Naslov
Controversis about antinociceptive action of botolinum toxin

Autori
Lacković, Zdravko

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
10th Central European Neuropsychopharmacological Symposium / Psychiatria Danubina 19(4) / Hofmann, Gustav ; Sartorius, Norman - Zagreb : Medicinska naklada, 2007, 385-385

Skup
10th Central European Neuropsychopharmacological Symposium

Mjesto i datum
Sarajevo, Bosna i Hercegovina, 17.10.2007. - 20.10.2007

Vrsta sudjelovanja
Pozvano predavanje

Vrsta recenzije
Nije recenziran

Ključne riječi
botulinum toxin ; pain

Sažetak
Active, proteolytic fragment of botulinum neurotoxin-A (BTX-A) enters cholinergic nerve endings and cleave SNAP-25 protein. While BTX-A disables its function, it consequently prevents vesicle release and causes prolonged weakness of voluntary muscles and symptoms of parasympathetic (muscarinic) inhibition. This is the basis of botulism toxicity as well as usefulness of small doses of BTX-A in treating pathological consequences of peripheral motor or parasympathetic cholinergic nerve hyperactivity. In addition to that more and more recent evidence indicate that BTX-A may have antinociceptive effect. Most hypotheses assume that BTX-A produces antinociceptive effect by inhibiting not only the exocytosis of acetylcholine but also other neurotransmitters from nociceptive nerve endings. Based on literature review and our own results we found that mentioned hypothesis is not sufficient to explain experimental and clinical data collected up to now. Why antinociceptive effect BTX-A lasts for weeks in experimental animals and for months in human? Why BTX-A relieves inflammatory and neuropathic pain and not acute nociceptive pain? Why BTX-A reduces formalin and not carrageenan induced inflammation? How is it possible that in some experimental models BTX-A reduces pain when injected on contralateral side? Some of these questions can not be explained by hypothesis that antinociceptive activity of BTX-A is mediated solely by cleavage of SNAP25 at peripheral ending of sensory nerves. Supported by Croatian Ministry of Education, Science and Sport, and Deutscher Akademischer Austausch Dienst.

Izvorni jezik
Engleski

Znanstvena područja
Kliničke medicinske znanosti

POVEZANOST RADA