Neuroanatomical and neuropharmacological approaches to postictal antinociception-related prosencephalic neurons: the role of muscarinic and nicotinic cholinergic receptors
Article first published online: 5 APR 2013
© 2013 The Authors. Brain and Behavior published by Wiley Periodicals, Inc.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Brain and Behavior
Volume 3, Issue 3, pages 286–301, May 2013
How to Cite
Brain and Behavior 2013; 3(3):286–301.
- Issue published online: 13 MAY 2013
- Article first published online: 5 APR 2013
- Manuscript Accepted: 20 OCT 2012
- Manuscript Revised: 3 OCT 2012
- Manuscript Received: 7 JUN 2012
- FAPESP. Grant Numbers: 96/08574-9, 02/01496-5, 07/01174-1
- CAPES. Grant Numbers: AUX-PE-PNPD 2400/2009, 23038.027801/2009-37
- FAEPA. Grant Numbers: 03/05256-1, 537/1995, 70/2002, 08/03402-4, 04/14786-7
- CNPq. Grant Numbers: 304421/2007-3, 200629/2005-0
- cholinergic neurotransmission;
- dorsal hippocampus;
- GABAergic neurotransmission;
- postictal analgesia
Several studies have suggested the involvement of the hippocampus in the elaboration of epilepsy. There is evidence that suggests the hippocampus plays an important role in the affective and motivational components of nociceptive perception. However, the exact nature of this involvement remains unclear. Therefore, the aim of this study was to determine the role of muscarinic and nicotinic cholinergic receptors in the dorsal hippocampus (dH) in the organization of postictal analgesia. In a neuroanatomical study, afferent connections were found from the somatosensory cortex, the medial septal area, the lateral septal area, the diagonal band of Broca, and the dentate gyrus to the dH; all these areas have been suggested to modulate convulsive activity. Outputs to the dH were also identified from the linear raphe nucleus, the median raphe nucleus (MdRN), the dorsal raphe nucleus, and the locus coeruleus. All these structures comprise the endogenous pain modulatory system and may be involved either in postictal pronociception or antinociception that is commonly reported by epileptic patients. dH-pretreatment with cobalt chloride (1.0 mmol/L CoCl2/0.2 μL) to transiently inhibit local synapses decreased postictal analgesia 10 min after the end of seizures. Pretreatment of the dH with either atropine or mecamylamine (1.0 μg/0.2 μL) attenuated the postictal antinociception 30 min after seizures, while the higher dose (5.0 μg/0.2 μL) decreased postictal analgesia immediately after the end of seizures. These findings suggest that the dH exerts a critical role in the organization of postictal analgesia and that muscarinic and nicotinic cholinergic receptor-mediated mechanisms in the dH are involved in the elaboration of antinociceptive processes induced by generalized tonic-clonic seizures.