BOTULINUM TOXIN TYPE A (150 kDa) DECREASES EXAGGERATED NEUROTRANSMITTER RELEASE FROM TRIGEMINAL GANGLION NEURONS AND RELIEVES NEUROPATHY BEHAVIORS INDUCED BY INFRAORBITAL NERVE CONSTRICTION
BOTULINUM TOXIN TYPE A (150 kDa) DECREASES EXAGGERATED NEUROTRANSMITTER RELEASE FROM TRIGEMINAL GANGLION NEURONS AND RELIEVES NEUROPATHY BEHAVIORS INDUCED BY INFRAORBITAL NERVE CONSTRICTION
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DOI：
10.1016/j.neuroscience.2009.01.066
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发表时间：
2009-04-10
期刊：
影响因子：
3.3
通讯作者：
Oguma, K.
中科院分区：
文献类型：
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作者：
Kitamura, Y.;Matsuka, Y.;Oguma, K.
Many patients with trigeminal neuropathies suffer severe chronic pain which is inadequately alleviated with centrally-acting drugs. These drugs also possess severe side effects making compliance difficult. One strategy is to develop new treatments without central side effects by targeting peripheral sensory neurons, since sensory neuron excitability and neurotransmitter release increase in chronic pain states. Such treatments may include the highly purified botulinum toxin type A 150 kDa (BoNT/A) which reportedly blocks vesicular neurotransmitter release. We set out to determine if experimental trigeminal neuropathy induced by infraorbital nerve constriction (IoNC) in rats could alter neurotransmitter release from somata of trigeminal sensory neurons and if it could be aften-uated by BoNT/A. Thus, we monitored the secretory activity of acutely dissociated trigeminal ganglion (TRG) neurons from naive and IoNC rats by measuring the fluorescence intensity of the membrane-uptake marker (N-(3-triethylammoniumpropyl)-4-(6-(4-(diethylamino)phenyl)hexatrienyl)pyridinium dibromide (FM4-64). FM4-64 staining showed that neurons possess a pool of recycled vesicles which could be released by high KCl (75 mM) application. BoNT/A pre-treatment of acutely dissociated TRG neurons from naive rats significantly reduced the rate of FM4-64 dye release. Neurons isolated from TRG ipsilateral to IoNC exhibited significantly faster onset of FM4-64 release than neurons contralateral to
