Naslov
EXPERIMENTAL FOCAL MUSCLE HYPERTONIA OFFERS NOVEL INSIGHTS INTO MOTOR EFFECTS OF BOTULINUM TOXIN TYPE A

Autori
Matak, Ivica ; Meglić, Patrik ; Šoštarić, Petra

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

Izvornik
10TH CROATIAN CONGRESS OF PHARMACOLOGY AND THE 1ST CROATIAN CONGRESS OF CLINICAL PHARMACOLOGY WITH INTERNATIONAL PARTICIPATION / Mršić Pelčić, Jasenka ; Vitezić, Dinko ; Janković, Tamara - : Pharmaca, 2022, 179-179

Skup
10. hrvatski kongres farmakologije ; 1. hrvatski kongres kliničke farmakologije s međunarodnim sudjelovanjem = 10th Croatian Congress of Pharmacology ; 1st Croatian Congress of Clinical Pharmacology and Therapeutics with International Participation

Mjesto i datum
Opatija, Hrvatska, 22.09.2022. - 25.09.2022

Vrsta sudjelovanja
Poster

Vrsta recenzije
Domaća recenzija

Ključne riječi
Botulinum toxin, hypertonic, focal paralysis

Sažetak
Introduction: Transient and reversible synaptic silencing by botulinum toxin type A (BoNT-A) is the basis of its therapeutic efficacy and safe use in movement disorders. Based on timing of BoNT-A actions and importance of appropriate muscle targeting, neuromuscular paralysis is considered its main therapeutic effect. Preclinical models have mostly focused on measurement of BoNT-A neuroparalytic effects in normal animals, in contrast to the possibly more relevant models of sustained or intermittent muscle hyperactivity. Moreover, clinical and experimental studies suggested that therapeutic effects of BoNT-A are not entirely explainable by peripheral neuromuscular site of action, suggesting the need for models of muscle hyperactivity. Results: In a series of experiments, we employed tetanus toxin (TeNT) as an elegant way to disinhibit the motoneuronal activity and evoke focal muscle hypertonia. We found that BoNTA induces simultaneous and non-mutually exclusive antispastic activity at both peripheral muscular and central spinal level. When separated from muscular action, central transsynaptic toxin action alone was effective in reducing the experimental muscle spasm. The central antispastic effect is masked by the toxin's peripheral action in the early period post injection, and becomes more prominent as the neuromuscular effect starts to weaken (2 months post BoNT-A). The toxin's activity at peripheral and central sites, as well as the duration of its beneficial antispastic action, was found to be dose-dependent. Conclusion: Preclinical models recapitulating some of the neurophysiological mechanisms of spastic and hyperkinetic movement disorders may be more helpful at explaining the factors and mechanisms of the BoNT-A’s long term clinical actions.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

POVEZANOST RADA