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Inhibition of central angiotensin converting enzyme ameliorates scopolamine induced memory impairment in mice: role of cholinergic neurotransmission, cerebral blood flow and brain energy metabolism.
Behav Brain Res. 2012 Jun 15; 232(1):66-76.BB

Abstract

Evidences indicate that inhibition of central Renin angiotensin system (RAS) ameliorates memory impairment in animals and humans. Earlier we have reported involvement of central angiotensin converting enzyme (ACE) in streptozotocin induced neurodegeneration and memory impairment. The present study investigated the role of central ACE in cholinergic neurotransmission, brain energy metabolism and cerebral blood flow (CBF) in model of memory impairment induced by injection of scopolamine in mice. Perindopril (0.05 and 0.1 mg/kg, PO) was given orally for one week before administration of scopolamine (3mg/kg, IP). Then, memory function was evaluated by Morris water maze and passive avoidance tests. CBF was measured by laser Doppler flowmetry. Biochemical and molecular parameters were estimated after the completion of behavioral studies. Scopolamine caused impairment in memory which was associated with reduced CBF, acetylcholine (ACh) level and elevated acetylcholinesterase (AChE) activity and malondialdehyde (MDA) level. Perindopril ameliorated scopolamine induced amnesia in both the behavioral paradigms. Further, perindopril prevented elevation of AChE and MDA level in mice brain. There was a significant increase in CBF and ACh level in perindopril treated mice. However, scopolamine had no significant effect on ATP level and mRNA expression of angiotensin receptors and ACE in cortex and hippocampus. But, perindopril significantly decreased ACE activity in brain without affecting its mRNA expression. The study clearly showed the interaction between ACE and cholinergic neurotransmission and beneficial effect of perindopril can be attributed to improvement in central cholinergic neurotransmission and CBF.

Authors+Show Affiliations

Division of Pharmacology, Central Drug Research Institute, Lucknow (UP), India.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22460064

Citation

Tota, Santoshkumar, et al. "Inhibition of Central Angiotensin Converting Enzyme Ameliorates Scopolamine Induced Memory Impairment in Mice: Role of Cholinergic Neurotransmission, Cerebral Blood Flow and Brain Energy Metabolism." Behavioural Brain Research, vol. 232, no. 1, 2012, pp. 66-76.
Tota S, Nath C, Najmi AK, et al. Inhibition of central angiotensin converting enzyme ameliorates scopolamine induced memory impairment in mice: role of cholinergic neurotransmission, cerebral blood flow and brain energy metabolism. Behav Brain Res. 2012;232(1):66-76.
Tota, S., Nath, C., Najmi, A. K., Shukla, R., & Hanif, K. (2012). Inhibition of central angiotensin converting enzyme ameliorates scopolamine induced memory impairment in mice: role of cholinergic neurotransmission, cerebral blood flow and brain energy metabolism. Behavioural Brain Research, 232(1), 66-76. https://doi.org/10.1016/j.bbr.2012.03.015
Tota S, et al. Inhibition of Central Angiotensin Converting Enzyme Ameliorates Scopolamine Induced Memory Impairment in Mice: Role of Cholinergic Neurotransmission, Cerebral Blood Flow and Brain Energy Metabolism. Behav Brain Res. 2012 Jun 15;232(1):66-76. PubMed PMID: 22460064.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of central angiotensin converting enzyme ameliorates scopolamine induced memory impairment in mice: role of cholinergic neurotransmission, cerebral blood flow and brain energy metabolism. AU - Tota,Santoshkumar, AU - Nath,Chandishwar, AU - Najmi,Abul Kalam, AU - Shukla,Rakesh, AU - Hanif,Kashif, Y1 - 2012/03/19/ PY - 2012/02/06/received PY - 2012/03/06/revised PY - 2012/03/09/accepted PY - 2012/3/31/entrez PY - 2012/3/31/pubmed PY - 2012/9/28/medline SP - 66 EP - 76 JF - Behavioural brain research JO - Behav Brain Res VL - 232 IS - 1 N2 - Evidences indicate that inhibition of central Renin angiotensin system (RAS) ameliorates memory impairment in animals and humans. Earlier we have reported involvement of central angiotensin converting enzyme (ACE) in streptozotocin induced neurodegeneration and memory impairment. The present study investigated the role of central ACE in cholinergic neurotransmission, brain energy metabolism and cerebral blood flow (CBF) in model of memory impairment induced by injection of scopolamine in mice. Perindopril (0.05 and 0.1 mg/kg, PO) was given orally for one week before administration of scopolamine (3mg/kg, IP). Then, memory function was evaluated by Morris water maze and passive avoidance tests. CBF was measured by laser Doppler flowmetry. Biochemical and molecular parameters were estimated after the completion of behavioral studies. Scopolamine caused impairment in memory which was associated with reduced CBF, acetylcholine (ACh) level and elevated acetylcholinesterase (AChE) activity and malondialdehyde (MDA) level. Perindopril ameliorated scopolamine induced amnesia in both the behavioral paradigms. Further, perindopril prevented elevation of AChE and MDA level in mice brain. There was a significant increase in CBF and ACh level in perindopril treated mice. However, scopolamine had no significant effect on ATP level and mRNA expression of angiotensin receptors and ACE in cortex and hippocampus. But, perindopril significantly decreased ACE activity in brain without affecting its mRNA expression. The study clearly showed the interaction between ACE and cholinergic neurotransmission and beneficial effect of perindopril can be attributed to improvement in central cholinergic neurotransmission and CBF. SN - 1872-7549 UR - https://www.unboundmedicine.com/medline/citation/22460064/Inhibition_of_central_angiotensin_converting_enzyme_ameliorates_scopolamine_induced_memory_impairment_in_mice:_role_of_cholinergic_neurotransmission_cerebral_blood_flow_and_brain_energy_metabolism_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0166-4328(12)00194-5 DB - PRIME DP - Unbound Medicine ER -