A photon entering the retina is absorbed by an 11-cis-retinal molecule bound to a protein called rhodopsin. This breaks a conjugated π bond in the retinal, allowing an isomerization to the all-trans form of retinal and subsequently a conformational change in the attached rhodopsin protein.
Rhodopsin then activates a G-protein, transducin, that activates a phosphodiesterase that hydrolyzes cGMP to GMP. Each step involves amplification: one active rhodopsin can activate many transducins which each activate multiple phosphodiesterase molecules, each of which can rapidly hydrolyze millions of cGMP molecules.
The decrease in cGMP levels causes the closure of cyclic-nucleotide-gated Na channels. The resting membrane potential, which is usually held at -40 by these channels, is then hyperpolarized towards the Nernst potential of K, which is approximately -70. These cells release NT constitutively, so this light-driven hyperpolarization leads to a decrease in chemical signaling to downstream cells.
Odorant molecules dissolve into the mucus in the dorsal posterior of the nasal cavity – hydrophobic compounds are bound by odorant-binding proteins to allow them to move in this aqueous/polar environment. There they come into contact with "cilia", or small, dendrite-like protuberances from odorant receptor neurons (ORNs).
These cilia express odorant receptor proteins – one or a small number per ORN – which non-covalently interact with the odorant molecules. Though these receptors are heterogeneous, they all activate a G-protein that activates adenylate cyclase, elevating cAMP levels and so activating a cAMP-gated Ca channel.
This is where the Kandel story stops, but recent work has indicated a further step: the influx of calcium opens a Ca-senstive chloride channel, leading to chloride efflux and so depolarization above threshold due to the unique chemical environs of the nasal mucus.
The least is known about the molecular mechanism of taste transduction. This is in part due to the system's complexity: each of the five tastes has a different chemical basis. Sweet, umami, and bitter use GPCRs, though the latter is a monomer of a different gene family than the heterodimers of the former two. Salty and sour are less understood, but the two competing hypotheses for both are the same: either direct influx of tastant molecules or ligand-gated ion channels (by Na for salty, H+ for sour).
†Note that we know the most about the visual system. I suspect that this is because man is a visual animal and so thinks visually and understands perception primarily through visual metaphors. Freud would have a lot to say about the relative primitiveness of our understanding of taste and smell and what that says about the neuroses and psychodynamics of scientists, but that's for another time.
- Kandel & Schwartz 5e, Phototransduction Links the Absorption of a Photon to a Change in Membrane Conductance, pp 582 - 3. (All you need to know)
- http://sites.sinauer.com/neuroscience5e/animations11.02.html - A nice animation that narrates and visualizes all of this information.
- Freud, S. 1929. Civilization and Its Discontents, pp. 19-20. URL. (For the footnote)
Kandel & Schwartz 5e, A Large Number of Olfactory Receptor Proteins Initiate the Sense of Smell, pp 714-5. (The basic story)
Su, C.-Y., Menuz, K., & Carlson, J. R. (2009). Olfactory Perception: Receptors, Cells, and Circuits. Cell, 139(1), 45–59. URL. (The last part about the role of Cl)
- Kandel & Schwartz 5e, Each Taste Is Detected by a Distinct Sensory Transduction Mechanism and Distinct Population of Taste Cells, pp 728-32.