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Introduction: Studies showed that following spontaneous epilepsy in rats, the permeability of CA1 region of Hypocampus to calcium is increased. In this study the role of voltage dependent calcium channels on the development of kindling induced by Pentylenetetrazol (PTZ) was investigated in rats.
Materials and Methods: In this experimental study rats were divided into two groups. In the test group, Verapamil (calcium channel blocker) was injected in the Hippocampus (4 g/4 min). After 20 minutes kindling was established by PTZ in subconvulsive dose (37.5 mg/kg ip). Convulsing activities were monitored for 20 min. The control group was the same age and undergone the same procedure exept for the injection, in which ACSF was injected without Verapamil.
Results: Verapamil significantly (p<0.01) reduced the number of needed stimulations to progress from stage 0 to 5 of the convulsion and also significantly (p<0.05) prolonged the fifth stage of seizure.
Conclusion: The results of this study suggested that interahippcampal injection of Verapamil facilitated the Pentylenetetrazol kindling in rats but had inhibitory effects on kindled animals.

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Background: Sumatriptan is a serotonin agonist. Hippocampal receptors contribute to the serotonergic control of learning. It seems that sumatriptan can also affect learning through serotonin receptors. Thus, this study was performed to investigate the effect of sumatriptan on cellular mechanisms of learning in male rats. Materials and Methods: In this experimental study, male Wistar rats were kept in standard conditions in the Animal Laboratory of the Department of Physiology, Arak University of Medical Sciences. After doing the surgical procedure and locating the electrodes in the CA1 region of hippocampus, synaptic transmission and long-term potentiation were measured, and the effect of three doses of sumatriptan on these parameters was compared to the control group. Results: Sumatriptan could significantly inhibit the effect of tetanic stimulation on long-term potentioation in the CA1 region of hippocampus, as compared to the control group. However, there was no significant difference in the synaptic transmission between the sumatriptan and control groups. Conclusion: This results show that sumatriprtan can probably impair learning and memory through inhibition of LTP in the CA1 region of hippocampus.

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Introduction: This study was to examine the effects of endurance training and high-fat diet in brain-derived neurotrophic factor (BDNF) in the male adult rat hippocampus.

Materials and Methods: Twenty eight Wistar rats were divided into four groups: (1) Regular diet-sedentary (RD-Sed), (2) Regular diet-Exercise (RD-Exe), (3) HF-sedentary (HF-Sed), and (4) HF- Exercise (HF- Exe) RD-Sed group was regarded as control. Animals in exercise groups received 8-wk endurance training and animals in HF groups were exposed to the HF diet for 8-wk. Hippocampal BDNF protein was assessed using commercial ELISA kits and the data were analyzed by one-way ANOVA. Statistical differences were considered significant at p<0.05.

Results: The results showed that the endurance training had no significant increase in BDNF protein level comparison with the RD-Sd and HF-Sed groups moreover the high-fat diet had no significant effect in BDNF protein level.

Conclusion: According to results of present study, looks applications of endurance training can increase amount of hippocampus BDNF protein level.

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Background: Considering the increased activity of hypothalamic orexinergic neurons due to morphine administration, and its extensive projections to the hippocampus, it is probable that morphine effect on CA1 neuronal function is mediated by orexinergic system. So the effect of hippocampal orexin-1 receptors (OX1R) blockade on CA1 baseline synaptic response and short term synaptic plasticity was investigated.

Materials and Methods: In this experimental study, animals received morphine 10 mg/kg/12h/(SC) for 10 days. SB-334867-A, OX1R antagonist (0.5&mug/0.5 &mul), was microinjected intrahippcampally for OX1R inhibition before each morphine injection. Baseline synaptic response and short term synaptic plasticity were evaluated by field potential recording. fEPSP was recorded from CA1 following Schaffer collaterals stimulation. After Input/Output construction, short term synaptic plasticity was induced by paired pulse stimulations.

Results: Chronic use of morphine did not affect the baseline synaptic response (p>0.05). SB- 334867-A microinjection in CA1 did not have any effect on baseline synaptic response in morphine dependent rats. Morphine increased paired pulse index (PPI) at 80 ms inter pulse interval (IPI, p<0.05). SB-334867-A pretreatment did not affect this morphine induced PPI change.

Conclusion: The results suggest that orexin-1 receptors (OX1R) do not mediate the effect of morphine on baseline synaptic response and short term synaptic plasticity in CA1 area of the hippocampus.

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Background: Considering the increased activity of hippocampal glial cells due to chronic morphine administration and the involvement of hippocampus in restoration of the addictive drug-associated experience, the role of these cells on morphine induced conditioned place preference (CPP) was investigated.

Materials and Methods: In this experimental study, four groups of animals were evaluated. After habituation to CPP apparatus on the first day, conditioning was done by injection of morphine (5 mg/kg) or its vehicle (saline) during three consecutive days. On the fifth day, the time spent in each compartment of CPP cage and locomotor activity was recorded for 20 min. To investigate the role of hippocampal glial cells in CPP, these cels were inbibited by bilaterally injecting fluorocitrate (1nmol/1ml), before each morphine injection. CPP testing in this group and animals received fluorocitrate vehicle (Phosphate buffer saline) was done before morphine injection.

Results: Fluorocitrate pretreatment reduced morphine induced conditioned place preference acquisition, so that a significant decrease was observed in conditioning score (unpaired t-test, p<0.01) in this group (n=8) compared to animals received morphine (n=9). Neither morphine nor fluorocitrate pretreatment did not affect locomotor activity (ANOVA, p>0.05).

Conclusion: The results suggest that glial cells in the hippocampus are involved in morphine induced conditioned place preference.

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Background: The Amyloid beta (Aβ) level increases in the brain of patients with Alzheimer's disease. The present study aimed to investigate the effects of eight weeks continuous training with low and high intensities on Aβ_1-42 levels in hippocampus of Alzheimer model rats.

Materials and Methods: Fifty male Wistar rats (12 weeks old and mean weight 219.82±13.10 g) were divided into five groups including: healthy control, Alzheimer’s control, Alzheimer's low-intensity training, Alzheimer's high-intensity training and sham. To induce Alzheimer's disease, homocysteine is infused into the rats cerebroventricular (dose of 0.6M). Low intensity groups trained with 20m/min (50-55% VO₂max) and high-intensity groups trained with 27m/min (75-80% VO₂max), 60min/day, and five days per week on the treadmill. For data analysis, one-way ANOVA and post hoc Tukey test were performed (p<0.05).

Results: The Aβ_1-42 levels in hippocampus of Alzheimer's control group was significantly higher than healthy control group (p=0.001) and in training groups with both low and high intensity was significantly lower than Alzheimer's control group (p=0.02). But no significant differences were found between two intensity (p=0.99).

Conclusion: It seems that continuous exercise training, through reducing the level of Aβ_1-42 in hippocampus, can be useful for Alzheimer’s disease model rats and continuous training can be studied as a complementary therapy in Alzheimer's disease.

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Introduction: The thickness of the molecular and pyramidal layers in the hippocampus represents a pivotal aspect of Alzheimer's research. This study was conducted to investigate the effect of swimming endurance, resistance, and combined exercises on the molecular and pyramidal layers of the hippocampus tissue thickness of Alzheimer's rats.
Methods: In this experimental study, 40 large white Wistar laboratory rats (6 weeks old; Weight 180-200 g) were randomly and equally divided into five groups: healthy control, Alzheimer's control, endurance, resistance, and combined. Alzheimer's disease was induced by intraperitoneal injection of trimethyltin chloride (8 mg/kg). Two weeks after the injection and confirmation of Alzheimer's induction, the training protocols of endurance (5-sessions/week, the first to the fourth week incrementally from 5-15-min to 45-min of swimming, the fifth to the twelfth week 60-min of swimming), resistance (5-sessions/week, The first week of familiarization with the exercise, week 2; 30%, week3-5; 70-90%, week6-8; 100-110%, week9-10; 120-130%, and week11-12; 140-150% of body weight), combined (2 resistance sessions/week and three endurance sessions/week) was performed for 12 weeks. Forty-eight hours post-intervention, animals were dissected, and hippocampus tissue was harvested. Finally, the data were analyzed at the significance level of P < 0.05.
Results: The thickness of the molecular and pyramidal layers of the hippocampal tissue of Alzheimer's animals decreased compared to healthy animals, and all three endurance, resistance, and combined exercise protocols increased layers (P < 0.001). However, the increase in the molecular and pyramidal layers thickness of the hippocampal tissue of combined group rats compared to the endurance and resistance group had a greater increase (P < 0.01).
Conclusions: These findings highlight the changes in the thickness of the hippocampal tissue layers concerning Alzheimer's pathology and the effect of combined exercises on this parameter. While exercise may have positively affected hippocampal volume and synaptic plasticity, more research is needed to fully understand the impact of exercise on hippocampal layer thickness in Alzheimer's.