NMDA receptors and voltage-dependent calcium channels mediate different aspects of acquisition and retention of a spatial memory task

• Published in: Neurobiology of learning and memory Vol. 81; no. 2; pp. 105 - 114
• Main Authors: Woodside, B.L, Borroni, A.M, Hammonds, M.D, Teyler, T.J
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 01-03-2004; Elsevier
• Subjects: Animal; Animals; Behavior, Animal - drug effects; Behavioral psychophysiology; Biological and medical sciences; Calcium Channels - drug effects; Dizocilpine Maleate - administration & dosage; Dizocilpine Maleate - pharmacology; Fundamental and applied biological sciences. Psychology; Injections; Learning. Memory; Long-term potentiation; LTP; Male; Maze Learning - drug effects; Memory; Memory - drug effects; Neuroprotective Agents - administration & dosage; Neuroprotective Agents - pharmacology; Neuropsychological Tests; Neurotransmission and behavior; nmdaLTP; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate - drug effects; Retention (Psychology) - drug effects; Space Perception - drug effects; Spatial Behavior - drug effects; Spatial learning; Spatial memory; vdccLTP; nmdaLTP; LTP; Long-term potentiation; Spatial learning; vdccLTP; Spatial memory; Potentiation; Rat; Rodentia; Glutamate receptor; Ionic channel; Experimental study; Retention; Acquisition; Long term; Vertebrata; Mammalia; Acquisition process; Calcium ion; Synaptic transmission; Animal; Synaptic plasticity; Antagonist; Working memory; NMDA receptor
• ISSN: 1074-7427; 1095-9564
• DOI: 10.1016/j.nlm.2003.10.003

Activity dependent calcium entry into neurons can initiate a form of synaptic plasticity called long-term potentiation (LTP). This phenomenon is considered by many to be one possible cellular mechanism underlying learning and memory. The calcium entry that induces this phenomenon can occur when
N-methyl-
d-aspartate receptors (NMDARs) and/or voltage-dependent calcium channels (VDCCs) are activated. While much is known about synaptic plasticity and the mechanisms that are triggered by activation of these two Ca
2+ channels, it is unclear what roles they play in learning. To better understand the role activation of these channels may play in learning we systemically administered pharmacological antagonists to block NMDARs, VDCCs, or both during training trials and retention tests in a radial arm maze task. Wistar rats injected with the NMDAR antagonist MK-801 (0.1
mg/kg) were impaired in the acquisition of this task. In contrast, rats injected with verapamil (10
mg/kg), an antagonist to VDCCs, acquired the task at the same rate as control animals, but were impaired on a 10-day retention test. A group of animals injected with both antagonists were unable to learn the task. The results suggest that each of the calcium channels and the processes they trigger are involved in a different stage of memory formation or expression.