Effects of treadmill running on spatial learning and memory in streptozotocin-induced diabetic rats

Reisi, Parham; Alaei, Hojjatallah; Babri, Shirin; Sharifi, Mohammad Reza; Mohaddes, Gisou

doi:10.1016/j.neulet.2009.03.052

Cited by 49 publications

(33 citation statements)

References 39 publications

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“…Diabetes alone could cause deficits in spatial learning in a rat model of STZinduced diabetes 3 months after STZ treatment. 20) In rats, DM could have caused the loss of choline acetyltransferase (ChAT) activity in the hippocampus. 21,22) DM also increased GFAP in brain homogenates.…”

Section: )mentioning

confidence: 99%

Cinepazide Maleate Improves Cognitive Function and Protects Hippocampal Neurons in Diabetic Rats with Chronic Cerebral Hypoperfusion

Zhang

et al. 2017

Biological & Pharmaceutical Bulletin

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To determine the combined effect of type 2 diabetes (T2D) and chronic cerebral hypoperfusion (CCH) on learning and spatial memory, we developed a rat model of CCH by permanent occlusion of bilateral common carotid arteries (2-vessel occlusion (2VO)) in high-fat diet (HFD)-fed rats injected with low-dose streptozotocin (STZ). Furthermore, we examined the effect of cinepazide maleate (CM) on cognitive deficits and brain damage in this rat model. Rats were maintained on HFD for 6 weeks and then injected with 35 mg/kg STZ to induce T2D. Sham or 2VO surgery was performed in non-diabetic or diabetic (DM) rats to obtain four groups: blank, DM, CCH, and DM-CCH groups. Cognitive function was tested by the Morris water maze (MWM) test. To determine the effects of the vasodilator cinepazide maleate (CM) on cognitive deficits and brain damage, DM-CCH rats were administered with 10 mg/kg CM or saline daily for 14 d. Neuronal damage in DM-CCH rats was associated with increased expression of glial fibrillary acidic protein (GFAP) and β-secretase 1 (BACE1), but decreased expression of choline acetyltransferase (ChAT). Moreover, the levels of all these proteins were significantly alleviated by CM treatment. These results suggest that T2D exacerbated CCH-induced brain damage and cognitive impairment, and CM ameliorated these effects.Key words diabetes; chronic cerebral hypoperfusion; cognitive impairment; cinepazide maleate Chronic cerebral hypoperfusion (CCH) is thought to be an important factor contributing to cognitive decline, both in aging and in age-related neurological disorders.1-3) The severity of memory dysfunction and the decline in cerebral blood flow are strongly correlated in disorders, such as Alzheimer's disease (AD), vascular dementia, and stroke.4,5) Diabetes is one of the fastest growing epidemics worldwide and diabetic patients are at a high risk for development of cognitive impairment or dementia. 6) Moreover, diabetes is often associated with CCH, and can further aggravate neurodegeneration.Permanent bilateral occlusion of both common carotid arteries (or 2-vessel occlusion, 2VO) is a widely used rodent model of CCH. As the model mimics several features of human AD and vascular dementia, it is used to investigate the consequences of hypoperfusion on cerebral blood flow, cognitive ability, and histopathology in these neurological disorders.2,7) Progressive cognitive impairment has been reported after 2VO in rats, 2,[8][9][10][11] and behavioral changes resulting from cognitive impairment are associated with delayed loss of neurons in the hippocampal CA1 region, a feature commonly observed in human aging and dementia.2) CA1 cell loss is characterized by gliosis, cholinergic dysfunction, 12) and activation of β-secretase 1 (BACE1).13) Consistent memory impairment after 2VO in rats occurs in the chronic phase of the ischemic event, i.e., up to 3 months after surgery, and not within 7 d, as assessed by water maze and object recognition tasks. 14)Cinepazide maleate (CM) is a calcium-channel blocker with vasodilato...

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Section: )mentioning

confidence: 99%

Cinepazide Maleate Improves Cognitive Function and Protects Hippocampal Neurons in Diabetic Rats with Chronic Cerebral Hypoperfusion

Zhang

et al. 2017

Biological & Pharmaceutical Bulletin

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“…1 Experimental protocol for different groups, the days on which memory acquisition or retrieval were tested. Co control group, Ex-Re exercise-rest (withdrawal exercise) group, Re-Ex rest-exercise (exercised group) group, Ex-Ex exerciseexercise (continual exercise) group likelihood of receiving shock was controlled by exposing the sham-exercised group to the treadmill apparatus without switching on the treadmill at the start of the experiment (Uda et al 2006;Alaei et al 2008;Chen et al 2008;Reisi et al 2009;Choi et al 2011). These rats received the same electric shock when they stepped onto the grid.…”

Section: Exercise Paradigmsmentioning

confidence: 99%

Effect of forced exercise and exercise withdrawal on memory, serum and hippocampal corticosterone levels in rats

et al. 2015

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Evidence suggests that there are positive effects of exercise on learning and memory. Moreover, some studies have demonstrated that forced exercise plays the role of a stressor. This study was aimed at investigating the effects of different timing of exercise and exercise withdrawal on memory, and serum and hippocampal corticosterone (CORT) levels. Wistar rats were randomly divided into five groups: control, sham, exercise-rest (exercise withdrawal), rest-exercise (exercised group), and exercise-exercise (continuous exercise). Rats were forced to run on a treadmill for 1 h/day at a speed 20-21-m/min. Memory function was evaluated by the passive avoidance test in different intervals (1, 7 and 21 days) after foot shock. Findings showed that after the exercise withdrawal, short-term and mid-term memories, had significant enhancement compared to the control group, while the long-term memory did not present this result. In addition, the serum and hippocampal CORT levels were at the basal levels after the rest period in the exercise-rest group. In the rest-exercise group, exercise improved mid- and long-term memories, whereas continuous exercise improved all types short-, mid- and long-term memories, particularly the mid-term memory. Twenty-one and forty-two days of exercise significantly decreased the serum and hippocampal CORT levels. It seems that exercise for at least 21 days with no rest could affect biochemical factors in the brain. Also, regular continuous exercise plays an important role in memory function. Hence, the duration and withdraw of exercise are important factors for the neurobiological aspects of the memory responses.

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“…Diabetic rat model Since Reisi and colleagues have demonstrated that streptozotocin (STZ)-induced diabetic SD rats show memory decline after 3 months (Reisi et al 2009), this model was employed in this work. To induce diabetes in male SD rats (2503 00 g), STZ was freshly dissolved in 0.05 M citrate buffer, pH 4.5, and a single intraperitoneal (i.p.)…”

Section: Animal Models and Brain Tissue Collectionmentioning

confidence: 99%

“…1g). Since Reisi and colleagues have demonstrated that STZ-induced diabetic SD rats show memory decline (Reisi et al 2009), we measured formaldehyde levels in the hippocampi of STZ-induced diabetic SD rats after 3 months. Similarly, there was a marked increase in hippocampal formaldehyde level of diabetic rats compared with controls (P<0.01) (Fig.…”

Section: Endogenous Formaldehyde Concentrations Increase In Age-relatmentioning

confidence: 99%

Accumulated hippocampal formaldehyde induces age-dependent memory decline

Tong

Han

Luo

et al. 2012

AGE

169

144

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Aging is an important factor in memory decline in aged animals and humans and in Alzheimer's disease and is associated with the impairment of hippocampal long-term potentiation (LTP) and downregulation of NR1/NR2B expression. Gaseous formaldehyde exposure is known to induce animal memory loss and human cognitive decline; however, it is unclear whether the concentrations of endogenous formaldehyde are elevated in the hippocampus and how excess formaldehyde affects LTP and memory formation during the aging process. In the present study, we report that hippocampal formaldehyde accumulated in memorydeteriorating diseases such as age-related dementia. Spatial memory performance was gradually impaired in normal Sprague-Dawley rats by persistent intraperitoneal injection with formaldehyde. Furthermore, excess formaldehyde treatment suppressed the hippocampal LTP formation by blocking N-methyl-D-aspartate (NMDA) receptor. Chronic excess formaldehyde treatment over a period of 30 days markedly decreased the viability of the hippocampus and down-regulated the expression of the NR1 and NR2B subunits of the NMDA receptor. Our results indicate that excess endogenous formaldehyde is a critical factor in memory loss in age-related memory-deteriorating diseases.

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Effects of treadmill running on spatial learning and memory in streptozotocin-induced diabetic rats

Cited by 49 publications

References 39 publications

Cinepazide Maleate Improves Cognitive Function and Protects Hippocampal Neurons in Diabetic Rats with Chronic Cerebral Hypoperfusion

Cinepazide Maleate Improves Cognitive Function and Protects Hippocampal Neurons in Diabetic Rats with Chronic Cerebral Hypoperfusion

Effect of forced exercise and exercise withdrawal on memory, serum and hippocampal corticosterone levels in rats

Accumulated hippocampal formaldehyde induces age-dependent memory decline

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