Projections from the medial geniculate body to primary auditory cortex in neonatally deafened cats

Abstract

In the present study, anatomical projections from the medial geniculate body (MGB) to primary auditory cortex (AI) were investigated in normal adult cats and in animals that were neonatally deafened with the ototoxic drug amikacin. Cochleotopic/tonotopic maps in AI (based on neural response characteristic frequency) were obtained with microelectrode recording techniques, and single or multiple injections of retrograde tracers (horseradish peroxidase and fluorescent dyes) were introduced into AI. The AI maps of the amikacin-treated cats had an abnormal cochleotopic organization, such that deprived cortical areas exhibited an expanded representation of intact regions of the damaged cochlea. However, retrograde tracer injections into different regions of AI produced a normal pattern of labeling in the ventral division of the medial geniculate body (MGBv). In both experimental and control animals, the main mass of labeled thalamic cells was found in the MGBv. Different isofrequency contours in AI receive input from different portions of the MGBv. Thus, cell arrays labeled by anterior AI injections were situated medially in MGBv, and injections into posterior AI labeled MGBv more laterally. Furthermore, the deafened cats did not develop a more divergent thalamocortical projection compared with normal control animals, indicating that an abnormal spread of the thalamocortical afferents across the frequency domain in AI (anterior-posterior axis) is not responsible for the altered cochleotopic map in these neonatally deafened animals. The relatively normal thalamocortical projection pattern suggests that, after neonatal cochlear lesions, the major reorganization of cochleotopic maps occurs at subthalamic levels.

Two thalamic pathways to primary auditory cortex

“…The dorso-ventral and rostral-caudal extent of the present labeling corresponds to that described previously (Andersen et al, 1980;Middlebrooks and Zook, 1983;Rodrigues-Dagaeff et al, 1989). Other studies found that input from MGBv to central AI was highly convergent, arising from over 3 mm in the MGBv dorso-ventral axis (Middlebrooks and Zook, 1983;Morel and Imig, 1987;Stanton and Harrison, 2000). These prior reports may have given the impression that the convergent input from superior and inferior parts of MGBv was similar.…”

Consequences of unilateral hearing loss: Cortical adjustment to unilateral deprivation

“…It implies simply that the auditory system contralateral to CA can still be driven, and that thalamocortical projections are intact and functional after CA (Stanton and Harrison, 2000). Nor do our findings of decreased activity in auditory cortex contralateral to CHL suggest an irretrievable loss of cortical function.…”

A morphometric analysis of auditory brain regions in congenitally deaf adults

“…However, it is unclear whether auditory deprivation from birth results in degeneration of primary auditory cortex in either animals or humans. The pattern of subcortical projections to primary auditory cortex in congenitally deaf cats is similar to that of normally hearing cats (4,5), suggesting that cortical auditory regions may continue to receive input from subcortical regions and might not exhibit degeneration. However, functional deficits are observed in synaptic activity and organization within auditory cortex (6), suggesting the possibility of variation in the structure of auditory cortex as a consequence of congenital deafness.…”