Neuroanatomical and neuropharmacological approaches to postictal antinociception‐related prosencephalic neurons: the role of muscarinic and nicotinic cholinergic receptors

Abstract

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.

Ictal analgesia in temporal lobe epilepsy – The mechanism of seizure-related burns

“…The dorsal hippocampus and the hippocampal CA1 region have an impact on the organization of postictal analgesia through muscarinergic and nicotinergic acetyl-cholin receptor-mediated mechanisms in experimental generalized tonic-clonic seizures [37][38][39]. The PAG has bidirectional projections from and to the central nucleus of the amygdala [14].…”

Analgesic activity of some aroylhydrazone-based molecular hybrids with antiseizure activity: in vivo and in silico evaluations

“…The rate of ictal non-epileptic headache ranges from 0.5 to 5%, and that of postictal headache ranges from 12 to 52% [13]. Increased pain sensitivity during the interictal period [14] and postictal analgesia [15] has been reported. Ictal/postictal analgesia was proposed as a contributing factor for increased traumatism in patients with epilepsy [16].…”

Intrinsic connections within the pedunculopontine tegmental nucleus are critical to the elaboration of post‐ictal antinociception

“…The blockade of the GABA‐mediated CL − influx has been used to elicit tonic and tonic‐clonic seizures followed by significant antinociception (Coimbra et al, ,b; de Oliveira et al, ; Freitas et al, , 2009; Felippotti et al, ; de Freitas et al, ). There is evidence that the cholinergic system is involved in post‐ictal antinociception (Coimbra et al, ; de Freitas et al, ). Curiously, the pretreatment with a GABA A receptor selective antagonist decreases the nicotine‐induced antinociception.…”