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Aging is accompanied by the deterioration of hearing that complicates our understanding of speech, especially in noisy environments. This deficit is partially caused by the loss of hair cells as well as by the dysfunction of the stria vascularis. However, the central part of the auditory system is also affected by processes accompanying aging that may run independently of those affecting peripheral receptors. Here, we review major changes occurring in the central part of the auditory system during aging. Most of the information that is focused on age-related changes in the central auditory system of experimental animals arises from experiments using immunocytochemical targeting on changes in the glutamic-acid-decarboxylase, parvalbumin, calbindin and calretinin. These data are accompanied by information about age-related changes in the number of neurons as well as about changes in the behavior of experimental animals. Aging is in principle accompanied by atrophy of the gray as well as white matter, resulting in the enlargement of the cerebrospinal fluid space. The human auditory cortex suffers not only from atrophy but also from changes in the content of some metabolites in the aged brain, as shown by magnetic resonance spectroscopy. In addition to this, functional magnetic resonance imaging reveals differences between activation of the central auditory system in the young and old brain. Altogether, the information reviewed in this article speaks in favor of specific age-related changes in the central auditory system that occur mostly independently of the changes in the inner ear and that form the basis of the central presbycusis.

To cite this version:Ladislav Ouda, Rastislav Druga, Josef Syka. Changes in parvalbumin immunoreactivity with aging in the central auditory system of the rat. Experimental Gerontology, Elsevier, 2008, 43 (8)

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SMI-32 antibody recognizes a non-phosphorylated epitope of neurofilament proteins, which are thought to be necessary for the maintenance of large neurons with highly myelinated processes. We investigated the distribution and quantity of SMI-32-immunoreactive(-ir) neurons in individual parts of the rat auditory system. SMI-32-ir neurons were present in all auditory structures; however, in most regions they constituted only a minority of all neurons (10-30%). In the cochlear nuclei, a higher occurrence of SMI-32-ir neurons was found in the ventral cochlear nucleus. Within the superior olivary complex, SMI-32-ir cells were particularly abundant in the medial nucleus of the trapezoid body (MNTB), the only auditory region where SMI-32-ir neurons constituted an absolute majority of all neurons. In the inferior colliculus, a region with the highest total number of neurons among the rat auditory subcortical structures, the percentage of SMI-32-ir cells was, in contrast to the MNTB, very low. In the medial geniculate body, SMI-32-ir neurons were prevalent in the ventral division. At the cortical level, SMI-32-ir neurons were found mainly in layers III, V and VI. Within the auditory cortex, it was possible to distinguish the Te1, Te2 and Te3 areas on the basis of the variable numerical density and volumes of SMI-32-ir neurons, especially when the pyramidal cells of layer V were taken into account. SMI-32-ir neurons apparently form a representative subpopulation of neurons in all parts of the rat central auditory system and may belong to both the inhibitory and excitatory systems, depending on the particular brain region.

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The inferior colliculus (IC) plays a strategic role in the central auditory system in relaying and processing acoustical information, and therefore its age-related changes may significantly influence the quality of the auditory function. A very complex processing of acoustical stimuli occurs in the IC, as supported also by the fact that the rat IC contains more neurons than all other subcortical auditory structures combined. GABAergic neurons, which predominantly co-express parvalbumin (PV), are present in the central nucleus of the IC in large numbers and to a lesser extent in the dorsal and external/lateral cortices of the IC. On the other hand, calbindin (CB) and calretinin (CR) are prevalent in the dorsal and external cortices of the IC, with only a few positive neurons in the central nucleus. The relationship between CB and CR expression in the IC and any neurotransmitter system has not yet been well established, but the distribution and morphology of the immunoreactive neurons suggest that they are at least partially non-GABAergic cells. The expression of glutamate decarboxylase (GAD) (a key enzyme for GABA synthesis) and calcium binding proteins (CBPs) in the IC of rats undergoes pronounced changes with aging that involve mostly a decline in protein expression and a decline in the number of immunoreactive neurons. Similar age-related changes in GAD, CB, and CR expression are present in the IC of two rat strains with differently preserved inner ear function up to late senescence (Long-Evans and Fischer 344), which suggests that these changes do not depend exclusively on peripheral deafferentation but are, at least partially, of central origin. These changes may be associated with the age-related deterioration in the processing of the temporal parameters of acoustical stimuli, which is not correlated with hearing threshold shifts, and therefore may contribute to central presbycusis.