Smell & Taste

No. A chemical changes what a sensory cell does. Ion movement changes its voltage, and electrical or chemical communication carries the information onward.

Odorants reach mucus around olfactory cilia. Dissolved tastants reach exposed tips of taste cells. Arrival is transport outside the cell, not yet an action potential. The stimulating molecule does not travel along the axon as the message.

A receptor protein is not the same thing as a whole sensory receptor cell. A receptor potential is a graded change in membrane voltage. An action potential is a regenerative electrical event. A transmitter is a chemical carrying information across a cell-to-cell contact. Keeping these levels separate makes the rest of the course easier.

Both olfactory neurons and several types of taste cell can generate electrical spikes. The important architectural difference is that the olfactory neuron has its own axon, whereas the taste epithelial cell communicates with a different sensory neuron.

Keep this boundary: A brighter stimulus symbol is not a measured voltage or a guarantee of stronger conscious perception.

Evidence: The Olfactory System, Introduction to Behavioral Neuroscience §8.3 · The Gustatory System, Introduction to Behavioral Neuroscience §8.2

A receptor activates an intracellular messenger pathway. cAMP opens channels, allowing positive ions to enter the cilium and change the neuron’s electrical state.

The receptor is a G-protein-coupled receptor. Its outside-facing stimulus interaction and its cytoplasmic signaling partners are on different sides of one membrane. AC3 produces cAMP inside the cell; cAMP acts on the intracellular face of CNG channels.

Under the relevant physiological conditions, inward sodium and calcium current through CNG channels helps depolarize the cilium. The graded receptor potential is not a spike located at the receptor protein. It changes neuronal excitability, and voltage-gated channels support propagated electrical output in the neuron.

Mouse loss-of-function studies of G_olf and AC3, together with channel experiments, support different links in this chain. They are converging experimental approaches, not one microscopic image proving every arrow or a genetic experiment performed in a person.

Keep this boundary: The illustrated membrane shapes locate a conceptual signaling interface; their colours or folds do not identify experimentally resolved OR, AC3 or CNG proteins.

Evidence: The Olfactory System, Introduction to Behavioral Neuroscience §8.3 · A cyclic nucleotide-gated conductance in olfactory receptor cilia · Mice deficient in G(olf) are anosmic · Disruption of the type III adenylyl cyclase gene leads to peripheral and behavioral anosmia in transgenic mice · The Ca2+-activated Cl− channel TMEM16B shapes the response time course of olfactory sensory neurons

In olfactory cilia, opening ANO2/TMEM16B can let negatively charged chloride leave. Loss of negative charge can reinforce depolarization, but a larger receptor current does not always mean more spikes.

The effect of a channel depends on the ion gradients and membrane voltage, not just the ion’s name. In this ciliary context, chloride can move out. That is electrically different from the familiar inhibitory chloride entry described in some other neurons.

A 2024 mouse study found that removing TMEM16B could permit better repeated spike firing despite a smaller receptor current. Amplification of receptor current, spike timing and conscious smell strength are therefore not interchangeable quantities.

Response termination is the subsiding of signaling and ion changes. Peripheral adaptation is altered responsiveness during sustained or repeated input. Central habituation concerns later processing. Calcium-dependent feedback and extrusion, including NCKX4 evidence from mice, interact with cAMP metabolism; no single universal reset switch explains every condition.

The NCKX4 source was available at abstract level for this review, so the course does not claim verified exchanger stoichiometry or detailed human kinetics. Human imaging supports a separate central processing level, not one universal time at which every familiar smell fades.

Keep this boundary: A smell fading from notice does not establish that the air is safe. No measured current gain, response duration or conscious intensity is encoded in the illustration.

Evidence: The Ca2+-activated Cl− channel TMEM16B shapes the response time course of olfactory sensory neurons · The Na+/Ca2+ exchanger NCKX4 governs termination and adaptation of the mammalian olfactory response · Olfactory CNG channel desensitization by Ca2+/CaM via the B1b subunit affects response termination but not sensitivity to recurring stimulation · Phosphodiesterase 1C is dispensable for rapid response termination of olfactory sensory neurons · Time course of odorant-induced activation in the human primary olfactory cortex

For sweet, bitter and umami pathways, intracellular calcium helps excite a taste cell. ATP released through CALHM1/3 channels then signals to a separate sensory nerve ending.

Sweet commonly uses T1R2/T1R3, umami uses T1R1/T1R3, and bitter uses members of the T2R family. Distinct receptor populations can share downstream machinery. A representative Type II cell does not mean all these receptor identities are mixed in every taste cell. Human receptors have been studied in expression systems, while much intact-cell causal evidence comes from mice.

PLCβ2 acts at the cytoplasmic membrane face and generates IP3 from membrane phosphoinositide. IP3 remains within the cytoplasm and opens a calcium-release channel in the ER membrane. Calcium leaves the internal ER store for cytoplasm, not from extracellular fluid directly through TRPM5.

TRPM5 is a monovalent-cation channel, not the calcium-release pore. Mouse evidence also implicates TRPM4, so TRPM5 is not presented as the only depolarizing conductance in every species. Electrical excitation in the taste cell and excitation in the nerve ending are distinct events.

CALHM1/3 forms an ATP-release pathway at the Type II cell’s channel synapse. ATP crosses into the extracellular contact space and activates purinergic receptors in the afferent membrane. The CALHM1 primary experiments help separate a cell’s own stimulus response from successful transmitter output. Type II ATP is not packaged into the conventional synaptic vesicles depicted in the sour comparison.

Keep this boundary: The diagram represents one mechanism-specific epithelial cell and a separate afferent, not a retrospectively identified cell in the old taste-bud artwork or an exact molecular structure.

Evidence: Human receptors for sweet and umami taste · T2Rs function as bitter taste receptors · Coding of sweet, bitter, and umami tastes: different receptor cells sharing similar signaling pathways · TRPM4 and TRPM5 are both required for normal signaling in taste receptor cells · CALHM3 is essential for rapid ion channel-mediated purinergic neurotransmission of GPCR-mediated tastes · CALHM1 ion channel mediates purinergic neurotransmission of sweet, bitter and umami tastes · ATP signaling is crucial for communication from taste buds to gustatory nerves · Taste transduction and channel synapses in taste buds

Protons enter through OTOP1 and help excite sour-responsive taste cells. Their conventional synaptic machinery is supported, but the source and release mechanism of the ATP needed for sour afferent signaling are not fully established.

The representative sour-responsive cell is Type III. OTOP1 carries protons rather than starting the same GPCR–IP3 chain described for Type II cells. Mouse knockout studies strongly weaken gustatory acid responses but do not remove every neural response to acid or every non-taste avoidance behavior.

Apical sensing and basal output are separate locations. Type III cells have conventional synaptic machinery and can release serotonin, but serotonin is not presented as the sole completely solved route to afferent firing. P2X-dependent afferent signaling does not itself identify where the required ATP comes from.

The 2025 SNAP25 study links conventional synaptic machinery with sour responses and Type III cell maintenance. It does not prove ATP-filled synaptic vesicles; that proposal requires further testing. The image therefore shows a vesicle-containing output context without naming its visible cargo as ATP.

Recent mouse localization also finds OTOP1 in Type I cells. OTOP1 positivity alone is not a sufficient cell-identity rule, and the colours of an old generated taste-bud illustration cannot identify Type III cells.

Keep this boundary: Uncertainty is part of this pathway, not a missing arrow to invent. Do not infer a solved Type III CALHM route, ATP vesicle or serotonin-to-P2X connection.

Evidence: ATP signaling is crucial for communication from taste buds to gustatory nerves · An evolutionarily conserved gene family encodes proton-selective ion channels · Cellular and neural responses to sour stimuli require the proton channel Otop1 · The K+ channel KIR2.1 functions in tandem with proton influx to mediate sour taste transduction · Dual functions of SNAP25 in mouse taste buds · Epitope tagging with genome editing in mice reveals that the proton channel OTOP1 is apically localized and not restricted to Type III sour taste receptor cells · Sour taste: receptors, cells and circuits · The enigma of type III taste bud cells

An olfactory sensory neuron carries its output along its own axon. A taste epithelial cell communicates across a contact with a different neuron, even though the taste cell can itself fire electrical spikes.

The key comparison is cell architecture, not “electrical versus non-electrical.” Taste cells can be electrically excitable without being neurons whose own axons form the cranial nerves. The receptor cell’s response and the receiving afferent’s response must remain distinguishable.

In the olfactory cascade, ATP is used inside the cell to make cAMP. In Type II taste output, ATP outside the cell is a transmitter. The same molecule can have different jobs in different compartments.

Mouse ENaC contributes to an amiloride-sensitive low-sodium pathway, while other salt responses remain. Human studies are variable and the molecular account is less settled. A neat set of five equally complete cartoons would hide this difference in certainty, so human salt is kept in an explicitly bounded evidence box.

A useful final test is to ask which stage an observation measures: chemical arrival, receptor-cell current, cellular spikes, transmitter release, afferent activity or conscious experience. Evidence at one stage does not automatically measure every later stage.

Keep this boundary: Animal loss-of-function experiments offer causal evidence but do not remove species differences. No tasting protocol, drug concentration or health inference is provided.

Evidence: The Gustatory System, Introduction to Behavioral Neuroscience §8.2 · CALHM1 ion channel mediates purinergic neurotransmission of sweet, bitter and umami tastes · ATP signaling is crucial for communication from taste buds to gustatory nerves · Human psychophysical studies of saltiness suppression by amiloride · The cells and peripheral representation of sodium taste in mice · Taste transduction and channel synapses in taste buds · Does ENaC work as sodium taste receptor in humans? · Receptors and signaling for sour and salty: the ionic taste qualities