Auditory: Mechanical basilar membrane displacement in the cochlea opens mechanoelectrical transduction channels in hair cells, allowing an influx of potassium (K+) mediated current. This leads to the downstream neural pathways for hearing. Amplification of this signal across the entire hearing range occurs as a result of one specific subset of these hair cells, the outer hair cells. In response to the transmembrane receptor potential, outer hair cells actively oscillate at the frequency of the incoming sound, in a process called electromotility. It is believed that these voltage-dependent cell vibrations are dependent upon a protein called prestin that is expressed highly in the lateral plasma membrane of the outer hair cells. This is supported based on Liberman et al’s homozygous gene disruption paradigm in mice that led to a greater than 100 fold loss of auditory sensitivity. Its mechanism seems to mediate the electroneutral exchange of two anions across the plasma membrane, chlorine (Cl -) and carbonate (CO2 -3), which causes a direct voltage to displacement conversion. The unique morphology of the outer hair cells allows them to operate at frequencies higher than 50 kHz if properly stimulated. This amplification via outer hair cells only occurs in mammals and allows for improved frequency selectivity, which is necessary for the complexities of human speech!
Olfactory: The mucous epithelial layer of the nose contains olfactory receptor neurons, each of which has 8-20 whip-like cilia that are each 30-200 microns long, and are where molecular reception of the odor commences. The incoming odor stimulates the transmembrane protein andenylate cyclase which catalyzes the conversion of ATP to 3′,5′-cyclic AMP (cAMP). cAMP is directly connected to an ion channel, allowing an influx of cations (primarily calcium) that depolarize the cell. The influx of calcium leads to an opening of calcium-dependent chloride channels. The chloride conductance is the amplification step and accounts for 80-90% of the odorant-induced depolarizing current, in sigmoidal fashion. Lowe and Gold (1993) had a classic study showing the effects of this. Using a newt olfactory receptor cell, they used flash photolysis of caged cAMP to simulate an upstream odor reception and analyzed the chloride influx. In addition to varying the intensity of the light source to uncage varying amounts of cAMP, and measuring the chloride amplitude, the researchers also used a condition with 5 millimoles of a chloride channel blocker, SITS. Here’s their figure 3D. The normal condition shows a sigmoidal amplification curve (black circles), and the SITS condition of open circles has no such amplification:
Inspired by CalTech’s Question #6 for cognitive scientists: “Every sensory system relies on receptor cells that transduce a stimulus into an electrical signal. This clearly requires some significant amplification. Describe two different sensory receptor cells, with attention to the location(s) and the mechanism(s) of this amplification.”
Liberman MC, et al. 2002 Prestin is required for electromotility of the outer hair cell and for the cochlear amplifier. doi:10.1038/nature01059.
Mistrik P, et al. 2009 Three-dimensional current flow in a large-scale model of the cochlea and the mechanism of amplification of sound. doi: 10.1098/rsif.2008.0201.
Stephan AB, et al. 2009 ANO2 is the cilial calcium-activated chloride channel that may mediate olfactory amplification. doi: 10.1073/pnas.0903304106.
Lowe G and Gold GH. 1993 Nonlinear amplification by calcium-dependent chloride channels in olfactory receptor cells. doi:10.1038/366283a0