Serotonin and sudden unexpected death in epilepsy

Petrucci, Alexandra N.; Joyal, Katelyn G.; Purnell, Benton S.; Buchanan, Gordon F.

doi:10.1016/j.expneurol.2019.113145

Cited by 70 publications

(74 citation statements)

References 249 publications

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“…The copyright holder for this this version posted December 5, 2020. ; https://doi.org/10.1101/2020.12.04.410969 doi: bioRxiv preprint 3 behavior [8][9] , administration of 5-HTP significantly reduced the incidence of S-IRA by anticonvulsant effects in our models. The anticonvulsant effects of 5-HTP was basically consistent with other studies that activation of 5-HT neurons can reduce the severity of seizure [14][15][16] . Meanwhile, administration of KET reversed the lower incidence of S-IRA by 5-HTP with producing only partly anticonvulsant effects, which suggested that 5-HT2AR in brainstem may be a specific target to prevent S-IRA and SUDEP.…”

Section: Introductionsupporting

confidence: 91%

“…Currently, to our certain knowledge, respiratory dysfunction during seizures has been regarded as a leading mechanism of SUDEP. Some studies indicated that several selective serotonin ( 5-HT) reuptake inhibitors (SSRIs) can prevent S-IRA in DBA/1 mice evoked by generalized audiogenic seizures (AGSz) by elevating 5-HT levels in the synaptic cleft [13][14][15][16] .…”

Section: Discussionmentioning

confidence: 99%

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Optogenetic activation of the serotonergic neural circuit between the dorsal raphe nucleus and pre-Bötzinger complex contributes to inhibition of seizure-induced respiratory arrest in the DBA/1 mouse SUDEP model

Shen

Lian

et al. 2020

Preprint

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Sudden unexpected death in epilepsy (SUDEP) is the fatal cause leading to the death of epilepsy patients with anti-epileptic drug resistance. However, the underlying mechanism of SUDEP remains to be elusive. Our previous study demonstrated that enhancement of serotonin (5-HT) synthesis by intraperitoneal (IP) injection of 5-hydroxytryptophan in brain significantly reduced the incidence of seizure-induced respiratory arrest (S-IRA) in DBA/1 mice SUDEP models. Given that 5-HT2A receptor (5-HT2AR) acts an important role in mediating respiration system in brain, we hypothesized that 5-HT2AR is of great significance to modulate S-IRA and SUDEP. To test this hypothesis, we examined whether the decreased incidence S-IRA evoked by either acoustic stimulation or PTZ by blocking 5-HT2AR by administration with ketanserin (KET), a selective antagonist of 5HT2AR, in DBA/1 mice SUDEP models to test the role of 5-HT2AR modulating S-IRA. Our results suggested that the decreased incidence of S-IRA by 5-Hydroxytryptophan (5-HTP), a precursor for central nervous system (CNS) serotonin (5-HT) synthesis, was significantly reversed by IP and intracerebroventricularly (ICV) injection of ketanserin in our models. Thus, our data suggested that 5-HT2AR in the brain may be a potential and specific target to prevent SUDEP.

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Section: Introductionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Optogenetic activation of the serotonergic neural circuit between the dorsal raphe nucleus and pre-Bötzinger complex contributes to inhibition of seizure-induced respiratory arrest in the DBA/1 mouse SUDEP model

Shen

Lian

et al. 2020

Preprint

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“…Seizure-induced changes in serotonin have been seen in epilepsy patients. 6 Lower levels of cerebrospinal fluid 5-HIAA (5-hydroxyindoleacetic acid), which is an indicator of serotonergic activity, have been measured in patients with high lethality suicide attempts, compared to low lethality attempts. 7 The Taiwan study suggests higher lethality of suicide attempts in the patients with epilepsy and the REP cohort showed people with epilepsy were significantly more likely to reattempt suicide.…”

Section: Commentarymentioning

confidence: 99%

Adolescence and Epilepsy: The Perfect Storm for Suicidal Behavior

Nickels¹

2021

Epilepsy Curr

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“…Perhaps a similar stimulation paradigm could be employed to reduce seizure sequelae thought to increase risk for SUDEP, such as respiratory and autonomic dysregulation, in addition to impaired arousal. 4 , 10 That said, these details are not critical to begin testing whether similar stimulation can reduce postictal arousal impairment in patients. Indeed, this group has a clinical trial underway through the NIH Brain Initiative.…”

Section: Commentarymentioning

confidence: 99%