Botulinum neurotoxin A subtype 2 reduces pathological behaviors more effectively than subtype 1 in a rat Parkinson’s disease model

•We compared the efficacy of BoNT/A1 and BoNT/A2 in a rat Parkinson’s disease model.•BoNT/A2 more effectively reduced rotation behavior in lesioned rats than BoNT/A1.•BoNT/A2 cleavage of SNAP-25 in the striatum was more efficient than that of BoNT/A1.•Treatment with BoNT/A2 may be a clinically usefu...

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Published inBiochemical and biophysical research communications Vol. 447; no. 2; pp. 311 - 314
Main Authors Itakura, Masanori, Kohda, Tomoko, Kubo, Takeya, Semi, Yuko, Azuma, Yasu-Taka, Nakajima, Hidemitsu, Kozaki, Shunji, Takeuchi, Tadayoshi
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 02.05.2014
Subjects
Acetylcholine
adverse effects
Animals
Botulinum neurotoxin
botulinum toxin
Botulinum Toxins, Type A - administration & dosage
Botulinum Toxins, Type A - adverse effects
Choline O-Acetyltransferase - metabolism
Corpus Striatum - drug effects
Corpus Striatum - metabolism
disease models
Disease Models, Animal
Female
Male
memory
Oxidopamine - pharmacology
Parkinson disease
Parkinson Disease, Secondary - chemically induced
Parkinson Disease, Secondary - drug therapy
Parkinson Disease, Secondary - physiopathology
Parkinson’s disease
Proteolysis
Rats
Rotation
Subtype
Synaptosomal-Associated Protein 25 - metabolism
PBS
PD
BoNT/A
ACh
ChAT
Rats
6-OHDA
CNS
Acetylcholine
Botulinum neurotoxin
Subtype
Parkinson’s disease
Online AccessGet full text
ISSN0006-291X
1090-2104
1090-2104
DOI10.1016/j.bbrc.2014.03.146

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Abstract •We compared the efficacy of BoNT/A1 and BoNT/A2 in a rat Parkinson’s disease model.•BoNT/A2 more effectively reduced rotation behavior in lesioned rats than BoNT/A1.•BoNT/A2 cleavage of SNAP-25 in the striatum was more efficient than that of BoNT/A1.•Treatment with BoNT/A2 may be a clinically useful therapy for Parkinson’s disease. Recent reports indicate that interruption of acetylcholine release by intrastriatal injection of botulinum neurotoxin type A (BoNT/A) in a rat Parkinson’s disease model reduces pathogenic behavior without adverse side effects such as memory dysfunction. Current knowledge suggests that BoNT/A subtype 1 (BoNT/A1) and BoNT/A subtype 2 (BoNT/A2) exert different effects. In the present study, we compared the effects of BoNT/A1 and BoNT/A2 on rotation behavior and in vivo cleavage of presynaptic protein SNAP-25 in a rat unilateral 6-hydroxydopamine-induced Parkinson’s disease model. BoNT/A2 more effectively reduced pathogenic behavior by efficiently cleaving SNAP-25 in the striatum compared with that of BoNT/A1. Our results suggest that BoNT/A2 has greater clinical therapeutic value for treating subjects with Parkinson’s disease compared to that of BoNT/A1.
AbstractList Recent reports indicate that interruption of acetylcholine release by intrastriatal injection of botulinum neurotoxin type A (BoNT/A) in a rat Parkinson's disease model reduces pathogenic behavior without adverse side effects such as memory dysfunction. Current knowledge suggests that BoNT/A subtype 1 (BoNT/A1) and BoNT/A subtype 2 (BoNT/A2) exert different effects. In the present study, we compared the effects of BoNT/A1 and BoNT/A2 on rotation behavior and in vivo cleavage of presynaptic protein SNAP-25 in a rat unilateral 6-hydroxydopamine-induced Parkinson's disease model. BoNT/A2 more effectively reduced pathogenic behavior by efficiently cleaving SNAP-25 in the striatum compared with that of BoNT/A1. Our results suggest that BoNT/A2 has greater clinical therapeutic value for treating subjects with Parkinson's disease compared to that of BoNT/A1.Recent reports indicate that interruption of acetylcholine release by intrastriatal injection of botulinum neurotoxin type A (BoNT/A) in a rat Parkinson's disease model reduces pathogenic behavior without adverse side effects such as memory dysfunction. Current knowledge suggests that BoNT/A subtype 1 (BoNT/A1) and BoNT/A subtype 2 (BoNT/A2) exert different effects. In the present study, we compared the effects of BoNT/A1 and BoNT/A2 on rotation behavior and in vivo cleavage of presynaptic protein SNAP-25 in a rat unilateral 6-hydroxydopamine-induced Parkinson's disease model. BoNT/A2 more effectively reduced pathogenic behavior by efficiently cleaving SNAP-25 in the striatum compared with that of BoNT/A1. Our results suggest that BoNT/A2 has greater clinical therapeutic value for treating subjects with Parkinson's disease compared to that of BoNT/A1.
Recent reports indicate that interruption of acetylcholine release by intrastriatal injection of botulinum neurotoxin type A (BoNT/A) in a rat Parkinson's disease model reduces pathogenic behavior without adverse side effects such as memory dysfunction. Current knowledge suggests that BoNT/A subtype 1 (BoNT/A1) and BoNT/A subtype 2 (BoNT/A2) exert different effects. In the present study, we compared the effects of BoNT/A1 and BoNT/A2 on rotation behavior and in vivo cleavage of presynaptic protein SNAP-25 in a rat unilateral 6-hydroxydopamine-induced Parkinson's disease model. BoNT/A2 more effectively reduced pathogenic behavior by efficiently cleaving SNAP-25 in the striatum compared with that of BoNT/A1. Our results suggest that BoNT/A2 has greater clinical therapeutic value for treating subjects with Parkinson's disease compared to that of BoNT/A1.
•We compared the efficacy of BoNT/A1 and BoNT/A2 in a rat Parkinson’s disease model.•BoNT/A2 more effectively reduced rotation behavior in lesioned rats than BoNT/A1.•BoNT/A2 cleavage of SNAP-25 in the striatum was more efficient than that of BoNT/A1.•Treatment with BoNT/A2 may be a clinically useful therapy for Parkinson’s disease. Recent reports indicate that interruption of acetylcholine release by intrastriatal injection of botulinum neurotoxin type A (BoNT/A) in a rat Parkinson’s disease model reduces pathogenic behavior without adverse side effects such as memory dysfunction. Current knowledge suggests that BoNT/A subtype 1 (BoNT/A1) and BoNT/A subtype 2 (BoNT/A2) exert different effects. In the present study, we compared the effects of BoNT/A1 and BoNT/A2 on rotation behavior and in vivo cleavage of presynaptic protein SNAP-25 in a rat unilateral 6-hydroxydopamine-induced Parkinson’s disease model. BoNT/A2 more effectively reduced pathogenic behavior by efficiently cleaving SNAP-25 in the striatum compared with that of BoNT/A1. Our results suggest that BoNT/A2 has greater clinical therapeutic value for treating subjects with Parkinson’s disease compared to that of BoNT/A1.
Author Kozaki, Shunji
Semi, Yuko
Kohda, Tomoko
Nakajima, Hidemitsu
Itakura, Masanori
Azuma, Yasu-Taka
Takeuchi, Tadayoshi
Kubo, Takeya
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Keywords PBS
PD
BoNT/A
ACh
ChAT
Rats
6-OHDA
CNS
Acetylcholine
Botulinum neurotoxin
Subtype
Parkinson’s disease
Language English
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Snippet •We compared the efficacy of BoNT/A1 and BoNT/A2 in a rat Parkinson’s disease model.•BoNT/A2 more effectively reduced rotation behavior in lesioned rats than...
Recent reports indicate that interruption of acetylcholine release by intrastriatal injection of botulinum neurotoxin type A (BoNT/A) in a rat Parkinson's...
Recent reports indicate that interruption of acetylcholine release by intrastriatal injection of botulinum neurotoxin type A (BoNT/A) in a rat Parkinson’s...
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SubjectTerms Acetylcholine
adverse effects
Animals
Botulinum neurotoxin
botulinum toxin
Botulinum Toxins, Type A - administration & dosage
Botulinum Toxins, Type A - adverse effects
Choline O-Acetyltransferase - metabolism
Corpus Striatum - drug effects
Corpus Striatum - metabolism
disease models
Disease Models, Animal
Female
Male
memory
Oxidopamine - pharmacology
Parkinson disease
Parkinson Disease, Secondary - chemically induced
Parkinson Disease, Secondary - drug therapy
Parkinson Disease, Secondary - physiopathology
Parkinson’s disease
Proteolysis
Rats
Rotation
Subtype
Synaptosomal-Associated Protein 25 - metabolism
Title Botulinum neurotoxin A subtype 2 reduces pathological behaviors more effectively than subtype 1 in a rat Parkinson’s disease model
URI https://dx.doi.org/10.1016/j.bbrc.2014.03.146
https://www.ncbi.nlm.nih.gov/pubmed/24713302
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https://www.proquest.com/docview/1825421987
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