Behavioural assessment of nicotinic acid, a GPR109a receptor agonist against memory deficit in rats

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Abstract

Present study was aimed at evaluating the neuroprotective role of nicotinic acid, GPR109a receptor agonist against aluminium chloride-induced dementia in rats. Dementia was induced in rats by chronic administration of aluminium chloride (10mg/kg, i.p.) for 42 days. Rats developed dementia as manifested by increased escape latency, total distance travelled to reach the target quadrant, latency to target quadrant in Morris water maze test. Fifteen days chronic oral treatment with nicotinic acid was able to reverse the elevated escape latency at higher doses (100 and 200 mg/kg), but found statistically insignificant. At 50 mg/kg, nicotinic acid failed to show any promising effect on behavioural parameters. Further, at 200 mg/kg dose, nicotinic acid reversed the elevated total distance and latency to target quadrant. However, statistically it was found insignificant as compared to AlCl3 control. This suggest the possibilities of nicotinic acid, a GPR109a receptor agonist, to have neuroprotective action against aluminium-induced memory deficit. However, detailed investigation is required to substantiate the above findings.

Original languageEnglish
Article number57
Pages (from-to)313-317
Number of pages5
JournalInternational Journal of Pharmaceutical Sciences Review and Research
Volume40
Issue number1
Publication statusPublished - 01-09-2016

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Niacin
Memory Disorders
Dementia
Aluminum
Water
aluminum chloride

All Science Journal Classification (ASJC) codes

  • Pharmaceutical Science

Cite this

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title = "Behavioural assessment of nicotinic acid, a GPR109a receptor agonist against memory deficit in rats",
abstract = "Present study was aimed at evaluating the neuroprotective role of nicotinic acid, GPR109a receptor agonist against aluminium chloride-induced dementia in rats. Dementia was induced in rats by chronic administration of aluminium chloride (10mg/kg, i.p.) for 42 days. Rats developed dementia as manifested by increased escape latency, total distance travelled to reach the target quadrant, latency to target quadrant in Morris water maze test. Fifteen days chronic oral treatment with nicotinic acid was able to reverse the elevated escape latency at higher doses (100 and 200 mg/kg), but found statistically insignificant. At 50 mg/kg, nicotinic acid failed to show any promising effect on behavioural parameters. Further, at 200 mg/kg dose, nicotinic acid reversed the elevated total distance and latency to target quadrant. However, statistically it was found insignificant as compared to AlCl3 control. This suggest the possibilities of nicotinic acid, a GPR109a receptor agonist, to have neuroprotective action against aluminium-induced memory deficit. However, detailed investigation is required to substantiate the above findings.",
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AU - Khurana, Shruti

AU - Nampoothiri, Madhavan

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N2 - Present study was aimed at evaluating the neuroprotective role of nicotinic acid, GPR109a receptor agonist against aluminium chloride-induced dementia in rats. Dementia was induced in rats by chronic administration of aluminium chloride (10mg/kg, i.p.) for 42 days. Rats developed dementia as manifested by increased escape latency, total distance travelled to reach the target quadrant, latency to target quadrant in Morris water maze test. Fifteen days chronic oral treatment with nicotinic acid was able to reverse the elevated escape latency at higher doses (100 and 200 mg/kg), but found statistically insignificant. At 50 mg/kg, nicotinic acid failed to show any promising effect on behavioural parameters. Further, at 200 mg/kg dose, nicotinic acid reversed the elevated total distance and latency to target quadrant. However, statistically it was found insignificant as compared to AlCl3 control. This suggest the possibilities of nicotinic acid, a GPR109a receptor agonist, to have neuroprotective action against aluminium-induced memory deficit. However, detailed investigation is required to substantiate the above findings.

AB - Present study was aimed at evaluating the neuroprotective role of nicotinic acid, GPR109a receptor agonist against aluminium chloride-induced dementia in rats. Dementia was induced in rats by chronic administration of aluminium chloride (10mg/kg, i.p.) for 42 days. Rats developed dementia as manifested by increased escape latency, total distance travelled to reach the target quadrant, latency to target quadrant in Morris water maze test. Fifteen days chronic oral treatment with nicotinic acid was able to reverse the elevated escape latency at higher doses (100 and 200 mg/kg), but found statistically insignificant. At 50 mg/kg, nicotinic acid failed to show any promising effect on behavioural parameters. Further, at 200 mg/kg dose, nicotinic acid reversed the elevated total distance and latency to target quadrant. However, statistically it was found insignificant as compared to AlCl3 control. This suggest the possibilities of nicotinic acid, a GPR109a receptor agonist, to have neuroprotective action against aluminium-induced memory deficit. However, detailed investigation is required to substantiate the above findings.

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