Conflict of Interest: The authors report no conflict of interest.
Involvement of AMPA Receptors in CSD-Induced Impairment of LTP in the Hippocampus
Article first published online: 3 AUG 2012
© 2012 American Headache Society
Headache: The Journal of Head and Face Pain
Volume 52, Issue 10, pages 1535–1545, November/December 2012
How to Cite
Maneepark, M., Srikiatkhachorn, A. and Bongsebandhu-phubhakdi, S. (2012), Involvement of AMPA Receptors in CSD-Induced Impairment of LTP in the Hippocampus. Headache: The Journal of Head and Face Pain, 52: 1535–1545. doi: 10.1111/j.1526-4610.2012.02229.x
- Issue published online: 15 NOV 2012
- Article first published online: 3 AUG 2012
- Accepted manuscript online: 11 JUL 2012 03:36AM EST
- Accepted for publication June 28, 2012.
- long-term potentiation;
- cortical spreading depression;
- α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor
Objective.— To investigate the alteration of hippocampal long-term plasticity and basal synaptic transmission induced by repetitive cortical spreading depressions (CSDs).
Background.— There is a relationship between migraine aura and amnesia attack. CSD, a state underlying migraine attacks, may be responsible for hippocampus-related symptoms. However, the precise role of CSD on hippocampal activity has not been investigated.
Methods.— Male Wistar rats were divided into CSD and control groups. Repetitive CSDs were induced in vivo by topical application of solid KCl. Forty-five minutes later, the ipsilateral hippocampus was removed, and hippocampal slices were prepared for a series of electrophysiological studies.
Results.— Repetitive CSDs led to a decrease in the magnitude of long-term potentiation in the hippocampus. CSD also reduced hippocampal synaptic efficacy, as shown by a reduction in post-synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor responses. In contrast, the post-synaptic N-methyl-d-aspartate receptor responses remained unchanged. In addition, there were no changes in paired-pulse profiles between the groups, indicating that CSD did not induce any presynaptic alterations.
Conclusion.— These findings suggest that a reduction of post-synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor responses is the mechanism responsible for impaired hippocampal long-term potentiation induced by CSD.