After auditory cortex lesion and stimulation with sound, ABRs (auditory brainstem recording analysis) shows, over a long term (15 and 30 days post lesion) a shortening in wave I latency. Could someone suggest a comprehensive physiological or molecular explanation for this finding?
Very interesting question.
I am envisaging two possibilities (guessing involved)
1. If there is a lesion to the cochlea, in addition to the cortical lesion, this can cause a broadening of cochlear (auditory) filters. A broader filter will take shorter time to buildup and will also recruit more afferent fibers, causing a reduction in ABR wave I latency.
2. If there is no lesion to the cochlea.
Could it be due to a loss of centrifugal cortical control over the olivocochlear efferents that innervate outer hair cells in the cochlea? The efferents could be causing larger than normal inhibition of outer hair cell activity, since they are not influenced (?inhibited) by top-down cortical responses, resulting in a broadened cochlear tuning. Again, this can cause a reduction in ABR wave I latency. This is a long shot.
I am interested to know what others think about this.
Controls show no changes, we can assume that the ears is working well in our experimental groups. Answer 2 is more solid for me. However my question now is why a broader freq tuning can reduce the latencies. This can affect the amplitude of waves (because more Type I fibres respond) but the two things that can alter latency, axonal conduction speed and synaptic delay, wich not changed by a less freq tuned response of Corti organ.( my e mail - [email protected])
I am not sure that the descending control may be inhibitory. Corticofugal connections to the MOCB may be excitatory and glutamatergic. Do you have any information about the effect of descending control on outher hair cell activity.
Look, you could not compare control group with experiment group because there are many variety between animals. So the latency in wave I effected by the place of electrodes under skin and the tempruture of plate when you put the animals.finaly I advice you to read liberman and kujawa 2009 paper which explain what happen after expose mice to noise
Thanks a lot for your advice. S. Kuwada help us in the design of our experiments.
Any shortening in Wave 1 must be due to a change in the cochlea. Meniere spectrum disorder is very likely, and follows any surgical operation where there is likely to be dehydration, weight loss or reduced CSF pressure. Audiosensitivity is very likely, so that the previous sound stimulus now sounds louder and will have shorter latency. I don't think audiosensitivity has anything to do with olivocochlear efferents.
Thanks a lot Dr. Gordon. I totally agree with you, however is evident for me that OC
efferent system strongly regulates hair cell activity and cochlear sensitivity to sound.
You could argue a case for this from animal work. All I can say is having seen and tested thousands of ENT patients complaining of audiosensitivity, this was due to (or more precisely correlated with) stapedial reflex abnormalities of peripheral origin. It was not necessary to postulate any neurological or psychological component. There is no other clinical syndrome left to explain. If anyone disputes this, all they need to do is to cite a case of oversensitivity to sound due to proven lesion of the olivocochlear efferents where cochlear hypersensitisation, especially from cochlear pressure reduction, has been excluded. Incidentally, my explanation for the Wave 1 shortening involves a reversible physiological dysfunction of the cochlea, not a lesion.
Reduced Wave 1 latency occurs with prolonged contraceptive use (Contraception 1987;35:41). Findings consistent with Meniere spectrum disorder on the pill include a plugged pressure sensation in the ear, and sensitivity to noise. Features consistent with dehydration include patulous Eustachian tube
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