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Article ; Online: Astrocyte-neuron circuits in epilepsy.

Purnell, Benton S / Alves, Mariana / Boison, Detlev

2023 Volume 179, Page(s) 106058

Abstract: The epilepsies are a diverse spectrum of disease states characterized by spontaneous seizures and associated comorbidities. Neuron-focused perspectives have yielded an array of widely used anti-seizure medications and are able to explain some, but not ... ...

Abstract	The epilepsies are a diverse spectrum of disease states characterized by spontaneous seizures and associated comorbidities. Neuron-focused perspectives have yielded an array of widely used anti-seizure medications and are able to explain some, but not all, of the imbalance of excitation and inhibition which manifests itself as spontaneous seizures. Furthermore, the rate of pharmacoresistant epilepsy remains high despite the regular approval of novel anti-seizure medications. Gaining a more complete understanding of the processes that turn a healthy brain into an epileptic brain (epileptogenesis) as well as the processes which generate individual seizures (ictogenesis) may necessitate broadening our focus to other cell types. As will be detailed in this review, astrocytes augment neuronal activity at the level of individual neurons in the form of gliotransmission and the tripartite synapse. Under normal conditions, astrocytes are essential to the maintenance of blood-brain barrier integrity and remediation of inflammation and oxidative stress, but in epilepsy these functions are impaired. Epilepsy results in disruptions in the way astrocytes relate to each other by gap junctions which has important implications for ion and water homeostasis. In their activated state, astrocytes contribute to imbalances in neuronal excitability due to their decreased capacity to take up and metabolize glutamate and an increased capacity to metabolize adenosine. Furthermore, due to their increased adenosine metabolism, activated astrocytes may contribute to DNA hypermethylation and other epigenetic changes that underly epileptogenesis. Lastly, we will explore the potential explanatory power of these changes in astrocyte function in detail in the specific context of the comorbid occurrence of epilepsy and Alzheimer's disease and the disruption in sleep-wake regulation associated with both conditions.
MeSH term(s)	Humans ; Astrocytes/metabolism ; Epilepsy/metabolism ; Neurons/metabolism ; Adenosine/metabolism ; Glutamic Acid/metabolism
Chemical Substances	Adenosine (K72T3FS567) ; Glutamic Acid (3KX376GY7L)
Language	English
Publishing date	2023-03-01
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2023.106058
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Article ; Online: Free-running circadian breathing rhythms are eliminated by suprachiasmatic nucleus lesion.

Purnell, Benton S / Buchanan, Gordon F

Journal of applied physiology (Bethesda, Md. : 1985)

2020 Volume 129, Issue 1, Page(s) 49–57

Abstract: It is widely agreed that breathing is subject to circadian regulation. Circadian differences in respiratory physiology significantly impact a number of diseases including sleep apnea, asthma, and seizure-induced death. The effect of time of day on ... ...

Abstract	It is widely agreed that breathing is subject to circadian regulation. Circadian differences in respiratory physiology significantly impact a number of diseases including sleep apnea, asthma, and seizure-induced death. The effect of time of day on breathing has been previously characterized; however, an endogenous free-running respiratory rhythm in mammals has not previously been described. Furthermore, it is assumed that circadian rhythms in breathing are dependent on the hypothalamic suprachiasmatic nucleus (SCN), the home of the mammalian central circadian oscillator, but this has not been shown experimentally. The breathing of mice was monitored during wakefulness using whole body plethysmography at six times of day while housed under light-dark conditions and at six circadian phases while housed under constant darkness. Respiratory frequency and minute ventilation, but not tidal volume, were significantly higher during the active phase in both entrained and free-running conditions. To determine whether circadian regulation of breathing requires the SCN, in separate sets of animals this structure was electrolytically lesioned bilaterally or a sham surgery was performed, and breathing was measured at six different time points. Time-dependent oscillations in breathing were lost in SCN-lesioned animals, but not those subjected to sham surgery. These results suggest that breathing is subject to circadian regulation via the SCN. Mechanistic insights into the circadian regulation of breathing may lead to targeted interventions to reduce the morbidity and mortality associated with diseases with respiratory pathophysiology.
MeSH term(s)	Animals ; Circadian Rhythm ; Hypothalamus ; Mice ; Seizures ; Suprachiasmatic Nucleus ; Wakefulness
Language	English
Publishing date	2020-06-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	219139-8
ISSN	1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
ISSN (online)	1522-1601
ISSN	0021-8987 ; 0161-7567 ; 8750-7587
DOI	10.1152/japplphysiol.00211.2020
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Article ; Online: The effect of time-of-day and circadian phase on vulnerability to seizure-induced death in two mouse models.

Purnell, Benton S / Petrucci, Alexandra N / Li, Rui / Buchanan, Gordon F

The Journal of physiology

2021 Volume 599, Issue 6, Page(s) 1885–1899

Abstract: Key points: Sudden unexpected death in epilepsy (SUDEP) is the leading cause of premature death in patients with refractory epilepsy. SUDEP typically occurs during the night, although the reason for this is unclear. We found that, in normally entrained ... ...

Abstract	Key points: Sudden unexpected death in epilepsy (SUDEP) is the leading cause of premature death in patients with refractory epilepsy. SUDEP typically occurs during the night, although the reason for this is unclear. We found that, in normally entrained mice, time-of-day alters vulnerability to seizure-induced death. We found that, in free-running mice, circadian phase alters the vulnerability to seizure-induced death. These findings suggest that circadian rhythmicity may be responsible for the increased night-time prevalence of SUDEP ABSTRACT: Sudden unexpected death in epilepsy (SUDEP) is the leading cause of epilepsy-related death. SUDEP typically occurs during the night following a seizure. Many aspects of mammalian physiology are regulated by circadian rhythms in ways that might make seizures occuring during the night more dangerous. Using two mouse models of seizure-induced death, we demonstrate that time-of-day and circadian rhythms alter vulnerability to seizure-induced death. We exposed normally entrained DBA/1 mice to a potentially seizure-inducing acoustic stimulus at different times of day and compared the characteristics and outcomes of the seizures. Time-of-day did not alter the probability of a seizure but it did alter the probability of seizure-induced death. To determine whether circadian rhythms alter vulnerability to seizure-induced death, we induced maximal electroshock seizures in free-running C57BL/6J mice at different circadian time points at the same time as measuring breathing via whole body plethysmography. Circadian phase did not affect seizure severity but it did alter postictal respiratory outcomes and the probability of seizure-induced death. By contrast to our expectations, in entrained and free-running mice, vulnerability to seizure-induced death was greatest during the night and subjective night, respectively. These findings suggest that circadian rhythmicity may be responsible for the increased night-time prevalence of SUDEP and that the underlying mechanism is phase conserved between nocturnal and diurnal mammals. All of the seizures in the present study were induced during wakefulness, indicating that the effect of time point on vulnerability to seizure-induced death was not the result of sleep. Understanding why SUDEP occurs more frequently during the night may inform future preventative countermeasures.
MeSH term(s)	Animals ; Death, Sudden/etiology ; Epilepsy ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Seizures
Language	English
Publishing date	2021-02-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP280856
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Article ; Online: Diaphragmatic pacing for the prevention of sudden unexpected death in epilepsy.

Purnell, Benton S / Braun, Alexander / Fedele, Denise / Murugan, Madhuvika / Boison, Detlev

Brain communications

2022 Volume 4, Issue 5, Page(s) fcac232

Abstract: Sudden unexpected death in epilepsy is the leading cause of epilepsy related death. Currently, there are no reliable methods for preventing sudden unexpected death in epilepsy. The precise pathophysiology of sudden unexpected death in epilepsy is unclear; ...

Abstract	Sudden unexpected death in epilepsy is the leading cause of epilepsy related death. Currently, there are no reliable methods for preventing sudden unexpected death in epilepsy. The precise pathophysiology of sudden unexpected death in epilepsy is unclear; however, convergent lines of evidence suggest that seizure-induced respiratory arrest plays a central role. It is generally agreed that sudden unexpected death in epilepsy could be averted if the patient could be rapidly ventilated following the seizure. The diaphragm is a muscle in the chest which contracts to draw air into the lungs. Diaphragmatic pacing is a surgical intervention which facilitates normal ventilation in situations, such as spinal cord injury and sleep apnoea, in which endogenous respiration would be inadequate or non-existent. In diaphragmatic pacing, electrodes are implanted directly onto diaphragm or adjacent to the phrenic nerves which innervate the diaphragm. These electrodes are then rhythmically stimulated, thereby eliciting contractions of the diaphragm which emulate endogenous breathing. The goal of this study was to test the hypothesis that seizure-induced respiratory arrest and death can be prevented with diaphragmatic pacing. Our approach was to induce respiratory arrest using maximal electroshock seizures in adult, male, C57BL6 mice outfitted with EEG and diaphragmatic electrodes (
Language	English
Publishing date	2022-09-16
Publishing country	England
Document type	Journal Article
ISSN	2632-1297
ISSN (online)	2632-1297
DOI	10.1093/braincomms/fcac232
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Article: Dead in the Night: Sleep-Wake and Time-Of-Day Influences on Sudden Unexpected Death in Epilepsy.

Purnell, Benton S / Thijs, Roland D / Buchanan, Gordon F

Frontiers in neurology

2018 Volume 9, Page(s) 1079

Abstract: Sudden unexpected death in epilepsy (SUDEP) is the leading cause of epilepsy-related death in patients with refractory epilepsy. Convergent lines of evidence suggest that SUDEP occurs due to seizure induced perturbation of respiratory, cardiac, and ... ...

Abstract	Sudden unexpected death in epilepsy (SUDEP) is the leading cause of epilepsy-related death in patients with refractory epilepsy. Convergent lines of evidence suggest that SUDEP occurs due to seizure induced perturbation of respiratory, cardiac, and electrocerebral function as well as potential predisposing factors. It is consistently observed that SUDEP happens more during the night and the early hours of the morning. The aim of this review is to discuss evidence from patient cases, clinical studies, and animal research which is pertinent to the nocturnality of SUDEP. There are a number of factors which might contribute to the nighttime predilection of SUDEP. These factors fall into four categories: influences of (1) being unwitnessed, (2) lying prone in bed, (3) sleep-wake state, and (4) circadian rhythms. During the night, seizures are more likely to be unwitnessed; therefore, it is less likely that another person would be able to administer a lifesaving intervention. Patients are more likely to be prone on a bed following a nocturnal seizure. Being prone in the accouterments of a bed during the postictal period might impair breathing and increase SUDEP risk. Sleep typically happens at night and seizures which emerge from sleep might be more dangerous. Lastly, there are circadian changes to physiology during the night which might facilitate SUDEP. These possible explanations for the nocturnality of SUDEP are not mutually exclusive. The increased rate of SUDEP during the night is likely multifactorial involving both situational factors, such as being without a witness and prone, and physiological changes due to the influence of sleep and circadian rhythms. Understanding the causal elements in the nocturnality of SUDEP may be critical to the development of effective preventive countermeasures.
Language	English
Publishing date	2018-12-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2018.01079
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Article ; Online: The role of adenosine in alcohol-induced respiratory suppression.

Purnell, Benton S / Thompson, Sydney / Bowman, Tenise / Bhasin, Jayant / George, Steven / Rust, Brian / Murugan, Madhuvika / Fedele, Denise / Boison, Detlev

Neuropharmacology

2022 Volume 222, Page(s) 109296

Abstract: Alcohol-related poisoning is the foremost cause of death resulting from excessive acute alcohol consumption. Respiratory failure is crucial to the pathophysiology of fatal alcohol poisoning. Alcohol increases accumulation of extracellular adenosine. ... ...

Abstract	Alcohol-related poisoning is the foremost cause of death resulting from excessive acute alcohol consumption. Respiratory failure is crucial to the pathophysiology of fatal alcohol poisoning. Alcohol increases accumulation of extracellular adenosine. Adenosine suppresses breathing. The goal of this investigation was to test the hypothesis that adenosine signaling contributes to alcohol-induced respiratory suppression. In the first experiment, the breathing of mice was monitored following an injection of the non-selective adenosine receptor antagonist caffeine (40 mg/kg), alcohol (5 g/kg), or alcohol and caffeine combined. Caffeine reduced alcohol-induced respiratory suppression suggesting that adenosine contributes to the effects of alcohol on breathing. The second experiment utilized the same experimental design, but with the blood brain barrier impermeant non-selective adenosine receptor antagonist 8-sulfophenyltheophylline (8-SPT, 60 mg/kg) instead of caffeine. 8-SPT did not reduce alcohol-induced respiratory suppression suggesting that adenosine is contributing to alcohol-induced respiratory suppression in the central nervous system. The third and fourth experiments used the same experimental design as the first, but with the selective A
MeSH term(s)	Animals ; Mice ; Adenosine/pharmacology ; Caffeine/pharmacology ; Ethanol ; Respiratory System ; Purinergic P1 Receptor Antagonists/pharmacology ; Respiratory Insufficiency ; Receptor, Adenosine A2A ; Adenosine A2 Receptor Antagonists/pharmacology ; Xanthines/pharmacology ; Receptor, Adenosine A1
Chemical Substances	Adenosine (K72T3FS567) ; Caffeine (3G6A5W338E) ; Ethanol (3K9958V90M) ; Purinergic P1 Receptor Antagonists ; Receptor, Adenosine A2A ; Adenosine A2 Receptor Antagonists ; Xanthines ; Receptor, Adenosine A1
Language	English
Publishing date	2022-10-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2022.109296
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Article ; Online: Serotonin and sudden unexpected death in epilepsy.

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

Experimental neurology

2019 Volume 325, Page(s) 113145

Abstract: Epilepsy is a highly prevalent disease characterized by recurrent, spontaneous seizures. Approximately one-third of epilepsy patients will not achieve seizure freedom with medical management and become refractory to conventional treatments. These ... ...

Abstract	Epilepsy is a highly prevalent disease characterized by recurrent, spontaneous seizures. Approximately one-third of epilepsy patients will not achieve seizure freedom with medical management and become refractory to conventional treatments. These patients are at greatest risk for sudden unexpected death in epilepsy (SUDEP). The exact etiology of SUDEP is unknown, but a combination of respiratory, cardiac, neuronal electrographic dysfunction, and arousal impairment is thought to underlie SUDEP. Serotonin (5-HT) is involved in regulation of breathing, sleep/wake states, arousal, and seizure modulation and has been implicated in the pathophysiology of SUDEP. This review explores the current state of understanding of the relationship between 5-HT, epilepsy, and respiratory and autonomic control processes relevant to SUDEP in epilepsy patients and in animal models.
MeSH term(s)	Animals ; Autonomic Nervous System/physiology ; Epilepsy/metabolism ; Epilepsy/physiopathology ; Humans ; Respiratory Physiological Phenomena ; Serotonin/metabolism ; Sudden Unexpected Death in Epilepsy
Chemical Substances	Serotonin (333DO1RDJY)
Language	English
Publishing date	2019-12-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2019.113145
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Article ; Online: Time-of-day influences on respiratory sequelae following maximal electroshock-induced seizures in mice.

Purnell, Benton S / Hajek, Michael A / Buchanan, Gordon F

Journal of neurophysiology

2017 Volume 118, Issue 5, Page(s) 2592–2600

Abstract: Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in refractory epilepsy patients. Although specific mechanisms underlying SUDEP are not well understood, evidence suggests most SUDEP occurs due to seizure-induced respiratory ... ...

Abstract	Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in refractory epilepsy patients. Although specific mechanisms underlying SUDEP are not well understood, evidence suggests most SUDEP occurs due to seizure-induced respiratory arrest. SUDEP also tends to happen at night. Although this may be due to circumstances in which humans find themselves at night, such as being alone without supervision or sleeping prone, or to independent influences of sleep state, there are a number of reasons why the night (i.e., circadian influences) could be an independent risk factor for SUDEP. We explored this possibility. Adult male WT mice were instrumented for EEG, EMG, and EKG recording and subjected to maximal electroshock (MES) seizures during wakefulness, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep during the nighttime/dark phase. These data were compared with data collected following seizures induced during the daytime/light phase. Seizures induced during the nighttime were similar in severity and duration to those induced during the daytime; however, seizures induced during the nighttime were associated with a lesser degree of respiratory dysregulation and postictal EEG suppression. Seizures induced during REM sleep during the nighttime were universally fatal, as is seen when seizures are induced during REM during the daytime. Taken together, these data implicate a role for time of day in influencing the physiological consequences of seizures that may contribute to seizure-induced death.
MeSH term(s)	Animals ; Death, Sudden/etiology ; Electroshock/adverse effects ; Epilepsy/etiology ; Epilepsy/physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Photoperiod ; Respiration ; Sleep Stages
Language	English
Publishing date	2017-08-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	80161-6
ISSN	1522-1598 ; 0022-3077
ISSN (online)	1522-1598
ISSN	0022-3077
DOI	10.1152/jn.00039.2017
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Article ; Online: Effect of monoamine reuptake inhibition and α

Kruse, Stephen W / Dayton, Kyle G / Purnell, Benton S / Rosner, Jared I / Buchanan, Gordon F

Epilepsia

2019 Volume 60, Issue 3, Page(s) 495–507

Abstract: Objective: Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in patients with refractory epilepsy. Although the mechanisms for SUDEP are incompletely understood, seizure-induced respiratory arrest (S-IRA) has been strongly and ... ...

Abstract	Objective: Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in patients with refractory epilepsy. Although the mechanisms for SUDEP are incompletely understood, seizure-induced respiratory arrest (S-IRA) has been strongly and consistently implicated. A body of evidence indicates that serotonin (5-HT), a modulator of breathing, plays a critical role in SUDEP. Because the 5-HT and norepinephrine (NE) systems interact in many biologic processes and NE is known to modulate breathing and seizures, we hypothesized that NE may play a role in S-IRA and SUDEP. Methods: We examined the effects of pharmacologic manipulation of 5-HT and NE on S-IRA and death following maximal electroshock (MES)-induced seizures in adult wild-type (WT) mice, genetically 5-HT neuron-deficient (Lmx1b Results: S-IRA and death was reduced in WT mice with NE reuptake inhibitors (NRIs), reboxetine and atomoxetine, selective serotonin reuptake inhibitors (SSRIs), fluoxetine and citalopram, and the dual 5-HT/NE reuptake inhibitor (SNRI), duloxetine. S-IRA and death was also reduced in Lmx1b Significance: These data suggest that 5-HT and NE critically interact in the modulation of breathing following a seizure and potentially inform preventive strategies for SUDEP.
MeSH term(s)	Adrenergic Uptake Inhibitors/therapeutic use ; Adrenergic alpha-1 Receptor Antagonists/therapeutic use ; Animals ; Atomoxetine Hydrochloride/therapeutic use ; Citalopram/therapeutic use ; Duloxetine Hydrochloride/therapeutic use ; Electroshock ; Fluoxetine/therapeutic use ; Male ; Mice ; Mice, Inbred C57BL ; Norepinephrine/agonists ; Norepinephrine/antagonists & inhibitors ; Norepinephrine/physiology ; Prazosin/therapeutic use ; Reboxetine/therapeutic use ; Seizures/prevention & control ; Serotonin/physiology ; Selective Serotonin Reuptake Inhibitors/therapeutic use ; Serotonin and Noradrenaline Reuptake Inhibitors/therapeutic use ; Sudden Unexpected Death in Epilepsy/prevention & control
Chemical Substances	Adrenergic Uptake Inhibitors ; Adrenergic alpha-1 Receptor Antagonists ; Serotonin Uptake Inhibitors ; Serotonin and Noradrenaline Reuptake Inhibitors ; Fluoxetine (01K63SUP8D) ; Citalopram (0DHU5B8D6V) ; Serotonin (333DO1RDJY) ; Atomoxetine Hydrochloride (57WVB6I2W0) ; Duloxetine Hydrochloride (9044SC542W) ; Reboxetine (947S0YZ36I) ; Norepinephrine (X4W3ENH1CV) ; Prazosin (XM03YJ541D)
Language	English
Publishing date	2019-02-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	216382-2
ISSN	1528-1167 ; 0013-9580
ISSN (online)	1528-1167
ISSN	0013-9580
DOI	10.1111/epi.14652
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Article ; Online: Suppression of phrenic nerve activity as a potential predictor of imminent sudden unexpected death in epilepsy (SUDEP).

Ashraf, Omar / Huynh, Trong / Purnell, Benton S / Murugan, Madhuvika / Fedele, Denise E / Chitravanshi, Vineet / Boison, Detlev

Neuropharmacology

2020 Volume 184, Page(s) 108405

Abstract: Sudden unexpected death in epilepsy (SUDEP) is a leading cause of death in patients with refractory epilepsy. Centrally-mediated respiratory dysfunction has been identified as one of the principal mechanisms responsible for SUDEP. Seizures generate a ... ...

Abstract	Sudden unexpected death in epilepsy (SUDEP) is a leading cause of death in patients with refractory epilepsy. Centrally-mediated respiratory dysfunction has been identified as one of the principal mechanisms responsible for SUDEP. Seizures generate a surge in adenosine release. Elevated adenosine levels suppress breathing. Insufficient metabolic clearance of a seizure-induced adenosine surge might be a precipitating factor in SUDEP. In order to deliver targeted therapies to prevent SUDEP, reliable biomarkers must be identified to enable prompt intervention. Because of the integral role of the phrenic nerve in breathing, we hypothesized that suppression of phrenic nerve activity could be utilized as predictive biomarker for imminent SUDEP. We used a rat model of kainic acid-induced seizures in combination with pharmacological suppression of metabolic adenosine clearance to trigger seizure-induced death in tracheostomized rats. Recordings of EEG, blood pressure, and phrenic nerve activity were made concomitant to the seizure. We found suppression of phrenic nerve burst frequency to 58.9% of baseline (p < 0.001, one-way ANOVA) which preceded seizure-induced death; importantly, irregularities of phrenic nerve activity were partly reversible by the adenosine receptor antagonist caffeine. Suppression of phrenic nerve activity may be a useful biomarker for imminent SUDEP. The ability to reliably detect the onset of SUDEP may be instrumental in the timely administration of potentially lifesaving interventions.
MeSH term(s)	Adenosine Kinase/antagonists & inhibitors ; Adenosine Kinase/metabolism ; Animals ; Kainic Acid/toxicity ; Male ; Phrenic Nerve/drug effects ; Phrenic Nerve/enzymology ; Phrenic Nerve/physiopathology ; Predictive Value of Tests ; Rats ; Rats, Wistar ; Seizures/chemically induced ; Seizures/enzymology ; Seizures/physiopathology ; Sudden Unexpected Death in Epilepsy ; Tubercidin/analogs & derivatives ; Tubercidin/pharmacology
Chemical Substances	5-iodotubercidin (24386-93-4) ; Adenosine Kinase (EC 2.7.1.20) ; Tubercidin (M351LCX45Y) ; Kainic Acid (SIV03811UC)
Language	English
Publishing date	2020-11-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2020.108405
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