Ok, here is why I am optimistic: Note the authors include Dr.Large (Autifony CEO) and Dr.Roland Schaette (Tinnitus researcher who predicted a cure for tinnitus within the next 10 years). Basically this is a tinnitus research dream team.
Also note- Aut3 returned Inferior colliculus spontaneous firing levels of noise exposed animals to those similar of non-exposed. Source below as always.
AUT3, a Kv3 channel modulator, counteracts elevation of spontaneous firing rates in the auditory midbrain following noise trauma
L. L. HESSE1,4, L. A. ANDERSON1,
C. H. LARGE 5, R. SCHAETTE 2, J. F. LINDEN3;1Ear Inst.,3Ear Inst. and Dept. of Neuroscience, Physiol. &Pharmacol.,2Univ. Col. London, London,United Kingdom;4Dept. of Otorhinolaryngology, Head &Neck Surgery, Univ. of Luebeck, Luebeck,Germany;
5Autifony Therapeutics
Ltd., London, United Kingdom
Abstract:
Exposure to loud noise is a common cause of tinnitus in humans, and can be used to generate
tinnitus like behaviour and neural pathologies in
animal models. Here we show that four weeks
after noise exposure, mice exhibit increased spontaneous neural activity in the inferior colliculus
(IC), and this elevation of spontaneous activity is normalized by intraperitoneal injections of AUT3,
a novel Kv3 channel modulator. CBA/Ca mice were exposed to octave
-band noise (8-16 kHz) at 105dB SPL for two hours under anaesthesia. Four weeks later, extracellular multiunit recordings wereobtained in vivo from the IC; similar recordings were made from control
mice. Spontaneousmultiunit activity in the IC was significantly higher in noise
-exposed than in control mice. Tone-response thresholds were also significantly higher in noise
-exposed mice, and distributions of characteristic frequencies and best frequencies were shifted toward lower frequencies than in
control animals. Intraperitoneal injections of 90 mg/kg AUT3, a positive modulator of Kv3.1
channels, decreased IC excitability in noise-exposed animals, returning spontaneous rates to levels
similar to those observed in control animals; no such effect was observed following injections of
vehicle. AUT3, but not vehicle, also reduced the probability of firing to clicks and maximum click
-evoked firing rates in noise
-exposed animals, but had no impact on frequency tuning or thresholds
of IC responses. In control animals, there were no significant differences in spontaneous rate,sound-
evoked firing, or tone-response thresholds between animals receiving 90 mg/kg AUT3 and
animals receiving vehicle. These results indicate that four weeks after noise exposure,
spontaneous activity is elevated in the IC; that the positive Kv3 channel modulator AUT3
counteracts this increase in spontaneous activity; and that AUT3 has minimal impact on IC
responses in control animals. AUT3 is therefore a potentially promising treatment for neural
pathologies that may underlie tinnitus.
http://www.autifonytherapeutics.com/publications/Hesse-et-al-SFN-2013-Abstract-FINAL.pdf
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