Protection of hippocampal CA1 neurons against ischemia/reper-fusion injury by exercise preconditioning via modulation of Bax/ Bcl-2 ratio and prevention of caspase-3 activation

Introduction: Ischemia leads to loss of neurons by apoptosis in specific brain regions, especially in the hippocampus. The purpose of this study was investigating the effects of exercise preconditioning on expression of Bax, Bcl-2, and caspase-3 proteins in hippocampal CA1 neurons after induction of cerebral ischemia

Methods: Male rats weighing 260-300 g were randomly allocated into three groups [sham, exercise, and ischemia]. The rats in exercise group were trained to run on a treadmill 5 days a week for 4 weeks. Ischemia was induced by the occlusion of both common carotid arteries [CCAs] for 20 min. Levels of expression of Bax, Bcl-2, and caspase-3 proteins in CA1 area of hippocampus were determined by immunohistochemical staining

Results: The number of active caspase-3-positive neurons in CA1 area were significantly increased in ischemia group, compared to sham-operated group [P<0.001], and exercise preconditioning significantly reduced the ischemia/reperfusion-induced caspase-3 activation, compared to the ischemia group [P<0.05]. Also, results indicated a significant increase in Bax/Bcl-2 ratio in ischemia group, compared to sham-operated group [P<0.001]

Discussion: This study indicated that exercise has a neuroprotective effects against cerebral ischemia when used as preconditioning stimuli

[Investigating the effects of 217 Hz frequency of cell phone on learning and spatial memory in rats]

Background: Extremely low frequency [0-300 Hz] fields from power lines, electronic equipment and medical devices, have been reported to produce various biological effects. Global system for mobile [GSM] is most largely used in everybody's life. This system utilizes a low frequency band as well as a high frequency range of electromagnetic field. This study investigated the effects of 217 Hz electromagnetic field [the modulating signal in GSM] on spatial learning and memory in rat

Methods: Twenty four male Wistar rat [200- 250 g] were randomly divided in to three groups as: test, sham and control. Using a Helmholtz coil system, the test group was exposed to a uniform pulsed EMF of 200 microT [micro Tesla] intensity for 4 h/day for 21 days [2 time in a day]. This procedure was repeated for the sham group but with no field. All groups were trained prior to the day 21 on the 15th day for five days four trial per day in Morris Water-Maze system. Then the probe test was carried out for 60 seconds with no platform

Results: The ANOVA test revealed that no significant differences were found between control and exposed rats in all day of learning acquisition. Also, in probe test for investigating the memory, no significant differences observed. [P

Conclusion: This finding is in consistent with previous studies and indicates low frequency band of electromagnetic fields [EMF] [200 microT intensity] in cell phone may not have any effect on the learning acquisition and spatial memory in rat

effect of acute ethanol and gabapentin administration on spatial learning and memory

Introduction: Patients with epilepsy can have impaired cognitive abilities. Many factors contribute to this impairment, including the adverse effects of antiepileptic drugs like Gabapentin [GBP]. Apart from anti-epilectic action, Gabapentin is used to relieve ethanol withdrawal syndrome. Because both GBP and ethanol act on GABA ergic system, the purpose of this study was to evaluate their effect and interaction on spatial learning and memory. Material and Methods: Male Sprague-Dawley rats were trained in the Morris water maze for 5 consecutive days. On the sixth day, a probe test was performed to assess the retention phase or spatial rats' memory ability. Ethanol [1.5 g/kg i.p.] and GBP [30 mg/kg i.p.] was administered each day 30 and 40 minutes before testing respectively. Results: Acute ethanol administration selectively impaired spatial memory [p<0.05], yet it failed to impair the acquisition phase [learning]. Contradictorily GBP selectively impaired learning on second and forth days. Conclusion: These findings demonstrate that GBP and acute ethanol impair different phases of learning probably by modifying different neuronal pathways in cognitive areas of the brain

Effect of angiotensin II on blood flow in acute and chronically inflamed knee joints of rabbits: the role of nitric oxide

Angiotensin converting enzyme [ACE] upregulation in stromal cells of joints affected by rheumatoid arthritis may lead to higher tissue angiotensin II that is a vasoconstrictor and mitogen factor. To date, the role of angiotensin II on regulating blood flow in inflamed joints has not been studied. Acute and chronic joint inflammation was induced in rabbits by intra-articular injection of carrageenan and antigen-induced arthritis method, respectively. The ACE level of synovial fluid and the response of joint blood flow to angiotensin II, angiotensin II receptor antagonist, and the role of nitric oxide [NO] in modulation of the effects of angiotensin II on joint blood vessels were examined The synovial fluid level of ACE was significantly increased during the process of inflammation and angiotensin II increased joint vascular resistance dose-dependently in both acute and chronically inflamed joints. The angiotensin 1 receptor antagonist losartan completely blocked the vasoconstrictor effect of angiotensin II on joint blood vessels and induced vasodilatation. Nitric oxide synthase inhibitor N-omega -nitro L- arginine methyl ester [L-NAME] increased joint vascular resistance and augmented vascular response of inflamed joints to angiotensin II. Angiotensin II receptors in joint blood vessels are angiotensin -1 subtype, and inflammation significantly increases the activity of synovial fluid ACE. Nitric oxide plays a significant role on regulating joint blood flow and in modulation of angiotensin 1 receptor-mediated vasoconstriction of inflamed joint blood vessels