Tags

Type your tag names separated by a space and hit enter

Inhibitory avoidance memory deficit induced by scopolamine: Interaction of cholinergic and glutamatergic systems in the ventral tegmental area.
Neurobiol Learn Mem. 2010 Jul; 94(1):83-90.NL

Abstract

Interaction of cholinergic and glutamatergic inputs in the ventral tegmental area (VTA) influencing a learned behavior is a topic of great interest. In the present study the effect of intra-VTA administration of a nonselective muscarinic acetylcholine antagonist, scopolamine, and N-methyl-d-aspartate (NMDA) receptor agents by themselves as well as their interactions on consolidation and retrieval of inhibitory avoidance (IA) memory have been investigated. A step-through inhibitory avoidance task was used for memory assessment in male Wistar rats. The results showed that intra-VTA administration of scopolamine (1 and 2microg/rat) and NMDA receptor antagonist, MK-801 (0.75 and 1microg/rat) immediately after training, impaired consolidation of IA memory. Interestingly, co-administration of an ineffective dose of MK-801 (0.5microg/rat) with ineffective doses of scopolamine (0.25 and 0.5microg/rat) significantly decreased the consolidation process. Post-training intra-VTA injections of NMDA (0.001 and 0.01microg/rat) had no effects by itself, whereas its co-administration with scopolamine (2microg/rat) prevented the effect of the later drug. The results also showed that pre-test intra-VTA administration of scopolamine (3 and 4microg/rat) and MK-801 (1 and 2microg/rat) impaired retrieval of the IA memory. Moreover, co-administration of an ineffective dose of MK-801 (0.5microg/rat) with ineffective doses of scopolamine (1 and 2microg/rat) increasingly reduced the retrieval of the IA memory. On the contrary to its post-training treatment, pre-test administration of NMDA either alone or in combination with scopolamine caused no significant effect on retrieval of IA memory. It can be concluded that muscarinic acetylcholine and NMDA glutamate receptors in the VTA are involved in the mechanism(s) underlying consolidation and retrieval of the IA memory.

Authors+Show Affiliations

Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

20403448

Citation

Mahmoodi, Gelavij, et al. "Inhibitory Avoidance Memory Deficit Induced By Scopolamine: Interaction of Cholinergic and Glutamatergic Systems in the Ventral Tegmental Area." Neurobiology of Learning and Memory, vol. 94, no. 1, 2010, pp. 83-90.
Mahmoodi G, Ahmadi S, Pourmotabbed A, et al. Inhibitory avoidance memory deficit induced by scopolamine: Interaction of cholinergic and glutamatergic systems in the ventral tegmental area. Neurobiol Learn Mem. 2010;94(1):83-90.
Mahmoodi, G., Ahmadi, S., Pourmotabbed, A., Oryan, S., & Zarrindast, M. R. (2010). Inhibitory avoidance memory deficit induced by scopolamine: Interaction of cholinergic and glutamatergic systems in the ventral tegmental area. Neurobiology of Learning and Memory, 94(1), 83-90. https://doi.org/10.1016/j.nlm.2010.04.004
Mahmoodi G, et al. Inhibitory Avoidance Memory Deficit Induced By Scopolamine: Interaction of Cholinergic and Glutamatergic Systems in the Ventral Tegmental Area. Neurobiol Learn Mem. 2010;94(1):83-90. PubMed PMID: 20403448.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibitory avoidance memory deficit induced by scopolamine: Interaction of cholinergic and glutamatergic systems in the ventral tegmental area. AU - Mahmoodi,Gelavij, AU - Ahmadi,Shamseddin, AU - Pourmotabbed,Ali, AU - Oryan,Shahrbanoo, AU - Zarrindast,Mohammad Reza, Y1 - 2010/04/18/ PY - 2009/08/18/received PY - 2010/04/08/revised PY - 2010/04/13/accepted PY - 2010/4/21/entrez PY - 2010/4/21/pubmed PY - 2010/9/30/medline SP - 83 EP - 90 JF - Neurobiology of learning and memory JO - Neurobiol Learn Mem VL - 94 IS - 1 N2 - Interaction of cholinergic and glutamatergic inputs in the ventral tegmental area (VTA) influencing a learned behavior is a topic of great interest. In the present study the effect of intra-VTA administration of a nonselective muscarinic acetylcholine antagonist, scopolamine, and N-methyl-d-aspartate (NMDA) receptor agents by themselves as well as their interactions on consolidation and retrieval of inhibitory avoidance (IA) memory have been investigated. A step-through inhibitory avoidance task was used for memory assessment in male Wistar rats. The results showed that intra-VTA administration of scopolamine (1 and 2microg/rat) and NMDA receptor antagonist, MK-801 (0.75 and 1microg/rat) immediately after training, impaired consolidation of IA memory. Interestingly, co-administration of an ineffective dose of MK-801 (0.5microg/rat) with ineffective doses of scopolamine (0.25 and 0.5microg/rat) significantly decreased the consolidation process. Post-training intra-VTA injections of NMDA (0.001 and 0.01microg/rat) had no effects by itself, whereas its co-administration with scopolamine (2microg/rat) prevented the effect of the later drug. The results also showed that pre-test intra-VTA administration of scopolamine (3 and 4microg/rat) and MK-801 (1 and 2microg/rat) impaired retrieval of the IA memory. Moreover, co-administration of an ineffective dose of MK-801 (0.5microg/rat) with ineffective doses of scopolamine (1 and 2microg/rat) increasingly reduced the retrieval of the IA memory. On the contrary to its post-training treatment, pre-test administration of NMDA either alone or in combination with scopolamine caused no significant effect on retrieval of IA memory. It can be concluded that muscarinic acetylcholine and NMDA glutamate receptors in the VTA are involved in the mechanism(s) underlying consolidation and retrieval of the IA memory. SN - 1095-9564 UR - https://www.unboundmedicine.com/medline/citation/20403448/Inhibitory_avoidance_memory_deficit_induced_by_scopolamine:_Interaction_of_cholinergic_and_glutamatergic_systems_in_the_ventral_tegmental_area_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1074-7427(10)00067-5 DB - PRIME DP - Unbound Medicine ER -