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ICV STZ induced impairment in memory and neuronal mitochondrial function: A protective role of nicotinic receptor.
Behav Brain Res. 2011 Oct 10; 224(1):50-7.BB

Abstract

The present study was planned to evaluate the cholinergic influence on mitochondrial activity and neurodegeneration associated with impaired memory in intracerebroventricular (ICV) streptozotocin (STZ) treated rats. STZ (3mg/kg), administered ICV twice with an interval of 48h between the two doses, showed significant impairment in spatial memory tested by water maze test 14 days after first dose without altering blood glucose level and locomotor activity. Animals were sacrificed on 21st day of ICV administration. STZ significantly increased malondialdehyde (MDA), reactive oxygen species (ROS), Ca(2+) ion influx, caspase-3 activity and decreased glutathione (GSH) level. Acetylcholinesterase inhibitors tacrine and donepezil (5mg/kg, PO) pretreatment significantly prevented STZ induced memory deficit, oxidative stress, Ca(2+) influx and caspase-3 activity. Carbachol, a muscarinic cholinergic agonist (0.01mg/kg, SC) did not show any significant effect on ROS generation, Ca(2+) ion influx and caspase-3 activity. While nicotinic cholinergic agonist, nicotine, significantly attenuated ICV STZ induced mitochondrial dysfunction and caspase-3 activity. The results indicate that instead of muscarinic receptors nicotinic receptors may be involved in neuroprotection by maintaining mitochondrial functions.

Authors+Show Affiliations

Division of Pharmacology, Central Drug Research Institute (CSIR), Lucknow 226001, India.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

21620901

Citation

Saxena, Gunjan, et al. "ICV STZ Induced Impairment in Memory and Neuronal Mitochondrial Function: a Protective Role of Nicotinic Receptor." Behavioural Brain Research, vol. 224, no. 1, 2011, pp. 50-7.
Saxena G, Patro IK, Nath C. ICV STZ induced impairment in memory and neuronal mitochondrial function: A protective role of nicotinic receptor. Behav Brain Res. 2011;224(1):50-7.
Saxena, G., Patro, I. K., & Nath, C. (2011). ICV STZ induced impairment in memory and neuronal mitochondrial function: A protective role of nicotinic receptor. Behavioural Brain Research, 224(1), 50-7. https://doi.org/10.1016/j.bbr.2011.04.039
Saxena G, Patro IK, Nath C. ICV STZ Induced Impairment in Memory and Neuronal Mitochondrial Function: a Protective Role of Nicotinic Receptor. Behav Brain Res. 2011 Oct 10;224(1):50-7. PubMed PMID: 21620901.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - ICV STZ induced impairment in memory and neuronal mitochondrial function: A protective role of nicotinic receptor. AU - Saxena,Gunjan, AU - Patro,Ishan K, AU - Nath,Chandishwar, Y1 - 2011/05/20/ PY - 2011/02/05/received PY - 2011/04/20/revised PY - 2011/04/25/accepted PY - 2011/5/31/entrez PY - 2011/5/31/pubmed PY - 2011/12/13/medline SP - 50 EP - 7 JF - Behavioural brain research JO - Behav Brain Res VL - 224 IS - 1 N2 - The present study was planned to evaluate the cholinergic influence on mitochondrial activity and neurodegeneration associated with impaired memory in intracerebroventricular (ICV) streptozotocin (STZ) treated rats. STZ (3mg/kg), administered ICV twice with an interval of 48h between the two doses, showed significant impairment in spatial memory tested by water maze test 14 days after first dose without altering blood glucose level and locomotor activity. Animals were sacrificed on 21st day of ICV administration. STZ significantly increased malondialdehyde (MDA), reactive oxygen species (ROS), Ca(2+) ion influx, caspase-3 activity and decreased glutathione (GSH) level. Acetylcholinesterase inhibitors tacrine and donepezil (5mg/kg, PO) pretreatment significantly prevented STZ induced memory deficit, oxidative stress, Ca(2+) influx and caspase-3 activity. Carbachol, a muscarinic cholinergic agonist (0.01mg/kg, SC) did not show any significant effect on ROS generation, Ca(2+) ion influx and caspase-3 activity. While nicotinic cholinergic agonist, nicotine, significantly attenuated ICV STZ induced mitochondrial dysfunction and caspase-3 activity. The results indicate that instead of muscarinic receptors nicotinic receptors may be involved in neuroprotection by maintaining mitochondrial functions. SN - 1872-7549 UR - https://www.unboundmedicine.com/medline/citation/21620901/ICV_STZ_induced_impairment_in_memory_and_neuronal_mitochondrial_function:_A_protective_role_of_nicotinic_receptor_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0166-4328(11)00349-4 DB - PRIME DP - Unbound Medicine ER -