Hippocampus Of Male Wistar Rats Research Articles

Melatonin is a Neuroprotective and Antioxidant Agent against Neurotoxicity Induced by an Intrahippocampal Injection of Nickel in Rats.

The investigation into the hippocampal function and its response to heavy metal exposure is crucial for understanding the mechanisms underlying neurotoxicity, this can potentially inform strategies for mitigating the adverse effects associated with heavy metal exposure. Melatonin is an essential neuromodulator known for its efficacy as an antioxidant. In this study, we aimed to determine whether melatonin could protect against Nickel (Ni) neurotoxicity. To achieve this, we performed an intracerebral injection of Ni (300 µM NiCl2) into the right hippocampus of male Wistar rats, followed by melatonin treatment. Based on neurobehavioral and neurobiochemical assessments, our results demonstrate that melatonin efficiently enhances Ni-induced behavioral dysfunction and cognitive impairment. Specifically, melatonin treatment positively influences anxious behavior, significantly reduces immobility time in the forced swim test (FST), and improves learning and spatial memory abilities. Moreover, neurobiochemical assays revealed that melatonin treatment modulates the Ni-induced alterations in oxidative stress balance by increasing antioxidant enzyme activities, such as superoxide dismutase (SOD) and catalase (CAT). Additionally, we observed that melatonin significantly attenuated the increased levels of lipid peroxidation (LPO) and nitric oxide (NO). In conclusion, the data from this study suggests that melatonin attenuates oxidative stress, which is the primary mechanism responsible for Ni-induced neurotoxicity. Considering that the hippocampus is the main structure involved in the pathology associated with heavy metal intoxication, such as Ni, these findings underscore the potential therapeutic efficacy of melatonin in mitigating heavy metal-induced brain damage.

Evaluation of the effect of Exercise Trainings and CGRP receptor antagonist (BIBN 4096) on mitochondrial dynamic in the hippocampus of male Wistar rats

BackgroundExercise training showed beneficial effects on brain. The purpose of the present study is to evaluate the effect of six weeks of high-intensity interval training (HIIT) and Endurance training (ET) with calcitonin gene-related peptide (CGRP) receptor antagonist on the expression of genes involved in mitochondrial dynamics and apoptosis in hippocampal tissue of male Wistar rats. MethodsIn this study, forty-two healthymale Wistar rats (8-week) were randomly divided into 6 groups (n = 7) as follow; 1) Control; 2) HIIT which performed 6 weeks of HIIT; 3) ET which performed 6 weeks of endurance training; 4) CGRPi received 10 mg/kg CGRP receptor antagonist every day at the last 2 weeks; 5) CGRPi-HIIT performed HIIT and received CGRP receptor antagonist; 6) CGRPi-ET performed ET and received CGRP receptor antagonist. Real-time PCR (2-ΔΔCT) and western blotting were employedto measure the expression of genes and protein, respectively. ResultsHIIT and ET significantly increased Bcl-2, Pgc-1α, Sirt3, and Nrf-1 gene expression in the hippocampal tissue (p < 0.05, p < 0.01, p < 0.01, and p < 0.001, respectively). ET-CGRPi and HIIT-CGRPi significantly increased Sirt3, Pgc-1α, and Nrf-1 gene expression compared to the control group (p < 0.05, p < 0.01, and p < 0.05, respectively). ConclusionET and HIIT-induced physiological alterations in the hippocampus. In fact, this modulation showed protective properties in the hippocampusvia up regulation of Bcl-2, Pgc-1α, Nrf-1, and Sirt3 gene expression. CGRPi did not cause gene or protein changes harmful to mitochondrial dynamic balance and apoptosis in the hippocampus of rats.

Ameliorative Effects of FMRFamide on 3,4-Methylenedioxyl-Methamphetamine /Tramadol-Induced Neurodegeneration in the Hippocampus

Objective: Tramadol and 3,4-methylenedioxy-methamphetamine (MDMA) use over an extended period is linked to deficits in memory encoding and retrieval. We aimed to determine the neurotoxic effects of co-administration of MDMA and tramadol (TRAM) on hippocampal function and investigate the potential of FMRFamide in attenuating resulting alterations in the Wistar rat model. Methods: Thirty adult male Wistar rats were grouped into six (n=5): Control, FMRFamide, TRAM, MDMA, TRAM+MDMA, and TRAM + MDMA + FMRFamide groups. The opiates were administered orally at 20mg/kg each, while 2mg/kg of FMRFamide was administered intraperitoneally for 12 days using normal saline as a vehicle. The Barnes and Morris water mazes were used to evaluate spatial learning and memory functions, followed by H&amp;E staining, and immunohistochemical staining for glial fibrillary acid protein (GFAP). Results: The opiates significantly increased total latencies in the Barnes Maze test, indicating that short- and long-term memory functions were impaired. Also, high levels of escape latency were observed following MDMA administration, suggesting that MDMA reduced the spatial navigation ability of the animals. These discrepancies were noticeably extreme in animals that received co-administration of opiates. However, FMRFamide showed significant potential in attenuating the damage induced by opiates, thus repairing and restoring memory formation and retention functions. Conclusion: FMRFamide may attenuate the Tramadol- and MDMA-mediated memory dysfunction by enhancing cholinergic and glutaminergic synthesis and transporting and restoring exploratory and navigational abilities in the hippocampus of male Wistar rats.

Prolonged Zaleplon Treatment Increases the Expression of Proteins Involved in GABAergic and Glutamatergic Signaling in the Rat Hippocampus.

Zaleplon is a positive allosteric modulator of the γ-aminobutyric acid (GABA)A receptor approved for the short-term treatment of insomnia. Previous publications on zaleplon have not addressed the proteins involved in its mechanism of action but have mostly referred to behavioral or pharmacological studies. Since both GABAergic and glutamatergic signaling have been shown to regulate wakefulness and sleep, we examined the effects of prolonged zaleplon treatment (0.625 mg/kg for 5 days) on these systems in the hippocampus of male Wistar rats. Western blot and immunohistochemical analyses showed that the upregulated components of GABAergic signaling (glutamate decarboxylase, vesicular GABA transporter, GABA, and α1 subunit of the GABAA receptor) were accompanied by increased protein levels in the glutamatergic system (vesicular glutamate transporter 1 and NR1, NR2A, and NR2B subunits of N-methyl-d-aspartate receptor). Our results, showing that zaleplon enhances GABA neurotransmission in the hippocampus, were not surprising. However, we found that treatment also increased glutamatergic signaling. This could be the result of the downregulation of adenosine A1 receptors, important modulators of the glutamatergic system. Further studies are needed to investigate the effects of the zaleplon-induced increase in hippocampal glutamatergic neurotransmission and the possible involvement of the adenosine system in zaleplon's mechanism of action.

A Brain Region-Dependent Alteration in the Expression of Vasopressin, Corticotropin-Releasing Factor, and Their Receptors Might Be in the Background of Kisspeptin-13-Induced Hypothalamic-Pituitary-Adrenal Axis Activation and Anxiety in Rats.

Previously, we reported that intracerebroventricularly administered kisspeptin-13 (KP-13) induces anxiety-like behavior and activates the hypothalamic-pituitary-adrenal (HPA) axis in rats. In the present study, we aimed to shed light on the mediation of KP-13's stress-evoking actions. The relative gene expressions of the corticotropin-releasing factor (Crf, Crfr1, and Crfr2) and arginine vasopressin (Avp, Avpr1a, and Avpr1b) systems were measured in the amygdala and hippocampus of male Wistar rats after icv KP-13 treatment. CRF and AVP protein content were also determined. A different set of animals received CRF or V1 receptor antagonist pretreatment before the KP-13 challenge, after which either an open-field test or plasma corticosterone levels measurement was performed. In the amygdala, KP-13 induced an upregulation of Avp and Avpr1b expression, and a downregulation of Crf. In the hippocampus, the mRNA level of Crf increased and the level of Avpr1a decreased. A significant rise in AVP protein content was also detected in the amygdala. KP-13 also evoked anxiety-like behavior in the open field test, which the V1 receptor blocker antagonized. Both CRF and V1 receptor blockers reduced the KP-13-evoked rise in the plasma corticosterone level. This suggests that KP-13 alters the AVP and CRF signaling and that might be responsible for its effect on the HPA axis and anxiety-like behavior.

Morphostructural changes in the brain of experimental animals after using mesenchymal stem cells in the temporomandibular joint inflammation model

The article presents the results of structural and functional transformations in cerebellum, trigeminal nuclei, and hippocampus of male Wistar rats against the background of injection of mesenchymal stem cells (MSCs) into Meckel’s space in the temporomandibular joint (TMJ) inflammation model.The aim of the study was to clarify the effect of MSCs injections into Meckel’s space on the morphostructural features of cerebellum, trigeminal nuclei, and hippocampus in the TMJ inflammation model.Injecting the mesenchymal stem cells into Meckel’s space in an inflammatory model of the right lower temporomandibular joint promotes the structure restoration of the ganglionic layer of the cerebellum, the spinal nuclei of the trigeminal nerve, and the hippocampus of rats by the 28th day. This is manifested in increasing the neuronal density, decreasing the neurodegeneration index, and in activating glia elements.

Prolonged Alprazolam Treatment Alters Components of Glutamatergic Neurotransmission in the Hippocampus of Male Wistar Rats—The Neuroadaptive Changes following Long-Term Benzodiazepine (Mis)Use

Alprazolam (ALP), a benzodiazepine (BDZ) used to treat anxiety, panic, and sleep disorders, is one of the most prescribed psychotropic drugs worldwide. The side effects associated with long-term (mis)use of ALP have become a major challenge in pharmacotherapy, emphasizing the unmet need to further investigate their underlying molecular mechanisms. Prolonged BDZ exposure may induce adaptive changes in the function of several receptors, including the primary target, gammaaminobutyric acid receptor type A (GABAAR), but also other neurotransmitter receptors such as glutamatergic. The present study investigated the potential effects of prolonged ALP treatment on components of glutamatergic neurotransmission, with special emphasis on N-Methyl-D-aspartate receptor (NMDAR) in the hippocampus of adult male Wistar rats. The study revealed behavioral changes consistent with potential onset of tolerance and involvement of the glutamatergic system in its development. Specifically, an increase in NMDAR subunits (NR1, NR2A, NR2B), a decrease in vesicular glutamate transporter 1 (vGlut1), and differential modulation of excitatory amino acid transporters 1 and 2 (EAAT1/2, in vivo and in vitro) were observed, alongside a decrease in α1-containing GABAAR following the treatment. By describing the development of compensatory actions in the glutamatergic system, the present study provides valuable information on neuroadaptive mechanisms following prolonged ALP intake.

The effect of crocin on cholestasis-induced spatial memory impairment with respect to the expression level of TFAM and PGC-1α and activity of catalase and superoxide dismutase in the hippocampus.

Large evidence has shown that cholestasis has a wide-range of deleterious effects on brain function, and also, on neurocognitive functions including learning and memory. On the other hand, crocin (derived from Crocus sativus) is a medicinal natural compound that induces neuroprotective and precognitive effects. In this study, we aimed to evaluate the effect of crocin on spatial learning and memory in cholestatic rats with respect to the level of mitochondrial transcriptional factor A (TFAM), peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), catalase (CAT), and superoxide dismutase (SOD) in the hippocampus of male Wistar rats. Bile duct ligation (BDL) was used to induce cholestasis. Y-maze apparatus was used to assess spatial memory performance and real-time PCR was used to assess TFAM and PGC-1α gene expression. Also, crocin was injected intraperitoneal at the doses of 15, 20, and 30mg/kg for thirty days. The results showed that BDL impaired spatial memory in rats. BDL also decreased SOD, TFAM, and PGC-1α level. In addition, crocin partially reversed the impairment effect of BDL on spatial memory. Crocin (30mg/kg) also reversed the effect of BDL on SOD, TFAM, and PGC-1α. Of note, the effect of BDL on CAT activity was controversial. It seems that BDL can increase CAT activity. In addition, crocin (30mg/kg) reversed the enhancement of CAT following BDL to its control level. In conclusion, crocin may induce a significant neuroprotective effect on cholestasis-induced memory impairment.

The Effect of Aerobic Training before Alzheimer’s Induction on the Expression of Calcineurin and Ca2+/Calmodulin-dependent Protein Kinase II Gene in the Hippocampus of Rats with Alzheimer’s Disease

Background and Objectives Regular aerobic exercise improves learning, memory, and cognitive and Synaptic Plasticity in Alzheimer’s disease (AD) patients. The aim of this study was to evaluate the levels of calcineurin and Ca2+/calmodulin-dependent protein kinase II mRNA after four weeks of aerobic training exercises and before AD induction in the hippocampus of male Wistar rats. Subjects and Methods Thirty 8-week-old rats with an average weight of 195±20 g were initially randomly divided into two groups of aerobic exercise or rest for four weeks. Then, each group was divided into three groups of AD, sham, and injection. Then, 48 hours after the last training session, Aβ1-42, or DMSO was injected into the hippocampus. Finally, after the isolation of the hippocampus, CaN mRNA and CaMKII mRNA levels were measured. Results The results of this study showed that there was a significant difference between the groups in mRNA CaN and CaMKII mRNA levels (P&lt;0.05). The results showed that aerobic exercise and AD pre-induction had a significant effect on increasing calcineurin and Ca2+/calmodulin-dependent protein kinase II levels. Conclusion Overall, the findings of the present study showed that four weeks of aerobic training improves the molecular signaling of neuroplasticity in AD rats.

Effects of ethanolic extract of Allium Sativum L on the hippocampus of male Wistar rats with Streptozotocin (STZ)- induced brain insulin resistance

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Harmine prevents 3-nitropropionic acid-induced neurotoxicity in rats via enhancing NRF2-mediated signaling: Involvement of p21 and AMPK

Oxidative stress induced neurotoxicity is increasingly perceived as an important neuropathologic mechanism underlying the motor and behavioral phenotypes associated with Huntington's disease (HD). Repeated exposure to 3-nitropropionic acid (3-NP) induces neurotoxic changes which closely simulate the neuropathological and behavioral characteristics of HD. This study aimed at evaluating the prophylactic effects of the dual-specificity tyrosine phosphorylation regulated kinase 1A (DYRK1A) inhibitor “harmine” against 3-NP-indued neurotoxicity and HD-like symptoms. The potential prophylactic effect of harmine (10 mg/kg/day; intraperitoneal) was investigated on 3-NP-induced motor and cognitive HD-like deficits, nuclear factor erythroid 2 like 2 (NRF2), AMP kinase (AMPK) and p21 protein levels and the gene expression of haem oxygenase-1 (Ho-1), NAD(P)H: quinone oxidoreductase-1 (Nqo-1) and p62 in addition to redox imbalance and histological neurotoxic changes in the striatum, prefrontal cortex, and hippocampus of male Wistar rats. Harmine successfully increased the protein levels of NRF2, AMPK and p21 and the gene expression of Ho-1, Nqo-1 and p62, restored redox homeostasis, and reduced CASPASE-3 level. This was reflected in attenuation of 3-NP-induced neurodegenerative changes and improvement of rats' motor and cognitive performance. This study draws attention to the protective role of harmine against 3-NP-induced motor and cognitive dysfunction that could be mediated via enhancing NRF2-mediated signaling with subsequent amelioration of oxidative stress injury via NRF2 activators, p21 and AMPK, in the striatum, prefrontal cortex, and hippocampus which could offer a promising therapeutic tool to slow the progression of HD.

Effects of Aerobic Training on Caspase-3 Expression and Apoptosis in Hippocampus of Rats after Brain Ischemic Stroke

Introduction: Although exercise is an effective strategy for preventing and treating stroke, the extent of this effect seems to depend on when exercise begins. Apoptosis plays a critical role after stroke. However, it is unclear whether early exercise inhibits apoptosis after stroke? The aim of this study was to determine the effect of eight weeks of early aerobic training after stroke induction on caspase-3 protein expression and apoptosis in the hippocampus of male Wistar rats.&#x0D; Methods: In this experimental study, 32 adult male Wistar rats (weighting 210-252 gr) were purchased and randomly divided into four groups: sham, ischemia, training and ischemia+ training groups. Ischemia was induced by the occlusion of both common carotid arteries (CCA) for 45 min. Aerobic training was initiated at 24 hours after induction of ischemia, for eight weeks for 20-50 minutes and at a speed of 18-30 meters per minute in each session and five sessions per week. Forty eight hours after the last training session, rats were sacrificed, then using immunohistochemical staining technique of caspase-3 protein expression and the rate of cell apoptosis were measured by hematoxylin and eosinophil (H&amp;E) staining method in hippocampus of rats.&#x0D; Results: The expression of caspase-3 protein and apoptosis in the hippocampus of rats in sham and training groups were significantly lower than in the ischemia and ischemia+ training groups (both; p&lt;0.0001). Moreover, in the ischemia+ training group, the expression of caspase-3 protein and apoptosis showed a significant decrease compared to the ischemia group (p&lt;0.0001).&#x0D; Conclusion: Based on the results of this study, it can be said that eight weeks of early aerobic training can reduce the lesions induced-cerebral ischemia by reducing the expression of cell death-causing factors.

A study on alpha-terpineol in Alzheimer’s disease with the use of rodent in vivo model, restraint stress effect and in vitro Amyloid beta fibrils

Alzheimer’s disease (AD) is a neurological disorder in which the neuronal degeneration is associated with inflammatory processes and oxidative stress. Since alpha-terpineol was shown to possess antioxidant and anti-inflammatory effects, the administration of this compound was studied on a rat model of AD. To create this model, Aβ1-42 was injected into the hippocampus of male Wistar rats. Generated AD models were divided into simple AD models and AD models in which short-term immobilization stress was added. Preventive and therapeutic (post-AD induction) effects of alpha-terpineol consumption (100 mg/Kg) were subsequently investigated in AD models, which were compared with control groups. Biochemical factors (superoxide dismutase and malondialdehyde), histological manifestations (amyloid plaques and neuron counts) and possible memory impairment (shuttle-box experiment) were investigated in all groups. For the in vitro experiment, alpha-terpineol effect was checked on Aβ1-42 fibril formation. In preventive and therapeutic modes, alpha-terpineol consumption could improve neurogenesis and long-term memory while reducing amyloid plaque counts and ameliorating biochemical factors (higher levels of superoxide dismutase and malondialdehyde and reduced levels of MDA). In vitro, shorter fibrillar structures were formed in the presence of alpha-terpineol, which indicates an anti-amyloid effect for this compound. In conclusion, alpha-terpineol significantly counteracted AD consequences.

Ghrelin Is Effective on Passive Avoidance Memory by Altering the Expression of NMDAR and HTR1a Genes in the Hippocampus of Male Wistar Rats.

Memory-dependent psychological behaviors have an important role in life. Memory strengthening in adulthood to prevent its defects in aging is a significant issue. The ghrelin endogenous hormone improves memory by targeting glutamatergic and serotonergic circuits. Also, citicoline, a memory strengthening drug in aging, is not recommended to adults due to its side effects. The current study aims to test that ghrelin treatment, like citicoline, would improve passive avoidance memory via expression of the genes encoding the N-methyl-D-aspartate receptor (NMDAR1) and the serotonin receptor 1A (HTR1α) involved in this process. Five groups of adult male rats received (1) saline (as control), (2) 0.5 mg/kg citicoline, or (3-5) 0.3, 1.5, and 3 nmol/μl ghrelin). The rats received the drugs via intra-hippocampal injection. Passive avoidance memory was determined using a shuttle box device. The latency to enter the dark chamber before (IL) and after (RL) injection and the total duration of the animal's presence in the light compartment (TLC) were evaluated. Then, the gene expression rates of NMDAR1 and HTR1α were measured by the Real-Time PCR. Ghrelin and citicoline had some similar and significant effects on passive avoidance memory, and both increased NMDAR1 and decreased HTR1α expression. Ghrelin, like citicoline, improves passive avoidance learning by altering the NMDAR1 and HTR1α expression in the hippocampus.

Effects of ethanol extract of allium sativum L. On the hippocampus of male wistar rats with streptozotocin-induced brain insulin resistance

Effects of ethanol extract of allium sativum L. On the hippocampus of male wistar rats with streptozotocin-induced brain insulin resistance

The Effect of 6 Weeks of Combination Training on NeuN and NF200 Factors and the Number of Living Cells in the CA1 Region of the Hippocampus of Male Wistar Rats: An Experimental Study

The Effect of 6 Weeks of Combination Training on NeuN and NF200 Factors and the Number of Living Cells in the CA1 Region of the Hippocampus of Male Wistar Rats: An Experimental Study

The Effect of NeuroAid (MLC901) on Cholestasis-Induced Spatial Memory Impairment with Respect to the Expression of BAX, BCL-2, BAD, PGC-1α and TFAM Genes in the Hippocampus of Male Wistar Rats.

Cholestasis is a bile flow reduction that is induced following Bile Duct Ligation (BDL). Cholestasis impairs memory and induces apoptosis. Apoptosis consists of two pathways: intrinsic and extrinsic. The intrinsic pathway is modulated by BCL-2 (B cell lymphoma-2) family proteins. BCL-2 (a pro-survival BCL-2 protein) has anti-apoptotic effect, while BAD (BCL-2-associated death) and BAX (BCL-2-associated X), the other members of BCL-2 family have pro-apoptotic effect. Furthermore, TFAM (mitochondrial transcriptional factor A) is involved in transcription and maintenance of mitochondrial DNA and PGC-1α (peroxisome proliferator-activated receptor γ coactivator-1α) is a master regulator of mitochondrial biogenesis. On the other hand, NeuroAid is a Traditional Chinese Medicine with neuroprotective and anti-apoptosis effects. In this study, we evaluated the effect of cholestasis on spatial memory and expression of BCL-2, BAD, BAX, TFAM, and PGC-1α in the hippocampus of rats. Additionally, we assessed the effect of NeuroAid on cholestasis-induced cognitive and genetic alterations. Cholestasis was induced by BDL surgery and NeuroAid was injected intraperitoneal at the dose of 0.4mg/kg. Furthermore, spatial memory was evaluated using Morris Water Maze (MWM) apparatus. The results showed cholestasis impaired spatial memory, increased the expression of BAD and BAX, decreased the expression of TFAM and PGC-1α, and did not alter the expression of BCL-2. Also, NeuroAid decreased the expression of BAD and BAX and increased the expression of TFAM, PGC-1α, and BCL-2. In conclusion, cholestasis impaired spatial memory and increased the expression of pro-apoptotic genes. Also, cholestasis decreased the expression of TFAM and PGC-1α. Interestingly, NeuroAid restored the effects of cholestasis.

Investigating the effect of crocin on memory deficits induced by total sleep deprivation (TSD) with respect to the BDNF, TrkB and ERK levels in the hippocampus of male Wistar rats.

Sleep deprivation (SD) induces cognitive impairments such as memory deficit. Brain-derived neurotrophic factor (BDNF) is considered as the most critical neurotrophin in the central nervous system that is involved in sleep and memory. The main receptor of BDNF, tropomyosin receptor kinase B (TrkB), is dramatically expressed in the hippocampus. Also, extracellular signal-regulated kinase (ERK) has a significant role in memory function. Crocin is a carotenoid chemical compound and the active component of the flower Crocus sativus L. (saffron) that improves memory function and increases the level of BDNF, TrkB and ERK. In this research, we aimed to investigate the effect of total SD (TSD, 24 h) and crocin on memory performance, and BDNF, TrkB and ERK hippocampal levels. Passive avoidance memory was assessed using step-through, and working memory was measured using Y-maze tasks. The level of proteins in both hemispheres of the hippocampus was evaluated using Western blotting. Crocin was injected intraperitoneally at doses of 1, 5 and 15 mg/kg. Twenty-four-hour TSD impaired both types of memories and decreased the level of all proteins in both hemispheres of the hippocampus. Crocin at all doses restored TSD-induced memory deficits. Crocin (15 mg/kg) reversed the effect of TSD on levels of all proteins. The adverse effect of TSD on the level of proteins in the hippocampus may disrupt synaptic plasticity and transmission, which induces memory impairment. Additionally, the restoration effect of crocin on the decrease in protein levels may be involved in its improvement effect on memory performance.

High intensity interval training increases the expression of hippocampus BDNF gene and decreases the serum tnf-α in Diabetic Rat

Background: Diabetics have many disabilities, including neuronal damege hippocampus, and BDNF is an effective factor in this field. This factor has the most impact on the hippocampus, also TNF-α is an inflammatory factor that increases in diabetes, the purpose of this study was to investigate the effect of 6 weeks of High Intensity interval training on the gene expression of brain-derived neurotrophic factor (BDNF) in the hippocampus of male Wistar rats. Methods: For this study, 48 male Wistar rats (4 weeks old) with 150± 10 g weight were categorized in 4 groups of: diabetic rats (n= 12), exercise diabetic (n= 12), control (n= 12) and exercise control (n= 12). For induction of diabetes, peritoneal injection of STZ solution (50 mg/kg) was used. After a week of familiarization with the environment and practice, high Intensity interval training protocol consisted of 3 days of training per week for 6 weeks with 50% to 110% of maximum oxygen consumption was performed. 24 hours after the completion of the exercise, the functional test was taken and the animals were autopsy 48 hours after the functional test. Finally, BDNF gene expression was evaluated using Real Time PCR technique. Results: Regarding the results, it was found that the high Intensity interval training intensified the expression of the BDNF gene and decreased the expression of the TNF-α protein. also The weight gain of the hippocampus has been observed along with increased expression of BDNF gene in the diabetic high Intensity interval training group. Conclusion: Exercise can help prevent hippocampus tissue loss, and also prevent memory damage that caused by diabetes. Also, high Intensity interval training are effective in maintaining the physical fitness of diabetics, therefore high Intensity interval training are recommended for improvement in the physical condition and life of diabetics.

The Effect of Four Weeks of Aerobic Training on the Expression of Sirt1, CREB and BDNF Genes in Hippocampus of Male Wistar Rats with Alzheimer’s Disease

The Effect of Four Weeks of Aerobic Training on the Expression of Sirt1, CREB and BDNF Genes in Hippocampus of Male Wistar Rats with Alzheimer’s Disease