Effect of insulin on spatial memory in aluminum chloride-induced dementia in rats

Abstract

Latest reports suggest the involvement of insulin in modulating memory. A few published in-vitro studies favor the antidementia effect of insulin. Thus, the present study aimed to evaluate the prophylactic role of insulin and its combination with glucose and its possible mechanism(s) in an aluminum chloride (AlCl3)-induced cognitive dysfunction model in rodents, with a special focus on memory centers namely, the hippocampus and the frontal cortex. Male Wistar rats were exposed to AlCl3 (175 mg/kg orally) for 60 days. Insulin (0.5 IU/kg), Insulin (0.5 IU/kg) in combination with glucose (200 mg/kg), and rivastigmine (1 mg/kg) were administered intraperitoneally 45 min before the administration of AlCl3 for 60 days. Spatial memory was assessed using the Morris water-maze test. After 60 days of treatment, animals were killed, and the hippocampus and frontal cortex were collected and analyzed for acetylcholinesterase activity and antioxidant enzyme level. Blood glucose levels were also analyzed. Treatment with the standard drug, rivastigmine (1 mg/kg), produced a significant reduction in escape latency and increased the time spent in the target quadrant compared with the AlCl3-treated group. Insulin and its combination with glucose could not inhibit the behavioral impairments in aluminum-exposed rats. Treatment with insulin alone and its combination with glucose reversed the increased glucose levels. Insulin alone and its combination with glucose could not inhibit aluminum-induced oxidative stress and impaired cholinergic transmission in the hippocampus and frontal cortex regions. The study suggests the inability of prophylactic insulin administration against cognitive dysfunction induced by environmental toxin (AlCl3) in the hippocampus and the frontal cortex.

Chenodeoxycholic Acid Ameliorates AlCl3-Induced Alzheimer’s Disease Neurotoxicity and Cognitive Deterioration via Enhanced Insulin Signaling in Rats

“…As shown in the current work, CDCA reduced AlCl 3 -induced cognitive defects as assessed by Morris Water Maze and Y-maze tests, these results were paralleled by a diminution in the measured AD markers; viz., BACE1 and Aβ 42 . The latter two parameters, however, were boosted in the AlCl 3 treated animals which match earlier findings reporting the effect of AlCl 3 on these markers [21,22] and spatial memory as well [23].…”

Dehydrozingerone protects temozolomide-induced cognitive impairment in normal and C6 glioma rats besides enhancing its anticancer potential

“…daily (Wick et al 2009 ; Anusha et al 2016 ). The cognitive function was assessed for episodic and spatial memory by NORT (Cheruku et al 2019 ) and Morris water maze test, respectively (Nampoothiri et al 2017 ). To assess the toxic effect of TMZ on locomotor activity, an actophotometer was used.…”

“…Animals were trained in four sessions (acquisition trial) to identify the hidden platform in the target quadrant. In the retention trail, the platform was removed and animals’ movements were recorded for 60 s. Parameters total zone entries, average speed, path efficiency, and escape latency to reach the platform were calculated using the software (Nayak et al 2017 ; Nampoothiri et al 2017 ).…”

Erratum: Effect of aluminum chloride on blood glucose level and lipid profile in normal, diabetic and treated diabetic rats

“…Reduction in AChE activity will result in increased level of ACh. [ 21 ] ACh is reported to increase the insulin secretion when glucose level is above 7 mM. The blood glucose level in the AlCl 3 and STZ-treated group at baseline was 21.24 mM (386.8 mg/dL).…”