RESPONSES OF INFERIOR COLLICULUS NEURONS IN C57BL 6J MICE WITH AND WITHOUT SENSORINEURAL HEARING-LOSS - EFFECTS OF CHANGING THE AZIMUTHAL LOCATION OF AN UNMASKED PURE-TONE STIMULUS/
Sl. Mcfadden et Jf. Willott, RESPONSES OF INFERIOR COLLICULUS NEURONS IN C57BL 6J MICE WITH AND WITHOUT SENSORINEURAL HEARING-LOSS - EFFECTS OF CHANGING THE AZIMUTHAL LOCATION OF AN UNMASKED PURE-TONE STIMULUS/, Hearing research, 78(2), 1994, pp. 115-131
Azimuth functions (discharge rates evoked by tone bursts as a function
of stimulus azimuth) were obtained from neurons in the inferior colli
culus (IC) of C57 mice aged 2, 7 and 12 months. Because of a gene that
affects the cochlea, C57 mice exhibit high-frequency sensorineural he
aring loss at 7 and 12 months. Azimuth functions were examined for dif
ferences that might be related to the decline in localization acuity t
hat accompanies hearing loss in this strain. Irrespective of age group
, nearly all neurons in the central area of the IC were sensitive to t
he azimuth of a best frequency (BF) stimulus, as revealed by azimuth f
unctions in which firing rates varied by more than 50% from maximum to
minimum at one or more intensities. The age groups were similar in ma
ny respects (e.g., there were no significant differences in the propor
tion of functions meeting the criterion for direction sensitivity, the
proportion of neurons with direction sensitive functions over a range
of intensities, azimuth function shapes, the locations or stability o
f 'borders' separating angles evoking high versus low discharge rates)
. However, in 7- and 12-month-olds: the proportion of IC neurons in wh
ich the strongest excitatory driving was evoked by ipsilateral stimula
tion was significantly larger; azimuth function borders were more like
ly to be 'reversed' (i.e., the high rates being evoked by the more ips
ilateral angle); and a greater proportion of azimuth functions met the
criterion for direction sensitivity only minimally. The findings sugg
est that binaural excitatory-inhibitory interactions are altered in IC
neurons of hearing-impaired mice.