that occurs early in the disease may contribute to cognitive decline by decreasing Αβ clearance. In contrast to conventional antioxidants, melatonin crosses the blood‐brain barrier, is relatively devoid of toxicity, and constitutes a straight‐forward potential therapeutic candidate in AD treatment.

The anxiolytic effect of salicylic acid is mediated via the GABAergic system in the fear potentiated plus maze behavior in rats.

Salicylic acid(SA) is a natural phenolic compound in plants with many beneficial effects for humans. The anxiolytic effect of this compound has been reported in animal models, but its mechanism of action remains unclear. In this study, by using the fear potentiated plus maze test, we evaluated the effect of salicylic acid on the gene expression of the main form of GABA (gamma aminobutyric acid) synthesizing enzyme i.e., the enzyme glutamic acid decarboxylase 67 (GAD67) which is called GAD1, in the ventral subiculum of the hippocampus, one of the main brain structures, in anxiety circuits. Also, the hypnotic effect of Salicylic acid was evaluated. Animals were divided into the solvent, (SA) and diazepam treated groups (n = 6). For evaluating the anxiolytic effect of Salicylic acid, animals were subjected to 2h of isolation, before placing them in the elevated plus maze (EPM). Afterward, the ventral part of the hippocampus was removed for evaluating the change in GAD1 gene expression by the reverse transcription-quantitative polymerase chain reaction (RTqPCR) technique. The hypnotic effect of Salicylic acidwas evaluated in the ketamine induced sleeping test. Salicylic acid at 10 and 30 (mg/kg) increased time spent and entries to the open arms in the (EPM) (p < 0.05). (RTqPCR) revealed that 30mg/kg of Salicylic acidincreased GAD1 gene expression (p < 0.001). Salicylic acid(30 and 300mg/kg) also increased the duration of sleep, in ketamine induced sleeping test (p < 0.05). Our results showed that Salicylic acidhas anxiolytic and hypnotic effects and it exerts its anxiolytic effect partly, via up the regulation of GAD1 in the ventral part of the hippocampus.

Red ginseng has stronger anti-aging effects compared to ginseng possibly due to its regulation of oxidative stress and the gut microbiota

BackgroundPanax ginseng (PG) and red ginseng (RG) are considered to be effective anti-aging treatments. However, evidence of their therapeutic mechanisms and difference in anti-aging effects is lacking. PurposeTo explore the potential therapeutic mechanisms of RG and PG in brain damage in D-Gal-induced aging mice, and evaluate the difference in anti-aging effects caused by their compositional differences. MethodsWe first tested the chemical components in PG and RG. In D-Gal aging mouse model, RG and PG (800 mg/kg) were orally administered for 9 weeks. The mice performed the Radial Arm Maze (RAM) behavior test. We collected blood, brain tissue, and fecal samples and performed biochemical analysis, histological examination, western blot, and Illumina MiSeq sequencing analysis. ResultsThe results of component analysis showed that the total polyphenols and rare ginsenosides were present in RG in 3.2, and 2.2 fold greater concentrations, respectively, compared to PG, while the proportion of non-starch polysaccharides in the crude polysaccharides of RG was 1.94 fold greater than that of PG. In D-Gal-induced aging mice, both PG and RG could prevent the increase in acetylcholinesterase (AChE), and malondialdehyde (MDA) levels, and improved the expression of superoxide dismutase (SOD), and catalase (CAT) in the serum. Meanwhile, both PG and RG could ameliorate brain tissue architecture and behavioral trial. In addition, the D-Gal-induced translocation of nuclear factor-κB (NF-κB), as well as activation of the pro-apoptotic factors Caspase-3 and the PI3K/Akt pathways were inhibited by PG and RG. Overall, both PG and RG exerted anti-aging effects, with RG stronger than PG. Finally, although both PG and RG regulated the diversity of gut microbes, RG appeared to aggravate the increase in probiotics, such as Bifidobacterium and Akkermania, and the decrease in inflammatory bacteria to a greater extent compared to PG. ConclusionOur results suggest that RG is more conducive to delay the D-Gal-induced aging process than PG, with possible mechanisms including beneficial changes in brain structure, cognitive functions, oxidative stress inhibition, and gut microbiome structure and diversity than PG, These mechanisms may rely on the presence of more total polyphenols, rare ginsenosides and non-starch polysaccharides in RG.

Trehalose Reduces Nerve Injury Induced Nociception in Mice but Negatively Affects Alertness

Trehalose, a sugar from fungi, mimics starvation due to a block of glucose transport and induces Transcription Factor EB- mediated autophagy, likely supported by the upregulation of progranulin. The pro-autophagy effects help to remove pathological proteins and thereby prevent neurodegenerative diseases such as Alzheimer’s disease. Enhancing autophagy also contributes to the resolution of neuropathic pain in mice. Therefore, we here assessed the effects of continuous trehalose administration via drinking water using the mouse Spared Nerve Injury model of neuropathic pain. Trehalose had no effect on drinking, feeding, voluntary wheel running, motor coordination, locomotion, and open field, elevated plus maze, and Barnes Maze behavior, showing that it was well tolerated. However, trehalose reduced nerve injury-evoked nociceptive mechanical and thermal hypersensitivity as compared to vehicle. Trehalose had no effect on calcium currents in primary somatosensory neurons, pointing to central mechanisms of the antinociceptive effects. In IntelliCages, trehalose-treated mice showed reduced activity, in particular, a low frequency of nosepokes, which was associated with a reduced proportion of correct trials and flat learning curves in place preference learning tasks. Mice failed to switch corner preferences and stuck to spontaneously preferred corners. The behavior in IntelliCages is suggestive of sedative effects as a “side effect” of a continuous protracted trehalose treatment, leading to impairment of learning flexibility. Hence, trehalose diet supplements might reduce chronic pain but likely at the expense of alertness.

Impact of Light–Dark Phase on Delay Discounting Behavior in Rats

Rodent models are commonly used in behavioral research because they offer increased experimental control and findings often generalizable to humans. However, one possible dilemma is that rodents are primarily nocturnal and research tasks often disrupt their light, rest phase. The present study used a within-subjects design to investigate possible effects of light-dark phase on delay discounting, motor coordination, open field, and elevated-plus maze behavior in Wistar rats. Rats spent significantly more time in the closed arms of the elevated plus maze when tested during the light, rest phase compared to the dark, active phase. There were no differences in motor coordination or delay discounting during the two phases. These results suggest possible important differences in certain behavioral tasks when testing in the light, rest versus dark, active phase for rats—researchers should be aware of these possible differences when planning and conducting experiments and when comparing research findings across laboratories.

The effect of rearing conditions during the milk-fed period on milk yield, growth, and maze behaviour of dairy cows during their first lactation.

The objective was to find whether cow growth, milk performance, and behaviour are affected by (1) rearing conditions until weaning after a milk-fed period of 84 d and (2) the sire lineage. Thirty-five Holstein heifers were assigned to one of three treatments: SM, , pen with mother to 21st day, then group pen (they received a maximum of 6 kg of milk daily); SN, , after 3 d with own mother in pen with nursing cow (they received a maximum of 6 kg of milk daily); H, , in hutch from the 2nd to 56th day (6 kg of milk replacer daily), then loose housing pen to weaning (6 kg of milk replacer daily). After weaning at the 84th day, all heifers were kept in pens with the same ration as during calving. During lactation, live body weight (LBW) was measured each month and milk yield each day. Maze learning was evaluated in the fifth month of lactation. The data were analysed using a general linear model ANOVA. At the 30th day, the LBW tended to be the highest in SN (SM 528.2 11.4 kg, SN 571.7 15.3 kg, H 533.2 12.3 kg). When lactation ended, the highest LBW was in SN and the lowest in H (SM 612.6 12.2 kg, SN 623.1 16.4 kg, H 569.8 13.2 kg; ). The SN tended to have the highest production of milk (SM 7143.9 241.5 kg, SN 7345.1 319.0 kg, H 7146.7 234 kg), and the H for FCM (SM 6290.3 203.2 kg, SN 6307.6 268.4 kg, H 6399.3 197.1 kg) for 305 d lactation. Group SN crossed the maze fastest (SM 1141.4 120.5 s, SN 810.3 160.5 s, H 1120.8 118.6 s). The vocalization number differed significantly (SM 32.3 5.7, SN 20.8 4.4, H 9.9 2.6; ). The results indicated that the rearing method up to weaning may have an impact on dairy cows' performance and behaviour.

Effects of test experience, closed-arm wall color, and illumination level on behavior and plasma corticosterone response in an elevated plus maze in male C57BL/6J mice: a challenge against conventional interpretation of the test

The elevated plus maze test is a widely used test for assessing anxiety-like behavior and screening novel therapeutic agents in rodents. Previous studies have shown that a variety of internal factors and procedural variables can influence elevated plus maze behavior. Although some studies have suggested a link between behavior and plasma corticosterone levels, the relationships between them remain unclear. In this study, we investigated the effects of experience with a battery of behavioral tests, the wall color of the closed arms, and illumination level on the behavior and plasma corticosterone responses in the elevated plus maze in male C57BL/6J mice. Mice were either subjected to a series of behavioral tests, including assessments of general health and neurological function, a light/dark transition test, and an open field test, or left undisturbed until the start of the elevated plus maze test. The mice with and without test battery experience were allowed to freely explore the elevated plus maze. The other two independent groups of naïve mice were tested in mazes with closed arms with different wall colors (clear, transparent blue, white, and black) or different illumination levels (5, 100, and 800 lx). Immediately after the test, blood was collected to measure plasma corticosterone concentrations. Mice with test battery experience showed a lower percentage of open arm time and entries and, somewhat paradoxically, had lower plasma corticosterone levels than the mice with no test battery experience. Mice tested in the maze with closed arms with clear walls exhibited higher open arm exploration than mice tested in the maze with closed arms with black walls, while there were no significant differences in plasma corticosterone levels between the different wall color conditions. Illumination levels had no significant effects on any measure. Our results indicate that experience with other behavioral tests and different physical features of the maze affect elevated plus maze behaviors. Increased open arm time and entries are conventionally interpreted as decreased anxiety-like behavior, while other possible interpretations are considered: open arm exploration may reflect heightened anxiety and panic-like reaction to a novel situation under certain conditions. With the possibility of different interpretations, the present findings highlight the need to carefully consider the test conditions in designing experiments and drawing conclusions from the behavioral outcomes in the elevated plus maze test in C57BL/6J mice.

Effect of raising method of calves during liquid milk nutrition on their open-field and maze behaviour after weaning

Effect of raising method of calves during liquid milk nutrition on their open-field and maze behaviour after weaning

Effects of Omega-3 Polyunsaturated Fatty Acids on Cognitive Function after Splenectomy in Rats.

Background Postoperative cognitive dysfunction (POCD) is a common complication after abdominal surgery. Several studies have reported that POCD is related to neuroinflammation caused by surgery. Omega-3 polyunsaturated fatty acids (PUFAs) can effectively inhibit the systematic inflammatory response. So, we use fish oil to study the effect of fish oil on inflammation, immunity, and cognitive behavior after splenectomy in rats. Methods 60 SD (Sprague-Dawley) rats were randomly divided into control group (group C, n = 20), surgery group (group S, n = 20), and omega-3 (fish oil) intervention group (group F, n = 20). Omega-3 PUFA was injected intraperitoneally from 3 days before operation to 7 days after operation in group F, and normal saline was injected simultaneously in group S. Rats in group S and group F received splenectomy under general anesthesia. Morris water maze behavioral evaluation was performed on the first, third, fifth, and seventh day after operation. The levels of IL-1β (interleukin-1β), IL-6 (interleukin-6), TNF-α (tumor necrosis factor-α), SOD (superoxide dismutase), and GSH-PX (glutathione peroxidase) were detected. Results Serums IL-1β, IL-6, and TNF-α concentrations in group S and group F were higher than those in group C (P < 0.01), while those inflammatory cytokines in group F were significantly lower than those in group S (P < 0.01); serum GSH-PX levels in group F were higher than group S (P < 0.01). The Morris water maze behavior test performance of group F was better than that of group S (P < 0.05). Conclusion Omega-3 PUFA can effectively improve postoperative inflammatory response, reduce the damage of antioxidant defense system, and improve postoperative cognitive function.

Adult neurogenesis alters response to an aversive distractor in a labyrinth maze without affecting spatial learning or memory.

Adult neurogenesis has been implicated in learning and memory of complex spatial environments. However, new neurons also play a role in nonmnemonic behavior, including the stress response and attention shifting. Many commonly used spatial tasks are very simple, and unsuitable for detecting neurogenesis effects, or are aversively motivated, making it difficult to dissociate effects on spatial learning and memory from effects on stress. We have therefore created a novel complex spatial environment, the flex maze, to enable reward-mediated testing of spatial learning in a flexibly configurable labyrinth. Using a pharmacogenetic method to completely inhibit neurogenesis in adulthood, we found that rats lacking new neurons (TK rats) and wild type controls completed and remembered most mazes equally well. However, control rats were slower to complete peppermint-scented mazes than other mazes, while neurogenesis-deficient rats showed no effect of mint on maze behavior, completing these mazes significantly faster than control rats. Additional testing found that wild type and TK rats showed similar detection of, avoidance of, and glucocorticoid response to the mint odor. These results suggest that spatial learning and memory in a labyrinth task is unaffected by the loss of new neurons, but that these cells affect the ability of an aversive stimulus to distract rats from completing the maze.

Hereditary determined diving behaviour in rats as a factor of fitness

Background. Rats natural ability to swim and dive provides adaptation in the wildlife and is widely applied as an instrument in experimental physiology. Nevertheless theres little scientific evidence on diving behaviour in rats itself. Meanwhile this behavioural pattern might be a notable trait to shed light on functional features of the nervous system, the higher nervous activity structure and evolutional adaptability in animals, including inherited ones.&#x0D; Materials and methods. In the present work we compared the performance of the spontaneous diving behaviour in the Morris water maze and forced diving behaviour in the Extrapolation escape task in two selected rat strains genetically differing in the nervous system excitability threshold.&#x0D; Results. We found a greater extent and adaptive pattern of both types of the diving behaviour in the high-excitable LT strain. This may be due to such basic features of this strain as high exploratory activity and an increased level of fear reactions. It was also shown that the second, low-excitable HT rat strain, demonstrates maladaptive jumping behaviour in the Extrapolation escape task due to higher anxiety level in the stress conditions.&#x0D; Conclusion. Observed differences between two strains allow us to consider the diving behaviour performed by high-excitable rats an inherited strain characteristic resembling adaptive rat behaviours in the wild and look forward to investigate its genetic mechanisms.