Name:

Zakaria Shenwari
Neurobiology 214, Fall 2022
Problem Set #3
Due Friday December 12 at noon. You can work on this with your fellow classmates, but
you must write your answers in your own words.
Please submit the answers in typewritten form



1. What is the known selectivity or function of each of the T1Rs and
how does activation of the T1R and T2R receptors lead to activation of afferent gustatory
neurons?

T1R and T2R are G protein couple receptors. The T1R consists of two subunits, T1R1 and T1R3,
which are receptors and functions as receptors for sweet and umami tastants. The T2R are
homodimer and are of many types that functions to detect bitter tastants.

The process of activation of afferent gustatory neurons is as follows:

- The tastants binds to GSPR
- G protein is activated
- By subunit activates specialized PLC (B2)
- PLC produces IP3
- IP3 releases Ca2+ from internal stores
- Ca2+ activates a Ca2+ gated Na+ channel causing depolarization
- Combination of CA2+ depolarization activates ATP channel causing ATP to be released
from the cell
- ATP binds to receptors on the gustatory afferent neuron causing a depolarization and
firing of APs

2. Explain how the transduction of sour tastants differs from salt tastants.

A common example of Salt (NaCl) activates the salty taste sensation. The Na+ ion from NaCl
enters through specialized Na+ channels and also opens the Ca that causes a depolarization. As
for sourness, it is the low acidity (low pH) caused by H+ ions that activates acidic sensing ion-
channel. The H+ ion, rather than Na+, enters the cell to depolarize. The H ion attaches to K
channels and block them further depolarizes the cell. The next steps are mostly the same for the
transduction of sourness and saltness. After depolarization, the graded potential causes Na and
Voltage-gated Calcium channels to open. Ca in turn causes the neurotransmitter release of
serotonin that activates a gustatory afferent neuron.

3. What are the molecular mechanisms that allow a specific odorant to initiate neuronal
 signaling in an olfactory receptive neuron?

When odorant molecule enters the nose, it encounters the olfactory epithelium, a layer of
tissue that contains the olfactory receptor neurons. The Odorant molecule binds to a
membrane odorant receptor protein. Each cell can respond to a variety of odors, but can
have odor preference.
Next, the receptor protein activates the G-olfactory protein. Adenylyl cyclase is activated
that stimulates synthesis of cAMP.
cAMP triggers Na+ and Ca2+ channels to open. Ca2+ influx activates the Ca channels
which allow the Cl ions to flow out of the cell, and cause depolarization in the membrane
that sends the signal from olfactory receptive neuron to olfactory bulb in the brain

4. What is the difference between fast- and slow-adapting mechanoreceptors? Give an

example of each and the type of stimuli they best respond to.

Fast-adapting Mechanoreceptors fires AP, at onset and offset of stimuli. The slow-adapting
mechanoreceptors respond to stimuli even after the it has been removed or remained constant.
An example of a fast-adapting mechanoreceptor is a Pacinian corpuscle, which is sensitive to
high-frequency vibrations or toa more forceful transient pressure. An example of a slow-adapting
mechanoreceptor is a Merkel cell, which is sensitive to sustained pressure on the skin and
respond to light pressure.

5. Explain the origin and effects of prostaglandins after a noxious stimulus. What is a
mechanism frequently used to counter the effects of prostaglandins?

Prostaglandins are chemicals derived from breakdown of lipid membranes produced in the brain
and other organs in response to noxious stimulus such as injury or inflammation by inducing pain
or fever. They increase greatly the sensitivity of nociceptors to other stimuli. Prostaglandins
attach to a GPCR nociceptor triggering a Gq protein, its subunit activating Phospholipase C, which
forms IP3 and DAG from the cleavage of PIP2. The DAG secondary messenger activates protein
kinase C, which then phosphorylates a nearby TRPV1 channel, allowing for it to be opened at
lower temperatures. When opened, Na+ and Ca2+ ions are allowed to pass through, depolarizing
the nociceptor and firing an AP that can travel down the pain pathway. The mechanism
frequently used to counter the effects of prostaglandins is anti-inflammation. The anti-
inflammatory drugs such as Aspirin from COAX inhibitors can be used to reduce the production of
prostaglandins and alleviate inflammation and pain.
 6. How do hair cells detect sound and transmit the information to the CNS?

Hair cells are mechanosensitive bundle composed of stereocilia , each of the stereocilium have
MET channels on top. The Hair cells encode, by the deflection of the hair bundle, the intensity
(magnitude) and Frequency (Rate) of the stimulus into APs in afferent neurons. After sound
vibrates the tympanic membrane in the form of waves, the ossicles, along with the tensor
tympani and stapedius muscles, amplify the waves through the oval window into the scala
tympani and perilymph, causing the basilar membrane to vibrate. The vibrations of the basilar
membrane cause the hair cells to open since they are mechanically gated by tip links at the
stereocilia. Because the endolymph is high in K+ concentration, the inside of the hair cell is
depolarized due to the endocochlear potential when the mechanically gated channels are
opened. This depolarization causes Ca2+ channels to open and, with the graded potential from
before, triggers the release of glutamate receptors into the ribbon synapse. In short, MET are
mechanically-gated channels that are depolarized. Next, Voltage-gated Calcium channels open.
Inward calcium ion flow. Calcium dependent vesicle is fused, and glutamate neurotransmitter is
released. This generates an AP electrical signal inside the auditory nerve that transmits the signal
to NS.

7. To test the neural circuitry of the leg, doctors tap the patellar tendon. Describe the
resulting tendon reflex.

Knee-jerk reflex is a Monosynaptic reflex that uses big, myelinated axon and a single synapse to
assess the proper functioning of a motor neuron. When the patellar tendon is tapped, it stretches
the quadriceps muscle. This stretch activates sensory receptors called muscle spindles. The
activation of the muscle spindles sends action potential signal through the sensory nerve fibers la
axon to the spinal cord (dorsal root).
In the spinal cord, the signal is quickly processed by interneurons. The interneurons (through
ventral root) then send a signal to the alpha motor neurons, which are neurons that control the
muscles.
The signal from the interneurons causes the motor neurons to activate the quadriceps muscle,
causing it to contract and resulting in the leg kicking out in response to the tap on the patellar
tendon.