Prestin is the motor protein of cochlear outer hair cells (OHCs). It is able to perform rapid and reciprocal electromechanical conversion that underlies OHC electromotility. Due to the inadequate size of a single pr...
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Prestin is the motor protein of cochlear outer hair cells (OHCs). It is able to perform rapid and reciprocal electromechanical conversion that underlies OHC electromotility. Due to the inadequate size of a single prestin molecule to form the2 nm intramembraneous protein particles (IMPs) in the OHC lateral membrane (LM), the possibility of prestin oligomerization has been proposed. It has been suggested that prestin molecules form highorder oligomers, most likely as the tetramer, in heterologous systems. In OHCs, however, the oligomeric structure of prestin remains unclear. Here we calculated the prestin-related charge density in both gerbil and guinea pig OHCs through measuring their nonlinear capacitance (NLC) and LM surface area, showing that the average charge density (22, 608 μm-2 in gerbils; 19, 460 μm-2 in guinea pigs) is statistically 4 times the average density of IMPs (5,686 μm-2 in gerbils; 5, 000 μm-2 in guinea pigs). This suggests that each IMP contains four prestin molecules based upon the notion that each prestin transfers a single elementary charge, implying that prestin forms tetramers in OHCs. To determine whether the prestin tetramer functions as a mechanical unit, we subsequently compared the slope factors (α) of electromotility and NLC simultaneously measured from the same OHC, showing that the α values of the two are statistically the same. This suggests that each prestin molecule in the tetramer is mechanically independent and equally contributes to OHC electromotility.
In most publications,animal models of diabetes have mainly been investigated for their multiple etiologies as well as for changes leading to diabetes and their genetic *** which seem important and need a special resea...
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In most publications,animal models of diabetes have mainly been investigated for their multiple etiologies as well as for changes leading to diabetes and their genetic *** which seem important and need a special research endeavor are the mechanism of the causes of diabetes and the lapse into complications in different species,their molecular basis and possible arrest and prevention.A concise list and and short discussion of the intensively studied rodents is present ed of spontaneous or nutritional background causing Type 2 diabetes but omitting diabetes evoked by transg enic manipulations or gene knockout techniques.
The etiology of sudden deafness or idiopathic sudden sensorineural hearing loss(ISSHL) remains unclear. Over the past 15 years, we have investigated the mechanisms of ischemic-induced hearing loss using a gerbil model...
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The etiology of sudden deafness or idiopathic sudden sensorineural hearing loss(ISSHL) remains unclear. Over the past 15 years, we have investigated the mechanisms of ischemic-induced hearing loss using a gerbil model of transient cochlear ischemia. In the gerbil, cochlear ischemia can be induced by occluding the bilateral vertebral arteries simultaneously at the neck, because the posterior communicating arteries of the Circle of Willis close spontaneously around 1 mo after birth. When 15 min ischemia was loaded on this animal, permanent hearing loss of about 25 d B and the death of hair cells, especially inner hair cells were induced. These pathological changes were mainly due to lack of an energy source, glutamate excitotoxicity, and the production of free radicals, especially superoxide and nitrous oxide species. Ischemic damage could be prevented by various procedures, such as cooling the cochlea, intratympanic administration of insulin-like growth factor 1 or AM-111(an anti-apoptotic agent), and systemic administration of prednisolone(steroid), edarabone(free radical scavenger), ginsenoside Rb1(Kanpo), hematopoietic stem cells, glia-cell derived neurotrophic factor, and liposome-encapsulated hemoglobin(artificial red blood cells). We also found that the cochlea was protected by the ischemic tolerance, indi-cating that minor cochlear ischemia alleviates or prevents inner ear damage in subsequent severe cochlear ischemia. As ISSHL usually occurs suddenly, with no preceding sign or symptom, we suggest that most ISSHL cases are caused by circulatory disturbance, probably at the stria vascularis.
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