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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    European archives of oto-rhino-laryngology and head & neck 246 (1989), S. 417-422 
    ISSN: 1434-4726
    Keywords: Hearing loss ; Cochlea ; Outer hair cells ; GABA receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The olivocochlear innervation has been postulated to regulate active mechanical processes in the mammalian cochlea. Histochemical studies led to the suggestion that a subpopulation of these efferent nerves, which predominantly terminate on outer hair cells (OHCs), are γ-aminobutyric acid (GABA)-ergic. By means of two monoclonal antibodies, we were able to visualize GABAA-receptor immunoreactivity at the basal pole of isolated sensory cells. Both subunits of the GABAA receptor, the α- and β-subunit, are known to form the transmembraneous GABA/ benzodiazepine-receptor complex and were present on OHCs. In addition, these inhibitory receptors were more numerous in the apical turns of the cochlea, indicating another criterion for distinguishing the apical from basal turns of the cochlea. These results support the concept that a subpopulation of axosomatic synapses at the basal pole of OHCs liberate the inhibitory neurotransmitter GABA into the synaptic cleft. Binding of the transmitter to these newly observed subsynaptic receptors is possibly followed by a change in OHC motility and a subsequent modulation of the movement of the basilar membrane.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European archives of oto-rhino-laryngology and head & neck 250 (1993), S. 351-357 
    ISSN: 1434-4726
    Keywords: Cochlea ; Efferent innervation ; Cochlear amplifier ; Olivocochlear bundle ; Hearing loss
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary There is evidence that the inhibitory neurotransmitter γ-aminobutyric acid (GABA) is released from some efferent olivocochlear nerve endings terminating at outer hair cells (OHCs). Using monoclonal antibodies against postsynaptic GABAA receptor from bovine cerebral cortex we confirm the presence of GABA and benzodiazepine bindings sites of α- and β-subunits of GABAA receptors at the basal pole of isolated OHCs. Whole-cell recording with viable OHCs revealed that the application of 10−3–10−8 M GABA to the cell surface was followed by a concentration-dependent hyperpolarization of the outer cell membrane. Hyperpolarization was increased in the presence of 2.5 × 10−5 M chlorazepate, a benzodiazepine derivative. Electrophysiological effects caused by GABA alone or in combination with chlorazepate were specifically inhibited by 10−6 M of the GABA-receptor antagonist picrotoxin. Moreover, 10−5–10−7 M GABA caused reversible slow elongation of the cylindrical hair cell body in OHCs examined. These neurotransmitter-induced motile responses were specifically blocked by 10−4 M picrotoxin. The results suggest that a subpopulation of OHCs express α- and β-subunits of GABAA receptors which both form a GABA/benzodiazepine-receptor complex at the basal pole of isolated OHCs. These receptors are thought to allow GABA which is released from efferent auditory nerve terminals to bind to the cell surface of OHCs, resulting in GABAAreceptor activation. This probably gates a GABAA-receptor-associated chloride channel in the postsynaptic OHC membrane, allowing hyperpolarization and elongation of the cell.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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