4-aminopyridine and Epilepsy studies

Epilepsy: A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)

Research Excerpts

Excerpt	Relevance	Reference
" We previously characterized the properties of distinct glutamatergic and GABAergic transmission-dependent synchronous epileptiform discharges in mouse hippocampal slices using the 4-aminopyridine model of epilepsy."	7.78	Hippocampal neuron firing and local field potentials in the in vitro 4-aminopyridine epilepsy model. ( Avoli, M; Dzakpasu, R; Gonzalez-Sulser, A; Queenan, BN; Vicini, S; Wang, J, 2012)
"Epileptiform discharges recorded in the 4-aminopyridine (4-AP) in vitro epilepsy model are mediated by glutamatergic and GABAergic signaling."	7.77	The 4-aminopyridine in vitro epilepsy model analyzed with a perforated multi-electrode array. ( Avoli, M; Dzakpasu, R; Gonzalez-Sulser, A; Motamedi, GK; Vicini, S; Wang, J, 2011)
"Infusion of the K(+) channel blocker 4-aminopyridine in the hippocampus induces the release of glutamate, as well as seizures and neurodegeneration."	7.70	Seizures and neurodegeneration induced by 4-aminopyridine in rat hippocampus in vivo: role of glutamate- and GABA-mediated neurotransmission and of ion channels. ( Peña, F; Tapia, R, 2000)
" Furthermore, real-time measurement of lactate and oxygen concentration dynamics concurrently with network electrical activity during status epilepticus induced by 4-aminopyridine (4-AP) demonstrated phasic changes in lactate levels that correlated with bursts of electrical activity, while tonic levels of lactate remained stable during seizures."	4.84	Amperometric bio-sensing of lactate and oxygen concurrently with local field potentials during status epilepticus. ( Barbosa, RM; Fernandes, E; Gerhardt, GA; Ledo, A, 2024)
"4-Aminopyridine was used in both in vivo and in vitro preparation to trigger seizures or epileptiform activity."	4.02	Neural recruitment by ephaptic coupling in epilepsy. ( Chiang, CC; Couturier, NH; Durand, DM; Pakalapati, N; Shivacharan, RS; Subramanian, M; Wei, X, 2021)
"To explore the role of cGKII in epilepsy, we investigated the expression of cGKII in patients with temporal lobe epilepsy (TLE) and in a pilocarpine-induced rat model and then performed behavioral, histological, and electrophysiological analyses by applying either a cGKII agonist or inhibitor in the hippocampus of the animal model."	3.88	Inhibition of Cgkii Suppresses Seizure Activity and Hippocampal Excitation by Regulating the Postsynaptic Delivery of Glua1. ( Gu, J; Lin, P; Lin, Z; Lu, S; Luo, J; Ma, Y; Tian, X; Wang, W; Wang, X; Xiao, F; Xiong, Y; Xu, D; Yang, Q; Yang, Y; Zhang, Y, 2018)
" Approximately 3-4 wk later recurrent electrographic seizures were evoked by local application of the chemoconvulsant 4-aminopyridine (4-AP); the ECoG and unit activity were monitored with extracellular silicone electrodes; and PV interneurons were activated optogenetically during the ictal and interictal phases."	3.83	The antiepileptic and ictogenic effects of optogenetic neurostimulation of PV-expressing interneurons. ( Assaf, F; Schiller, Y, 2016)
" We previously characterized the properties of distinct glutamatergic and GABAergic transmission-dependent synchronous epileptiform discharges in mouse hippocampal slices using the 4-aminopyridine model of epilepsy."	3.78	Hippocampal neuron firing and local field potentials in the in vitro 4-aminopyridine epilepsy model. ( Avoli, M; Dzakpasu, R; Gonzalez-Sulser, A; Queenan, BN; Vicini, S; Wang, J, 2012)
" Using a conditional transgenic mouse model, selective ablation of adult neural stem and progenitor cells in the subventricular zone induced a dramatic increase in morbidity and mortality of central nervous system disorders characterized by excitotoxicity-induced cell death accompanied by reactive inflammation, such as 4-aminopyridine-induced epilepsy and ischaemic stroke."	3.78	Subventricular zone neural progenitors protect striatal neurons from glutamatergic excitotoxicity. ( Bacigaluppi, M; Bari, M; Brambilla, E; Butti, E; Cambiaghi, M; Cebrian Silla, A; Centonze, D; Comi, G; D'Adamo, P; De Ceglia, R; De Chiara, V; Garcia-Verdugo, JM; Leocani, L; Maccarrone, M; Martino, G; Musella, A; Muzio, L; Quattrini, A; Rossi, S; Teneud, L, 2012)
"Epileptiform discharges recorded in the 4-aminopyridine (4-AP) in vitro epilepsy model are mediated by glutamatergic and GABAergic signaling."	3.77	The 4-aminopyridine in vitro epilepsy model analyzed with a perforated multi-electrode array. ( Avoli, M; Dzakpasu, R; Gonzalez-Sulser, A; Motamedi, GK; Vicini, S; Wang, J, 2011)
" We have addressed this issue in the 4-aminopyridine model of epilepsy in vitro by comparing GABAergic epileptiform currents and their sensitivity to gap junction blockers in wild-type vs."	3.77	Is connexin36 critical for GABAergic hypersynchronization in the hippocampus? ( Beaumont, M; Maccaferri, G, 2011)
"Morphological aspects of the formation and fate of neurons that underwent dramatic ultrastructural compaction ("dark" neurons) induced by 4-aminopyridine epilepsy were compared in an excitotoxic and a neighboring normal-looking area of the rat brain cortex."	3.74	The mode of death of epilepsy-induced "dark" neurons is neither necrosis nor apoptosis: an electron-microscopic study. ( Baracskay, P; Czurkó, A; Gallyas, F; Juhász, G; Kiglics, V, 2008)
"The functional significance of gap-junction (GJ) channels in seizure susceptibility and induction and maintenance of seizures in the developing rat brain was investigated on the 4-aminopyridine (4-AP) in vivo epilepsy model."	3.73	The functional significance of gap junction channels in the epileptogenicity and seizure susceptibility of juvenile rats. ( Gajda, Z; Gyengési, E; Hermesz, E; Szente, M; Szupera, Z, 2006)
"The purpose of the present study was to investigate if the sodium channel blocker and memory enhancer, vinpocetine, was capable to overcome the epileptic cortical activity, the abnormalities in the later waves of the auditory brainstem responses (ABRs) and the hearing loss induced by 4-AP at a convulsing dose in the guinea pig in vivo."	3.72	Vinpocetine prevents 4-aminopyridine-induced changes in the EEG, the auditory brainstem responses and hearing. ( Nekrassov, V; Sitges, M, 2004)
"The possible role of gap junctions in the manifestation and control of the duration of seizures was tested on the 4-aminopyridine-induced epilepsy model in rats in vivo, by using electrophysiologic, pharmacologic, and molecular biologic techniques."	3.72	Involvement of gap junctions in the manifestation and control of the duration of seizures in rats in vivo. ( Ali, KS; Gajda, Z; Gyengési, E; Hermesz, E; Szente, M, 2003)
"In order to determine whether the anticonvulsant effect of 2, 3-benzodiazepines is also displayed in a model of in vitro epilepsy, such as the "epileptiform" hippocampal slice, we studied the effects of 2,3-benzodiazepine 1-(4-aminophenyl)-4-methyl-7, 8-methylenedioxe-5H 2,3-benzodiazepine hydrochloride (GYKI 52466) and some new 2,3-benzodiazepine derivatives on CA1 basal neuronal excitability and on CA1 epileptiform burst activity produced by 4-aminopyridine in rat hippocampal slices."	3.70	Effects of GYKI 52466 and some 2,3-benzodiazepine derivatives on hippocampal in vitro basal neuronal excitability and 4-aminopyridine epileptic activity. ( Gatta, F; Marinelli, S; Sagratella, S, 2000)
"Infusion of the K(+) channel blocker 4-aminopyridine in the hippocampus induces the release of glutamate, as well as seizures and neurodegeneration."	3.70	Seizures and neurodegeneration induced by 4-aminopyridine in rat hippocampus in vivo: role of glutamate- and GABA-mediated neurotransmission and of ion channels. ( Peña, F; Tapia, R, 2000)
"The anticonvulsant activity of U-54494A was studied in a 4-aminopyridine (4-AP) epilepsy model using extracellular recordings in in vitro hippocampal slices."	3.68	U-54494A reduces 4-AP-induced afterdischarges of CA1 pyramidal cells in the hippocampal slice of the rat. ( Camacho-Ochoa, M; Hoffmann, WE; Piercey, MP; VonVoigtlander, PF, 1992)
"The effects of ketamine and (+)cyclazocine on three in vitro models of epilepsy: the "Mg2+ free", the 4-aminopyridine (4-AP) and, for comparison, the penicillin model were studied."	3.67	Effects of ketamine and (+)cyclazocine on 4-aminopyridine and "magnesium free" epileptogenic activity in hippocampal slices of rats. ( de Carolis, AS; Frank, C; Sagratella, S, 1987)
"Limbic seizures can be mimicked in vitro using preparations of combined hippocampus-entorhinal cortex slices perfused with artificial cerebrospinal fluid containing convulsants or nominally zero Mg(2+), in order to produce epileptiform synchronization."	2.41	Network and pharmacological mechanisms leading to epileptiform synchronization in the limbic system in vitro. ( Avoli, M; Biagini, G; D'Antuono, M; D'Arcangelo, G; Köhling, R; Louvel, J; Pumain, R; Tancredi, V, 2002)
"During epileptic seizures, neuronal network activity is hyper synchronized whereby GABAergic parvalbumin-interneurons may have a key role."	1.91	Cell-specific switch for epileptiform activity: critical role of interneurons in the mouse subicular network. ( Andersson, M; Kokaia, M; Ledri, M; Wickham, J, 2023)
"Focal epilepsy is thought to be a network disease, in which epileptiform activity can spread noncontiguously through the brain via highly interconnected nodes, or hubs, within existing networks."	1.91	Excitatory-inhibitory mismatch shapes node recruitment in an epileptic network. ( Estin, J; Li, D; Li, J; Lin, W; Liou, JY; Luo, P; Ma, H; Niemeyer, JE; Schwartz, TH; Yang, F; Zhan, F; Zhao, M, 2023)
"Epilepsy is a group of neurological disorders which affects millions of people worldwide."	1.51	Electrophoretic Delivery of γ-aminobutyric Acid (GABA) into Epileptic Focus Prevents Seizures in Mice. ( Kaszas, A; Malliaras, GG; Proctor, CM; Slezia, A; Williamson, A, 2019)
"Focal seizure propagation is classically thought to be spatially contiguous."	1.48	Role of inhibitory control in modulating focal seizure spread. ( Baird-Daniel, E; Daniel, A; Emerson, R; Liou, JY; Ma, H; Schevon, CA; Schwartz, TH; Smith, EH; Wenzel, M; Yuste, R; Zhao, M, 2018)
"Traditionally, seizure activity is believed to arise from the breakdown of this delicate balance in favor of excitation with loss of inhibition."	1.48	Role of KCC2-dependent potassium efflux in 4-Aminopyridine-induced Epileptiform synchronization. ( Avoli, M; Bazhenov, M; González, OC; Krishnan, GP; Myers, TL; Shiri, Z; Williams, S, 2018)
"Epilepsy is a highly prevalent neurological disorder."	1.46	Propylparaben suppresses epileptiform activity in hippocampal CA1 pyramidal cells in vitro. ( Galván, EJ; Lara-Valderrábano, L; Rocha, L, 2017)
"We induced focal neocortical seizures using microinjection of 4-aminopyridine into premotor cortex in five anesthetized cynomolgus monkeys."	1.46	Rapid focal cooling attenuates cortical seizures in a primate epilepsy model. ( Fu, Y; Gan, Y; Li, D; Ren, G; Tao, G; Wang, L; Wang, W; Yan, J; Yan, X; Yang, X; Yue, F; Zhang, Z, 2017)
"Epilepsy is a disease of neuronal hyper-synchrony that can involve both neocortical and hippocampal brain regions."	1.42	Coalescence of deep and superficial epileptic foci into larger discharge units in adult rat neocortex. ( Andrade, R; Loeb, JA; Serafini, R, 2015)
"Epilepsy is a chronic brain disease characterised by recurrent seizures."	1.42	Heterogeneous effects of antiepileptic drugs in an in vitro epilepsy model--a functional multineuron calcium imaging study. ( Hasegawa, M; Hongo, Y; Ikegaya, Y; Ogawa, K; Sakaguchi, G; Takasu, K, 2015)
"Epilepsy is a neurological disorder produced by an imbalance between excitatory and inhibitory neurotransmission, in which transporters of both glutamate and GABA have been implicated."	1.38	Rapid compensatory changes in the expression of EAAT-3 and GAT-1 transporters during seizures in cells of the CA1 and dentate gyrus. ( López-Pérez, SJ; Medina-Ceja, L; Morales-Villagrán, A; Sandoval-García, F, 2012)
"Treatment with bicuculline and 4-aminopyridine (Bic + 4-AP), which induced burst firing, inhibited metabotropic-induced suppression of excitation (MSE) and prolonged the duration of depolarization-induced suppression of excitation (DSE)."	1.38	Epileptic stimulus increases Homer 1a expression to modulate endocannabinoid signaling in cultured hippocampal neurons. ( Krogh, KA; Li, Y; Thayer, SA, 2012)
"Pretreatment with levetiracetam failed to exert any antiepileptogenic effect."	1.37	Protein kinase inhibitor as a potential candidate for epilepsy treatment. ( Gajda, Z; Horváth, Z; Kéri, G; Orfi, L; Szántai-Kis, C; Szente, M; Török, R, 2011)
"Zonisamide (ZNS) is an anticonvulsant drug known to affect various neuronal channels and transmitter systems."	1.35	Antiepileptic activity of zonisamide on hippocampal CA3 neurons does not depend on carbonic anhydrase inhibition. ( Leniger, T; Splettstösser, F; Thöne, J; Wiemann, M, 2008)
"Similar to neuropathic pain, spinal dorsal horn epileptiform activity was much less reduced by classical analgesics than by anticonvulsant agents."	1.32	Epileptiform activity in rat spinal dorsal horn in vitro has common features with neuropathic pain. ( Ruscheweyh, R; Sandkühler, J, 2003)
"Furosemide was not found to alter synaptic field responses, excitatory postsynaptic currents or intrinsic membrane properties of principal hippocampal neurons."	1.32	A potential role for astrocytes in mediating the antiepileptic actions of furosemide in vitro. ( Baraban, SC; Barbaro, NM; Takahashi, DK, 2004)
"Remacemide is a potential anticonvulsant drug with an active metabolite, desglycinyl-remacemide (DGR)."	1.31	Differential effects of remacemide and desglycinyl-remacemide on epileptiform burst firing in the rat hippocampal slice. ( Brodie, MJ; Santangeli, S; Sills, GJ; Stone, TW, 2002)

Research

Studies (167)

Authors

Clinical Trials (3)

Trial Overview

Trial Outcomes

Standard Alcoholic Drinks Per Treatment Period

Timeframe	Studies, this research(%)	All Research%
pre-1990	3 (1.80)	18.7374
1990's	36 (21.56)	18.2507
2000's	61 (36.53)	29.6817
2010's	58 (34.73)	24.3611
2020's	9 (5.39)	2.80

Authors	Studies
Fedor, FZ	1
Paraczky, C	1
Ravasz, L	1
Tóth, K	1
Borhegyi, Z	1
Somogyvári, Z	2
Juhász, G	2
Fekete, Z	1
Volnova, A	1
Tsytsarev, V	3
Ganina, O	1
Vélez-Crespo, GE	1
Alves, JM	1
Ignashchenkova, A	1
Inyushin, M	1
Maghbooli, M	2
Jourahmad, Z	2
Golizadeh, M	2
Wickham, J	1
Ledri, M	1
Andersson, M	1
Kokaia, M	1
Müller, P	1
Takacs, DS	1
Hedrich, UBS	1
Coorg, R	1
Masters, L	1
Glinton, KE	1
Dai, H	1
Cokley, JA	1
Riviello, JJ	1
Lerche, H	1
Cooper, EC	2
Luo, P	1
Yang, F	1
Li, J	1
Niemeyer, JE	1
Zhan, F	1
Estin, J	1
Zhao, M	5
Li, D	3
Lin, W	1
Liou, JY	3
Ma, H	5
Schwartz, TH	5
Fernandes, E	1
Ledo, A	1
Gerhardt, GA	1
Barbosa, RM	1
Kong, S	1
Chen, TX	1
Jia, XL	1
Cheng, XL	1
Zeng, ML	1
Liang, JY	1
He, XH	1
Yin, J	1
Han, S	1
Liu, WH	4
Fan, YT	1
Zhou, T	1
Liu, YM	1
Peng, BW	1
Shivacharan, RS	2
Chiang, CC	3
Wei, X	1
Subramanian, M	1
Couturier, NH	1
Pakalapati, N	1
Durand, DM	5
Baird-Daniel, E	2
Daniel, AGS	1
Wenzel, M	2
Laffont, P	1
Yuste, R	2
Ren, G	1
Yan, J	1
Tao, G	1
Gan, Y	1
Yan, X	1
Fu, Y	1
Wang, L	1
Wang, W	2
Zhang, Z	1
Yue, F	1
Yang, X	1
Zhang, C	2
Tabatabaei, M	1
Bélanger, S	2
Girouard, H	1
Moeini, M	1
Lu, X	1
Lesage, F	3
Lara-Valderrábano, L	1
Galván, EJ	1
Rocha, L	1
González, OC	1
Shiri, Z	2
Krishnan, GP	1
Myers, TL	1
Williams, S	1
Avoli, M	33
Bazhenov, M	1
Wu, X	1
Muthuchamy, M	1
Reddy, DS	1
Gu, J	1
Tian, X	1
Yang, Q	1
Lin, P	1
Ma, Y	1
Xiong, Y	1
Xu, D	1
Zhang, Y	1
Yang, Y	2
Lu, S	1
Lin, Z	1
Luo, J	1
Xiao, F	1
Wang, X	1
Smith, EH	1
Daniel, A	1
Emerson, R	1
Schevon, CA	1
Zhang, M	1
Gonzalez-Reyes, LE	2
Slezia, A	1
Proctor, CM	1
Kaszas, A	1
Malliaras, GG	2
Williamson, A	1
Rao, B	1
Maslov, KI	2
Li, L	1
Wang, LV	2
Rubi, L	1
Schandl, U	1
Lagler, M	1
Geier, P	1
Spies, D	1
Gupta, KD	1
Boehm, S	1
Kubista, H	1
Guevara, E	1
Pouliot, P	2
Nguyen, DK	1
Ladas, TP	1
Herrington, R	3
Lévesque, M	5
Wang, Y	1
Toprani, S	1
Tang, Y	1
Vrabec, T	1
Harris, S	1
Boorman, L	1
Bruyns-Haylett, M	1
Kennerley, A	1
Overton, PG	1
Berwick, J	1
Hamidi, S	3
Serafini, R	2
Andrade, R	1
Loeb, JA	2
Kano, T	1
Inaba, Y	2
D'Antuono, M	5
Biagini, G	4
Hongo, Y	1
Takasu, K	1
Ikegaya, Y	1
Hasegawa, M	1
Sakaguchi, G	1
Ogawa, K	1
Alfonsa, H	1
Merricks, EM	1
Codadu, NK	1
Cunningham, MO	1
Deisseroth, K	1
Racca, C	1
Trevelyan, AJ	1
Dettloff, S	1
Ahn, S	1
Jun, SB	1
Lee, HW	1
Lee, S	1
Assaf, F	1
Schiller, Y	1
Jonsson, A	1
Inal, S	1
Uguz, I	1
Williamson, AJ	1
Kergoat, L	1
Rivnay, J	1
Khodagholy, D	1
Berggren, M	1
Bernard, C	1
Simon, DT	1
Ristori, C	2
Cammalleri, M	4
Martini, D	2
Pavan, B	2
Liu, Y	5
Casini, G	2
Dal Monte, M	2
Bagnoli, P	3
Gallyas, F	1
Kiglics, V	1
Baracskay, P	1
Czurkó, A	1
Kobayashi, K	1
Nishizawa, Y	1
Sawada, K	1
Ogura, H	1
Miyabe, M	1
Világi, I	4
Dobó, E	1
Borbély, S	2
Czégé, D	1
Molnár, E	1
Mihály, A	4
Pineau, J	2
Guez, A	1
Vincent, R	1
Panuccio, G	1
Fernández, M	1
Lao-Peregrín, C	1
Martín, ED	2
Hill, AJ	1
Jones, NA	1
Williams, CM	1
Stephens, GJ	1
Whalley, BJ	1
Carriero, G	1
Uva, L	1
Gnatkovsky, V	1
de Curtis, M	1
Medina-Ceja, L	3
Ventura-Mejía, C	1
Gonzalez-Sulser, A	2
Wang, J	2
Motamedi, GK	1
Vicini, S	2
Dzakpasu, R	2
Wirtz, PW	1
Titulaer, MJ	1
Gerven, JM	1
Verschuuren, JJ	1
Beaumont, M	1
Maccaferri, G	1
Gajda, Z	4
Török, R	1
Horváth, Z	1
Szántai-Kis, C	1
Orfi, L	1
Kéri, G	1
Szente, M	5
Streit, AK	1
Derst, C	1
Wegner, S	1
Heinemann, U	6
Zahn, RK	2
Decher, N	1
Vincent, RD	1
Courville, A	1
Ketzef, M	1
Kahn, J	1
Weissberg, I	1
Becker, AJ	1
Friedman, A	1
Gitler, D	1
He, D	1
Yin, XQ	2
Sitges, M	2
Sanchez-Tafolla, BM	1
Chiu, LM	1
Aldana, BI	1
Guarneros, A	1
De la Cruz, E	1
Guo, L	1
Anderson, SA	1
Yao, J	1
Parameswar, AR	1
Demchenko, AV	1
Addae, JI	1
Stone, TW	2
Sah, N	1
Rajput, SK	1
Singh, JN	1
Meena, CL	1
Jain, R	1
Sikdar, SK	1
Sharma, SS	1
Vera, G	1
Tapia, R	5
Liotta, A	1
Kim, S	1
Sandow, N	1
Wang, SB	2
Yu, X	1
Coiret, G	1
Ster, J	1
Grewe, B	1
Wendling, F	1
Helmchen, F	1
Gerber, U	1
Benquet, P	1
Li, Y	1
Krogh, KA	1
Thayer, SA	1
Sandoval-García, F	1
Morales-Villagrán, A	2
López-Pérez, SJ	1
Queenan, BN	1
Butti, E	1
Bacigaluppi, M	1
Rossi, S	1
Cambiaghi, M	1
Bari, M	1
Cebrian Silla, A	1
Brambilla, E	1
Musella, A	1
De Ceglia, R	1
Teneud, L	1
De Chiara, V	1
D'Adamo, P	1
Garcia-Verdugo, JM	1
Comi, G	1
Muzio, L	1
Quattrini, A	1
Leocani, L	1
Maccarrone, M	1
Centonze, D	1
Martino, G	1
Gulyás-Kovács, A	1
Dóczi, J	1
Tarnawa, I	1
Détári, L	2
Banczerowski-Pelyhe, I	1
Smyth, MD	1
Barbaro, NM	2
Baraban, SC	5
Lee, AC	1
Wong, RK	1
Chuang, SC	1
Shin, HS	1
Bianchi, R	1
Louvel, J	4
Köhling, R	3
Pumain, R	3
D'Arcangelo, G	2
Tancredi, V	5
Said Ali, K	1
Hermesz, E	3
Szakács, R	1
Weiczner, R	2
Krisztin-Péva, B	2
Zádor, Z	1
Zádor, E	1
Sayin, U	1
Rutecki, PA	3
Ayala, GX	2
Ruscheweyh, R	1
Sandkühler, J	1
Roshan-Milani, S	1
Ferrigan, L	1
Khoshnood, MJ	1
Davies, CH	2
Cobb, SR	1
Mattia, D	3
Olivier, A	1
Esposito, V	1
Gyengési, E	2
Ali, KS	1
Klueva, J	1
Munsch, T	1
Albrecht, D	1
Pape, HC	1
Harrison, PK	1
Tattersall, JE	1
Clement, RA	1
Merlo, D	1
Cifelli, P	1
Cicconi, S	1
Pisani, A	1
Bonsi, P	1
Martella, G	1
De Persis, C	1
Costa, C	1
Pisani, F	1
Bernardi, G	2
Calabresi, P	2
Takahashi, DK	1
Vizi, S	1
Bagosi, A	1
Gulya, K	1
Nekrassov, V	1
Cervia, D	2
Langenegger, D	1
Hoyer, D	1
Kaminski, RM	1
Marini, H	1
Kim, WJ	1
Rogawski, MA	2
Thuault, SJ	1
Brown, JT	1
Calver, AR	1
Collingridge, GL	1
Randall, A	1
Fabene, PF	1
Marzola, P	1
Nicolato, E	1
Calderan, L	1
Andrioli, A	1
Farkas, E	1
Süle, Z	1
Sbarbati, A	1
Kang, N	1
Xu, J	1
Xu, Q	1
Nedergaard, M	1
Kang, J	1
Lees, G	1
Stöhr, T	1
Errington, AC	1
Peña, F	3
Alavez-Pérez, N	1
Halasy, K	1
Kilb, W	1
Dierkes, PW	1
Syková, E	1
Vargová, L	1
Luhmann, HJ	2
Skov, J	1
Andreasen, M	1
Nedergaard, S	1
Szupera, Z	1
Fernández de Sevilla, D	1
Garduño, J	1
Galván, E	1
Buño, W	2
Cataldi, M	1
Lariccia, V	1
Marzaioli, V	1
Cavaccini, A	1
Curia, G	1
Viggiano, D	1
Canzoniero, LM	1
di Renzo, G	1
Annunziato, L	1
Cordero-Romero, A	1
Thöne, J	1
Leniger, T	1
Splettstösser, F	1
Wiemann, M	1
Fueta, Y	3
Siniscalchi, A	3
Arvanov, VL	1
Holmes, KH	1
Keele, NB	1
Shinnick-Gallagher, P	1
Yonekawa, WD	1
Kapetanovic, IM	1
Kupferberg, HJ	1
Lücke, A	2
Nagao, T	3
Hoffman, SN	1
Prince, DA	1
Hwa, GG	1
Watts, AE	1
Jefferys, JG	3
Longo, R	1
Zeng, YC	1
Sagratella, S	3
Barbarosie, M	2
Lopantsev, V	2
Higashima, M	2
Kinoshita, H	1
Yamaguchi, N	1
Koshino, Y	1
Traub, RD	1
Borck, C	1
Colling, SB	1
Psarropoulou, C	2
Mercuri, NB	1
Truyen, L	1
Barkhof, F	1
Frequin, ST	1
Polman, CH	1
Tobi, H	1
Hommes, OR	1
Valk, J	1
Hochman, DW	3
D'Ambrosio, R	1
Janigro, D	1
Schwartzkroin, PA	3
Armand, V	1
Rundfeldt, C	1
Sinha, SR	1
Saggau, P	1
Gutschmidt, KU	1

Trial	Phase	Enrollment	Study Type	Start Date	Status
Placebo-Controlled Crossover Trial of Levetiracetam on Ethanol Intake[NCT01168687]		46 participants (Actual)	Interventional	2008-11-30	Completed
Treatment Efficacy of 1-Octanol Compared to Placebo in Adults With Essential Tremor[NCT00080366]	Phase 2	14 participants	Interventional	2004-03-31	Completed
Clinical Trial Characterizing the Bioavailability of 1-Octanol in Adults With Ethanol-responsive Essential Tremor[NCT00102596]	Phase 2	21 participants (Actual)	Interventional	2005-01-31	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

The primary outcome of this study is to determine the effect of levetiracetam on alcohol consumption as measured by change in # of drinks during each treatment period. (NCT01168687)
Timeframe: During each 14 day treatment period

Blood Plasma Levels of Octanoic Acid After 64 mg/kg 1-Octanol Dose

Intervention	number of drinks per treatment period (Mean)
All Subjects (n = 46) Placebo	41.2
All Subjects (n = 46) Levetiracetam	45.4

Octanoic Acid is a metabolite of 1-octanol. Blood plasma levels of octanoic acid were measured at 5, 20, 45, 70, 100, 130, 160, 210, 270 and 360 minutes post-dose. (NCT00102596)
Timeframe: 5, 20, 45, 70, 100, 130, 160, 210, 270 and 360 minutes post-dose

Heart Rate Post 1-Octanol Dose

Intervention	ng/ml (Mean)
	Plasma Octanoic Acid Level at 5 min post-dose	Plasma Octanoic Acid Level at 20 min post-dose	Plasma Octanoic Acid Level at 45 min post-dose	Plasma Octanoic Acid Level at 70 min post-dose	Plasma Octanoic Acid Level at 100 min post-dose	Plasma Octanoic Acid Level at 130 min post-dose	Plasma Octanoic Acid Level at 160 min post-dose	Plasma Octanoic Acid Level at 210 min post-dose	Plasma Octanoic Acid Level at 270 min post-dose	Plasma Octanoic Acid Level at 360 min post-dose
64 mg/kg 1-Octanol Cellulose-based (CEL) Formulation	62.94	5064.12	7967.97	6788.58	5701.60	5448.23	4662.88	3179.10	2248.74	1266.37
64 mg/kg 1-Octanol Soybean Oil Embedded (SOY) Formulation	74.16	3885.52	9645.55	13315.26	9289.39	9605.68	6678.69	4307.74	2618.25	872.51

(NCT00102596)
Timeframe: 0 minutes, 15 minutes, 100 minutes and 24 hours post-dose

Normalized Mean Tremor Amplitude for Both Formulations of 64 mg/kg 1-Octanol in Part B

Intervention	beats per minute (Least Squares Mean)
	Heart Rate at 0 min	Heart Rate at 15 min	Heart Rate at 100 min	Heart Rate at 24 hours
1-Octanol Dose	70.8	66.6	67.1	72.4

Spirography mean tremor amplitudes were measured in the right hand of each participant at 0, 15, 30, 60, 90, 120, 150, 180, 240 and 360 minutes post-dose. Then, the scores of each participant were normalized (i.e., divided by) by their baseline tremor severity scores so that all scores are expressed as a proportion of the baseline score. Therefore, 1 is the baseline tremor severity, and lower scores indicate tremor reduction. (NCT00102596)
Timeframe: 0, 15, 30, 60, 90, 120, 150, 180, 240 and 360 minutes post-dose

PR and QTc Intervals Post 1-Octanol Dose

Intervention	normalized score on a scale (Mean)
	Normalized score at 0 minutes	Normalized score at 15 minutes post-dose	Normalized score at 30 minutes post-dose	Normalized score at 60 minutes post-dose	Normalized score at 90 minutes post-dose	Normalized score at 120 minutes post-dose	Normalized score at 150 minutes post-dose	Normalized score at 180 minutes post-dose	Normalized score at 240 minutes post-dose	Normalized score at 360 minutes post-dose
64 mg/kg 1-Octanol Cellulose-based (CEL) Formulation	1	1.009	0.826	0.786	0.670	0.662	0.680	0.645	0.791	0.894
64 mg/kg 1-Octanol Soybean Oil Embedded (SOY) Formulation	1	0.901	0.738	0.766	0.685	0.709	0.746	0.707	0.683	0.122