Inner ear hair cells of lower vertebrates regenerate following physical or chemical insults. In the present study we aimed to define the damage and recovery of the pre and postsynaptic activity in the frog crista ampullaris after ototoxic insult with the antibiotic, gentamicin. Frogs were treated with a single dose of gentamicin sulphate (GM-5mM) administered intraotically. The presynaptic activity was monitored by recording in isolated canal preparations the endoampullar (receptor) potential (Adc). The postsynaptic activity was monitored by recording the resting and evoked spike activity from the whole ampullar nerve and from single canal afferents. We found that Adc was abolished 5 days after GM administration and that it progressively recovered close to control values 20 days after treatment. These results well fitted with the morphological damage and recovery of hair cells in the crista epithelium. Consistently with the presynaptic damage, the canal afferent activity was abolished 5 days after GM treatment, while the recovery of the background and the evoked afferent activity showed a different sequence. Background activity reappeared 7-8 days after GM treatment and in this period it was not driven by canal mechanical stimulation. In addition, background activity reached control values around 15 days post-treatment, while the evoked activity was detected 9 days after GM treatment and appeared normal close to 20 days. Intracellular recordings from single canal afferents confirmed the above mentioned results and revealed that the EPSP evoked discharge, together with the spike activity, reached normal values close to 20 days post-treatment. The present results show that the frog semicircular canal rapidly and completely recovers its pre -and postsynaptic function following severe ototoxic insult and that during the recovery, the afferent activity at rest becomes functional and mature before the mechano-transduction function.
Recovery of pre- and postsynaptic activity in frog semicircular canal after gentamicin treatment
PRIGIONI, IVO;CALZI, DANIELA MARIA;RUSSO, GIANCARLO;GIOGLIO, LUCIANA;
2008-01-01
Abstract
Inner ear hair cells of lower vertebrates regenerate following physical or chemical insults. In the present study we aimed to define the damage and recovery of the pre and postsynaptic activity in the frog crista ampullaris after ototoxic insult with the antibiotic, gentamicin. Frogs were treated with a single dose of gentamicin sulphate (GM-5mM) administered intraotically. The presynaptic activity was monitored by recording in isolated canal preparations the endoampullar (receptor) potential (Adc). The postsynaptic activity was monitored by recording the resting and evoked spike activity from the whole ampullar nerve and from single canal afferents. We found that Adc was abolished 5 days after GM administration and that it progressively recovered close to control values 20 days after treatment. These results well fitted with the morphological damage and recovery of hair cells in the crista epithelium. Consistently with the presynaptic damage, the canal afferent activity was abolished 5 days after GM treatment, while the recovery of the background and the evoked afferent activity showed a different sequence. Background activity reappeared 7-8 days after GM treatment and in this period it was not driven by canal mechanical stimulation. In addition, background activity reached control values around 15 days post-treatment, while the evoked activity was detected 9 days after GM treatment and appeared normal close to 20 days. Intracellular recordings from single canal afferents confirmed the above mentioned results and revealed that the EPSP evoked discharge, together with the spike activity, reached normal values close to 20 days post-treatment. The present results show that the frog semicircular canal rapidly and completely recovers its pre -and postsynaptic function following severe ototoxic insult and that during the recovery, the afferent activity at rest becomes functional and mature before the mechano-transduction function.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
