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Hear Res. 2002 Oct;172(1-2):14-7.
CGRP- and cholinergic-containing fibers project to guinea pig outer hair cells.

Cabanillas LA, Luebke AE.

Department of Otolaryngology, University of Miami School of Medicine, 1600 NW 10th Avenue, RMSB 3160, Miami, FL 33136, USA.

MU33, an antibody to calcitonin gene-related peptide (CGRP), was used to investigate the magnitude of CGRP-containing nerve fiber endings, compared to acetylcholinesterase (AChE)-containing nerve fiber endings on outer hair cells (OHCs). Results showed that CGRP-containing nerve fiber immunoreactivity mimicked the AChE fiber OHC staining pattern across the cochlea suggesting that CGRP can function as both a medial efferent (contacting primarily OHCs) and as a lateral efferent (contacting primarily inner hair cell afferents) neurotransmitter.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12361863&dopt=Abstract

J Comp Neurol. 2003 Jan 13;455(3):406-16.
Olivocochlear innervation in the mouse: immunocytochemical maps, crossed versus uncrossed contributions, and transmitter colocalization.

Maison SF, Adams JC, Liberman MC.

Department of Otology and Laryngology, Harvard Medical School and Eaton-Peabody Laboratory, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts 02114-3096, USA. sfpl.meei.harvard.edu

To further understand the roles and origins of gamma-aminobutyric acid (GABA) and calcitonin gene-related peptide (CGRP) in the efferent innervation of the cochlea, we first produced in the mouse an immunocytochemical map of the efferent terminals that contain acetylcholine (ACh), CGRP, and GABA. Olivocochlear (OC) terminals in inner and outer hair cell (IHC and OHC) regions were analyzed quantitatively along the cochlear spiral via light-microscopic observation of cochlear wholemounts immunostained with antibodies to glutamic acid decarboxylase (GAD), vesicular acetylcholine transporter (VAT), or the peptide CGRP. Further immunochemical characterization was performed in mice with chronic OC transection at the floor of the fourth ventricle to distinguish crossed from uncrossed contributions and, indirectly, the contributions of lateral versus medial components of the OC system. The results in mouse showed that (1) there are prominent GABAergic, cholinergic, and CGRPergic innervations in the OHC and IHC regions, (2) GABA and CGRP are extensively colocalized with ACh in all OC terminals in the IHC and OHC areas, (3) the longitudinal gradient of OC innervation peaks roughly at the 10-kHz region in the OHC area and is more uniform along the cochlear spiral in the IHC area, (4) in contrast to other mammalian species there is no radial gradient of OC innervation of the OHCs, and (5) all OHC efferent terminals arise from the medial OC system and terminals in the IHC area arise from the lateral OC system. 2002 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12483691&dopt=Abstract

nifty.ne.jp

A theoretical consideration is given on how the constituent cells of the cochlear partition can amplify its motion and increase its momentum without resorting to external forces, and it leads to a micromechanical model that explains the role of the cells in the active amplification. The triangle composed of the outer hair cell, the phalanx of Deiters cell and the reticular lamina forms a mechanical unit that stores up and releases strain. When outer hair cells contract in a region along the cochlear partition, strain accumulates in the triangle causing deformation of the region that pushes down the basilar membrane, and hence it appears as a transverse pressure that drives the basilar membrane. The momentum of the region increases at the cost of the momentum of neighboring regions, and the total momentum of the cochlear partition is not altered by the internal forces generated by the outer hair cells. The model can produce a frequency-response curve that compares favorably with experimental data.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12361866&dopt=Abstract

Hear Res. 2002 Oct;172(1-2):81-6.
Rescue of auditory hair cells from aminoglycoside toxicity by Clostridium difficile toxin B, an inhibitor of the small GTPases Rho/Rac/Cdc42.

Bodmer D, Brors D, Pak K, Gloddek B, Ryan A.

Department of Surgery, Division of Otolaryngology, UCSD School of Medicine and VA Medical Center, 9500 Gilman Drive #0666, La Jolla, CA 92093, USA.

The hair cells (HCs) are the most vulnerable elements in the cochlea and damage to them is the most common cause of sensorineural hearing loss. Understanding the intracellular events that lead to the death of HCs is a key to developing protective strategies. Recently, it has been shown that the c-Jun-N-terminal kinase (JNK) pathway is activated in HCs in response to aminoglycosides (J. Neurosci. 20 (2000) 43). We have studied the upstream events leading to JNK activation in aminoglycoside toxicity in vitro. The small GTPases Rac and Cdc42 are well known upstream activators of JNK in other cell types. Clostridium difficile toxin B monoglucosylates all members of the Rho GTPase subfamily (Rho, Rac and Cdc42 isoforms) and inhibits GTP binding by steric interference (Nature 341 (1989) 209). Organ of Corti explants from p5 rat basal turns were maintained in tissue culture and treated with C. difficile toxin B for 12 h. They were then treated with toxin B plus gentamicin for 72 h. Significantly less HC death was observed compared to with gentamicin alone. Toxin B alone had no effect on HCs at the highest concentration used. Using antibodies against phospho-c-Jun, we observed background immunoreactivity in control explants, strong staining of outer hair cell nuclei in gentamicin treated explants, and weaker immunostaining in explants treated with gentamicin and C. difficile toxin B. We conclude that Rho family small GTPases play a role in aminoglycoside toxicity signaling as upstream activators of the JNK signaling pathway.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12361869&dopt=Abstract

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