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Comparison of neuroprotective effects induced by alpha-phenyl-N-tert-butyl nitrone (PBN) and N-tert-butyl-alpha-(2 sulfophenyl) nitrone (S-PBN) in lithium-pilocarpine status epilepticus.
Neurotoxicology. 2005 Dec; 26(6):969-79.N

Abstract

The status epilepticus (SE) induced in rats by lithium-pilocarpine (Li-pilo) shares many common features with soman-induced SE including extensive limbic neuropathology. Reactive oxygen species are hypothesized to play a role in the SE induced neuropathology and we propose that the free radical scavengers alpha-phenyl-N-tert-butyl nitrone (PBN) and N-tert-butyl-alpha-(2 sulfophenyl) nitrone (S-PBN) may be neuroprotective. PBN or S-PBN were administered either immediately following pilocarpine (exposure treatment) or 5 min after the onset of SE as determined by ECoG activity. SE was allowed to continue for 3 h before termination with propofol. The rats were sacrified 24 h following pilocarpine administration. S-PBN induced minor effects to reduce SE duration and improve neurological deficit 24 h following pilocarpine administration. One hundred and fifty milligrams per kilograms PBN administered 5 min after SE onset produced significant neuroprotection in the parietal, occipital, perirhinal and piriform cortices as well as the lateral amygdala. One hundred and fifty milligrams per kilograms S-PBN was neuroprotective only in the occipital and perirhinal cortex while 300 mg/kg S-PBN exacerbated cortical neuropathology. S-PBN administered 5 min after SE onset exacerbated neuropathology in thalamic regions. In contrast, PBN and S-PBN administered as exposure treatment exacerbated neuropathology in thalamic and CA3 regions. The differential neuroprotective effects of PBN and S-PBN may be the result of the poor brain penetration by S-PBN. The results suggest that free radical scavenger activity is neuroprotective in cortical regions during cholinergic convulsions. Regional variations in drug-induced neuroprotectant activity in Li-pilo SE are common and suggest multiple mechanisms of neuropathology.

Authors+Show Affiliations

College of Pharmacy, MSC09 5360, 1 University of New Mexico, Albuquerque, NM 87131-0001, USA. bonfire@unm.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

15890407

Citation

Peterson, Steven L., et al. "Comparison of Neuroprotective Effects Induced By alpha-phenyl-N-tert-butyl Nitrone (PBN) and N-tert-butyl-alpha-(2 Sulfophenyl) Nitrone (S-PBN) in Lithium-pilocarpine Status Epilepticus." Neurotoxicology, vol. 26, no. 6, 2005, pp. 969-79.
Peterson SL, Purvis RS, Griffith JW. Comparison of neuroprotective effects induced by alpha-phenyl-N-tert-butyl nitrone (PBN) and N-tert-butyl-alpha-(2 sulfophenyl) nitrone (S-PBN) in lithium-pilocarpine status epilepticus. Neurotoxicology. 2005;26(6):969-79.
Peterson, S. L., Purvis, R. S., & Griffith, J. W. (2005). Comparison of neuroprotective effects induced by alpha-phenyl-N-tert-butyl nitrone (PBN) and N-tert-butyl-alpha-(2 sulfophenyl) nitrone (S-PBN) in lithium-pilocarpine status epilepticus. Neurotoxicology, 26(6), 969-79.
Peterson SL, Purvis RS, Griffith JW. Comparison of Neuroprotective Effects Induced By alpha-phenyl-N-tert-butyl Nitrone (PBN) and N-tert-butyl-alpha-(2 Sulfophenyl) Nitrone (S-PBN) in Lithium-pilocarpine Status Epilepticus. Neurotoxicology. 2005;26(6):969-79. PubMed PMID: 15890407.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Comparison of neuroprotective effects induced by alpha-phenyl-N-tert-butyl nitrone (PBN) and N-tert-butyl-alpha-(2 sulfophenyl) nitrone (S-PBN) in lithium-pilocarpine status epilepticus. AU - Peterson,Steven L, AU - Purvis,Rebecca S, AU - Griffith,James W, PY - 2005/01/07/received PY - 2005/04/04/accepted PY - 2005/5/14/pubmed PY - 2006/4/6/medline PY - 2005/5/14/entrez SP - 969 EP - 79 JF - Neurotoxicology JO - Neurotoxicology VL - 26 IS - 6 N2 - The status epilepticus (SE) induced in rats by lithium-pilocarpine (Li-pilo) shares many common features with soman-induced SE including extensive limbic neuropathology. Reactive oxygen species are hypothesized to play a role in the SE induced neuropathology and we propose that the free radical scavengers alpha-phenyl-N-tert-butyl nitrone (PBN) and N-tert-butyl-alpha-(2 sulfophenyl) nitrone (S-PBN) may be neuroprotective. PBN or S-PBN were administered either immediately following pilocarpine (exposure treatment) or 5 min after the onset of SE as determined by ECoG activity. SE was allowed to continue for 3 h before termination with propofol. The rats were sacrified 24 h following pilocarpine administration. S-PBN induced minor effects to reduce SE duration and improve neurological deficit 24 h following pilocarpine administration. One hundred and fifty milligrams per kilograms PBN administered 5 min after SE onset produced significant neuroprotection in the parietal, occipital, perirhinal and piriform cortices as well as the lateral amygdala. One hundred and fifty milligrams per kilograms S-PBN was neuroprotective only in the occipital and perirhinal cortex while 300 mg/kg S-PBN exacerbated cortical neuropathology. S-PBN administered 5 min after SE onset exacerbated neuropathology in thalamic regions. In contrast, PBN and S-PBN administered as exposure treatment exacerbated neuropathology in thalamic and CA3 regions. The differential neuroprotective effects of PBN and S-PBN may be the result of the poor brain penetration by S-PBN. The results suggest that free radical scavenger activity is neuroprotective in cortical regions during cholinergic convulsions. Regional variations in drug-induced neuroprotectant activity in Li-pilo SE are common and suggest multiple mechanisms of neuropathology. SN - 0161-813X UR - https://www.unboundmedicine.com/medline/citation/15890407/Comparison_of_neuroprotective_effects_induced_by_alpha_phenyl_N_tert_butyl_nitrone__PBN__and_N_tert_butyl_alpha__2_sulfophenyl__nitrone__S_PBN__in_lithium_pilocarpine_status_epilepticus_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0161-813X(05)00034-3 DB - PRIME DP - Unbound Medicine ER -