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

Madhavan Nampoothiri, Nitesh Kumar, Grandhi Venkata Ramalingayya, Nampurath Gopalan Kutty, Nandakumar Krishnadas, Chamallamudi Mallikarjuna Rao

Research output: Contribution to journalArticle

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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.

Original languageEnglish
Pages (from-to)540-544
Number of pages5
JournalNeuroReport
Volume28
Issue number9
DOIs
Publication statusPublished - 01-05-2017

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Dementia
Insulin
Rivastigmine
Frontal Lobe
Glucose
Hippocampus
Aluminum
aluminum chloride
Spatial Memory
Acetylcholinesterase
Cholinergic Agents
Blood Glucose
Wistar Rats
Rodentia
Oxidative Stress
Antioxidants
Water
Enzymes
Pharmaceutical Preparations

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

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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.",
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Effect of insulin on spatial memory in aluminum chloride-induced dementia in rats. / Nampoothiri, Madhavan; Kumar, Nitesh; Ramalingayya, Grandhi Venkata; Kutty, Nampurath Gopalan; Krishnadas, Nandakumar; Rao, Chamallamudi Mallikarjuna.

In: NeuroReport, Vol. 28, No. 9, 01.05.2017, p. 540-544.

Research output: Contribution to journalArticle

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