Cranial Nerves and Taste Buds

Study Notes

The glossopharyngeal nerve connects to taste buds in the posterior two-thirds of the tongue.
The vagus nerve connects to taste buds in the extreme posterior of the tongue, which are more sensitive to noxious stimuli like bitterness.
Axons from the three cranial nerves carrying taste information travel to the medulla.
The primary gustatory cortex, located near the inferior margin of the post-central gyrus, is responsible for our sensations of taste.

Olfactory receptor neurons are incorporated into a limited region of the nasal epithelium in the superior nasal cavity.
The olfactory epithelium contains bipolar sensory neurons with dendrites extending from the apical surface of the epithelium into the mucus lining the nasal cavity.
Odorant molecules bind to proteins that keep them dissolved in the mucus and help transport them to the olfactory dendrites.
The odorant-protein complex binds to a receptor protein on the membrane of the olfactory cell.
Each cilia may have as many as 40 specific receptor membrane proteins for interaction with different odorant molecules.
Rapid adaptation and removal of the odorants permit continued recognition and discrimination of new aromas.
Action potentials generated in the axon terminals of activated neurons are propagated into the glomeruli within the olfactory bulb.
The axons of the olfactory neurons extend into the olfactory bulb located on the ventral surface of the frontal lobe.
Smell is the one sensory modality that does not require a synaptic connection in the thalamus before connecting to the cerebral cortex.

The efferent nervous system can be divided into two functional parts: the somatic nervous system and the autonomic nervous system.
The major differences between the two systems are evident in the responses that each produces.
The somatic nervous system causes contraction of skeletal muscles.

Light reduces cGMP, causing the Na channels to close, and the membrane potential becomes more negative.
The hyperpolarizing response to light is initiated by the absorption of electromagnetic radiation by the photopigment in the membrane of the stacked disks in the rod outer segments.
Rhodopsin can be thought of as a receptor protein with a prebound chemical agonist.
The bleaching of rhodopsin stimulates a G-protein called transducin in the disk membrane, which in turn activates the effector enzyme phosphodiesterase (PDE), which breaks down the cGMP that is normally present.

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