BIOL 546 - Exam 1 Review

Where: Budig 130

When: Thursday (2/23) from 8-10 pm
Exam Info Bring form of identification (KU ID, driver’s license, etc)

Topics: any material covered after

Monday’s lecture (Wednesday’s
lecture not included) ● True or False
- Intro to Physiology ● Multiple choice
- Metabolism and Enzymes ● Around 40-50 questions total
- Neurophysiology
- Sensory Physiology
Best way to prepare/study

❖ These slides/review
❖ Highlighted slides
❖ Poll questions
❖ Sample questions
Chapter 1: Introduction to Physiology and Energy
Physiology

❖ Concerned with normal functions of cells

❖ How mechanisms work

❖ Explain using cause and effect

❖ Derived from scientific experiments

The Scientific Method

1. Observation
2. Question what’s wrong
3. Hypothesis
4. Prediction
5. Experiment

Then becomes theory if experiment proves hypothesis right

 Homeostasis
Homeostasis: keeping the
internal environment the same
regardless of changes in the
external environment

❖ is dynamic (not static)

❖ deviation from = disease

Feedback Loops
❖ Negative Feedback Loops
❖ Examples: body temperature, blood sugar, and blood pressure
❖ DECREASES original stimulus

❖ Positive Feedback Loops

❖ Examples: blood clotting, production of action potentials in neurons, Hodgkins
Cycle
❖ AMPLIFIES the changes
❖ Known as the SNOWBALL effect
➢ STOPS when a process or necessary component becomes a limiting
factor
Negative Feedback Example
 Energy

- Universal energy carrier: ATP

- Energy released when break a phosphate, turns it into ADP
- A lot of other energy rich compounds
- Energy metabolism is multi-step and bi-directional
- Cellular respiration is process of producing ATP using
oxygen
 How do cells make ATP?

- If oxygen is present, use cellular/ aerobic respiration

- Consist of glycolysis, citric acid cycle, electron transport chain
- Makes about 38 ATP per molecule of glucose
- If oxygen is NOT present, use anaerobic respiration/ fermentation
- Still do glycolysis as normal but then produces lactic acid to
regenerate NAD+
- Only produces the 2 ATP from glycolysis
 Glycolysis
- In cytosol
- Produces ATP via substrate-level
phosphorylation
- Produces 2 ATP per molecule of glucose
- Energy investment and energy payoff phase
- Energy investment:
- Invest glucose, 2 ATP ,and 2 NAD+
- Energy payoff
- Gain 2 pyruvate, 4 ATP, and 2 NADH
 Citric Acid Cycle/Krebs Cycle/ TCA Cycle

❖ In the mitochondrial matrix

❖ The pyruvate from Glycolysis was
converted into acetyl CoA for the
beginning of the CAC
❖ Also produces ATP via substrate level
phosphorylation
❖ The CAC moves through a series of
reactions to generate 6 NADH, 2 FADH,
1 ATP, and 4 CO2 per glucose molecule
 Electron Transport Chain (ETC)
- In mitochondria
- Uses oxidative phosphorylation to produce
most of the ATP gained from cellular respiration
- Uses electrons from NADH and FADH2
(electron carriers)
- Oxygen is final electron acceptor → turns into
water
- Chemiosmotic Theory: creating a huge H+
concentration difference across mitochondrial
membrane, allowing these H+ to move down
gradient (through ATP synthase) turns ADP into
ATP
 Anaerobic Glycolysis/ Fermentation

❖ Glycolysis like normal to produce 2 ATP

❖ Use pyruvic acid generated to make Lactic acid
❖ This regenerates NAD+ so they can be used
again
❖ Lactic acid can then be used in Cori Cycle
➢ Where lactic acid transported to the liver and
converted to pyruvic acid
❖ Therefore, if 12 moles of glucose are used, only
24 moles of ATP can be used
Metabolism and Enzymes
Metabolism

❖ Metabolism: sum of all chemical reactions in the body that involve energy
➢ Catabolism + Anabolism

❖ Anabolism: making larger molecules from small ones

➢ Uses ATP (energy)

❖ Catabolism: breaking down large molecules into smaller ones

➢ Produces ATP (energy)
 Reaction Types and ATP
Endergonic reactions

- requires input of energy to make product

- (ex: making glycogen chains)

Exergonic reactions

- produce energy (breaking glucose)

Couple Reactions

- Connecting two reaction through an intermediate

 Reduction and Oxidation
❖ Reduction: gaining electrons
➢ Also known as oxidizing agent because it
allows for the other molecule to be oxidized

❖ Oxidation: losing electrons

➢ Also known as reducing agent because it
allows for the other molecule to be reduced
 Enzymes

● Enzymes are biological catalysts

➢ They increase reaction rate by lowering the activation energy
➢ Are not consumed or change by the reaction
➢ Only change the speed of the reaction, can't change products or reactants
● Activation energy- the energy required for reactants to start a chemical
reaction
➢ Most reactants don't have enough AE to start the reaction
➢ Heat increases the rate of reaction
➢ Enzymes increase rate of reaction at natural temperature
 Enzymatic activity
❖ Each enzyme has a 3D shape or conformation, with pockets that
contain an active site
➢ The reactants (substrates) fit into the active site like a lock and key
❖ Lock and Key
➢ When substrates bind to the active site, it forms temporary bonds
with the enzyme (key-lock). Then, breaking of the temporary enzyme
substrate complex yields the products of the reaction
➢ Substrate= Key, Enzyme= Lock
➢ Enzymes have specificity to which “lock” and “key” can fit together
❖ Induced Fit- The enzyme adjust the shape when bound to
substrate to enhance or inhibit activity
Enzymes continued…

❖ Zymogen: inactive form of enzyme

➢ Activated when needed Ex) pepsinogen → pepsin in digestive
system
❖ Reaction rate: rate at which reactants are being converted into
products
➢ As substrate concentration increases, so does the rate until
enzyme is SATURATED
➢ Saturated: every enzyme is being used and maximum reaction rate
is reached
 What affects Enzymatic Rate?

1) Temperature
a) Temp increases rate, but also can denature (optimum temp for the reaction)
2) pH
a) pH optimum (stomach-2 vs saliva- 7 vs small intestine-9)
3) Concentration of Cofactors and Coenzymes
a) These are additional small molecules that aid in enzymatic reactions
4) Concentration of Enzyme and Substrate
a) Reaction rate increases until the enzyme becomes saturated with substrate. It will reach a
maximum rate eventually.
5) Stimulatory or inhibitory effects
 Enzyme Inhibitors
Competitive Inhibitor
❖ The substrate and inhibitor compete for active site
Non- Competitive Inhibitor
❖ The substrate and inhibitor DO NOT compete for active site. The inhibitor binds to the
allosteric site, which changes the conformation of the active site and does not allow
the enzyme to bind
End-Product Inhibition
❖ This occurs when one of the final products inhibit a branch point enzyme (glycolysis)
❖ This is negative feedback
Chapter 4: Movement of Solutes and Water Across
Cell Membranes
 Diffusion
❖ Diffusion: the dispersion of particles due to random thermal motion
❖ Net movement: from high concentration to low concentration until equilibrium is
reached → DO NOT require carrier proteins
➢ At equilibrium there is still movement, but no net movement
❖ Rate of diffusion: How much solute (s) is transported per unit time
➢ Rate diffusion of solute (s) = D x A x ΔC/X
■ D= diffusion coefficient, depends on a lot of factors
■ A = Cross sectional area= area through which (s) diffuses
■ Δ C =Concentration Difference= difference in concentrations of (s) across
membrane
■ X = distance
 Osmotic Pressure
❖ Osmosis: movement of water from area of low solute
concentration to area of high solute concentration
❖ Must have a semipermeable membrane: allows water
to pass but not solutes
❖ Osmotic /Hydrostatic Pressure: pressure needed to
stop osmosis
➢ Determined by number of solutes per volume
➢ Higher solute concentration = higher osmotic pressure
❖ Water moves from low osmotic pressure to
higher osmotic pressure !!!!
Osmotonicity of Cell
Membrane Permeability

● Permeability: how easily a solute can move through the

membrane
● Equation = P(C1-C2)
○ P = permeability constant, depends on a lot of factors
○ C1-C2: concentration gradient of solute across the membrane

*Similar concept to diffusion rate equation, know both to be safe

 Facilitated Diffusion

❖ Also moves from high concentration to low concentration

❖ Uses channels and carriers
❖ No ATP is needed
Primary Active Transport

❖ Requires ATP
❖ Goes against concentration
gradient: from area of low
concentration to area of high
concentration
❖ Ex) Na/K pump
 Secondary Active Transport

❖ Set up by primary active transport

❖ Allowing one atom to flow back down its
concentration (Na+) gradient to bring another
molecule (glucose) against its concentration
gradient
❖ Antiport: one molecule is exchanged for another
❖ Symport: two molecules are transported
together
➢ Ex) solute-coupled water transport across the
epithelial cells into the kidney/ stomach
 Passive and Active Transport

Passive: down
gradient

Active: against
gradient so
requires ATP
Chapter 6: Neurophysiology Part 1
 CNS vs PNS

Central Nervous System

● Brain and Spinal cord

Peripheral Nervous System

● All neural tissue outside of the CNS

● Includes afferent and efferent divisions
 Afferent vs Efferent

❖ Afferent: brings message from outside to

central nervous system (CNS) via sensory
neurons
❖ Efferent: sends signals from CNS to
effectors (muscles) via motor neurons
➢ Somatic and Autonomic
➢ Autonomic can be divided again insto
parasympathetic and sympathetic
 Nerve Cell Structure

Dendrites: receives signals

Body: contains genetic info
Axon hillock (aka trigger zone):
spike (AP) initiation due to high
concentration of Na channels
Axon: transmits electrical
impulses
Axon terminals: releases signal
to next neuron
 2 Types of Cells in Nervous System

1. Neurons
- Transmit information via electrical impulses
- ELECTRICALLY EXCITABLE

2. Glial Cells
- Maintain environment and support neurons
- None are able to produce electrical impulses
 Six types of Glial cells
1) Astrocytes: support/ regulate, blood-brain barrier
2) Oligodendrocytes: myelin-forming
3) Microglia: protection
4) Ependymal cells: control CSF (cerebral spinal fluid)

5) Schwann cells: myelin- forming

6) Satellite cells: support

* First 4 are in CNS and last 2 are in PNS*

Ohm’s Law: How electrical signals arise

V=IxR
V: voltage, I: Current, R: Resistance
Units: V (volt), I (ampere), R (ohm)
Electrical Signals

• Resting membrane potential =

-70mV
• Depolarization: charge increases
(becomes less negative)
• Repolarization: charge moves
back toward resting membrane
potential
• Hyperpolarization: charge
becomes more negative than
-70mV (dips below resting
membrane potential)
Types of Ion channels
Non-gated: Gated:
● Always open ● Opened by a physiological
● Such as leaky channels
stimuli
● Voltage-gated: open due to
change in voltage → AP
● Ligand-gated: open due to
extracellular chemical stimuli
● Signal-gated: open due to
intracellular chemical
● Mechanically gated: open due
to stretching or pressure
Resting Membrane Potential

resting membrane potential: -70mV

close to K+ equilibrium
K+ equilibrium potential (EK): -90mV
Na+ equilibrium potential (ENa): +60mV
- established by difference in ion concentrations, K+ leaky
channels, and Na/K pump
 K+ Leaky channels and Na/K pump
❖ High conc of K inside cell
❖ High conc of Na outside of cell
❖ A lot of K leaky channels allows for K+ to leave the
inside
➢ This helps make inside of cell more negative compared to
outside
❖ Na/K pump brings 2 K back in for every 3 Na that leave
➢ This also makes the inside of the cell more negative
➢ Pump requires ATP
➢ Necessary to maintain concentration difference → keep
the inside more negative
Information Flow Through the Neuron

1) Graded Potential
a) The signal decreases as the distance traveled increases through a neuron
i) This can occur at the membranes of sensory cells on the postsynaptic
membrane
2) Action Potential
a) This is an all or nothing potential
b) There is no change in size of the stimulus
i) Amplitude is not dependent on stimulus strength, if the threshold for
an action potential is met, then an AP will be generated
Graded Potentials

• Local changes in membrane potential

• Short-lived
• Signal weakens the farther it travels
• Stimulus strength determines magnitude of signal
• Aka, stronger stimulus = stronger signal; weaker stimulus =
weaker signal
• Graded potentials can add up and initiate an action
potential if it adds to a strong enough signal
Graded Potentials
• EPSPs and IPSPs make up graded potentials (summation)
• EPSP = Excitatory Postsynaptic Potential
• Open Na+ or Ca2+ channels 🡪 graded depolarization
• Moves toward threshold
• IPSP = Inhibitory Postsynaptic Potential
• Open K+ or Cl- 🡪 graded hyperpolarization
• Moves away from threshold
• Temporal Summation: one neuron with summation over time
• E1 + E1 + E1 … over time, threshold is finally reached→ action potential
• Spatial Summation: two or more neurons with summation over
space
• E1 + E2 add together to reach threshold → action potential
What about action potentials?

*initiated at axon hillock (highest

V-G Na+ channel density)

Can undergo summation Cannot undergo summation (cannot combine)

Action Potentials
• All-or-nothing... must reach
a threshold potential, and
once that threshold is
reached, we will get the
same AP every time Depolarization
Repolarization

• Stronger stimulus ≠ stronger

signal; weaker stimulus ≠
weaker signal
• Stronger stimulus WILL lead
to higher FREQUENCY of AP’s
• Amplitude will not decrease Repolarization
with distance Hyperpolarization
 Action Potential Steps

❖ Starts at resting potential

❖ Depolarization via activation of voltage-gated Na
channels
➢ Na flows into cell
❖ Repolarization via de-activation of Na channels and
opening of voltage gated K channels
➢ K flows out of cell
❖ Hyperpolarizes when some voltage gated K
channels are still open
❖ Returns to resting potential when all voltage gated
K channels are closed
Equilibrium Potential for Ions
● Denoted by “Eion”
● Each ion has its own equilibrium potential
● Based on diffusion and electrostatic forces
○ First: flow down gradient by diffusion
○ Next: Can’t all flow down because then get repulsed by
similar charges so some move back
○ These two together establish the equilibrium potential
● Equation for this: Nernst Equation
○Eion = .058 log [ion outside]/ [ion inside]
○ Know simple logs: log (10) = 1, log (100) = 2, log (1/100)= -2
and how to solve any variable in the equation
● Net movement stops once this potential is reached
 Membrane permeability and conductance
- Conductance (g) is inversely related to
resistance

- During rising phase (depolarization), the

membrane potential (Vm) is reaching the
equilibrium potential for Na (ENa) and Na
conductance (gNa) is rising

- During falling phase (repolarization), the

membrane potential (Vm) is reaching the
equilibrium potential for K (EK)and K
conductance (gK) is rising
Hodgkin Cycle
• Positive feedback drives the regeneration of APs
• Na+ brought into cell by diffusion → greater change in
membrane potential (hits threshold potential) →
voltage-gated Na+ channels open → rapid depolarization
• Stopped by inactivation of Na channels and activation of K
channels
 Conformations of voltage-gated Na+
channels

1) Active: channel is open

2) Inactive: channel is closed and
cannot be opened again
3) De-activated: channel is closed but
can we activated again
- These three stages cause the
domino effect and refractory
periods
 Domino Effect
- One Na channel is opened into
active conformation and allows
current flow
- This depolarizes the membrane
so the next channel is opened
but while this one opens, the
previous one becomes
inactivated
- This makes it so the flow of AP
propagation has to occur in one
direction and can’t backflow at
all
 Refractory Periods
• Absolute Refractory Period: no AP possible
• All Na+ channels inactivated
• Relative Refractory Period: strong stimulus may
produce AP of smaller amplitude
• After absolute refractory period
• Some of Na+ channels are re-opening, but K+ channels
are also still open
• This is why action potentials do not combine… once
one ends, there is a mandatory waiting period
before another can form
 Accommodation
- Excitability of membrane decrease and
the threshold increase
- This means it is harder to reach
threshold and produce another AP

1) Fast accommodation (aka→ phasic

response): the membrane quickly becomes
un-excitable and unable to produce another
AP

2) Slow accommodation (aka → tonic

response): takes the membrane longer to
become un-excitable and unable to produce
another AP
Chapter 6: Neurophysiology Part 2
Safety Factor
- “Overshoot” is extra
depolarization past the
threshold
- This causes membrane
ahead of AP to also
depolarize and produce
another AP
 Length constant
- property of the membrane
- numeric way of representing how far a graded potential can
travel down an axon
- Larger the length constant → further away it can travel
- Increase length constant = increase in conduction velocity
- Based on rm and rl
- rm: resistance across and rl: resistance along the
membrane
- What could increase length constant- specifically rm?
MYELINATION
Saltatory Conduction
- “Saltatory” means jumping
- Occurs at Node of Ranviers
- Electrical impulses skip from node to node along axon due
to myelination
- This speeds up the transmission of impulse by increasing
resistance across the membrane
- Therefore, conduction speed is fastest with myelination
and a larger diameter
Chapter 6 Part 3: Chemical Synapse
 Two Types of Synapses
• Synapse: connection between
two neurons
• Electrical synapse
• AP spreads from one neuron to
another
• Chemical synapse
• Release of neurotransmitters to
bind to another neuron
 Electrical synapse
- Faster
- Used to synchronize
neurons (ex: heart)
- Information transfers in
both directions (cell A to
cell B or cell B to cell A)
- Neurons connect via gap
junctions (join cells
together)
 Chemical Synapse
1. Arrival of AP in axon terminal
2. Ca2+ channels activated by
depolarization
3. Ca2+ influx into presynaptic terminal
4. Synaptic vesicles fuse with
presynaptic membrane
5. NTs diffuse across synaptic cleft
6. NTs bind to postsynaptic receptors
1. Ionotropic receptors (faster)
2. Metabotropic receptors (slower)
7. This can cause either an EPSP or IPSP
in the postsynaptic neuron
 Postsynaptic Receptors
• Ionotropic
• Fast
• Small synaptic vesicles
• Receptor and channel in the same complex
• NT binds → ion channel directly opened
• Metabotropic
• Receptor and ion channel separate
• Direct G-Protein Coupling
• NT binds to receptor → G protein activated → G protein opens/closes ion channel
• Second Messenger Coupling
• NT binds to receptor →G protein activated → enzyme produces second messenger
→ 2nd messenger performs cellular functions and opens/closes ion channel
Types of NTs
● Small-molecules
○ Include many groups such as Ach, amino acids, purines,
biogenic amines
● Peptides
○3-30 amino acids long
○Precursors and their activating enzymes are transported
in vesicles
● Gases
○ NO (nitric oxide) and CO (carbon monoxide)
○ Both are not packaged in vesicles
 How NTs are released

1. Vesicles holding NTs dock to presynaptic membrane

2. Vesicles primed for fusion
3. Vesicles begin fusing with membrane until NTs are released → Ca 2+
is needed for fusion
• Full fusion: vesicle cannot be reused
• Kiss-and-run: vesicle partially fuses with membrane, releases NTs, vesicle able
to be reused

• Most all NTs are packaged in vesicles for transport and release
• Exceptions: NO (nitric oxide) and CO (carbon monoxide) → two gases that
both function as neurotransmitters
 How NT release is regulated
● Autoreceptors
○ Controls release of NT
○ Receptors present on the
presynaptic neuron that bind to
the NT it is releasing
○ Similar idea to feedback inhibition
○ If there is a lot of NT in the
synaptic cleft, it binds to these
autoreceptors and lets the
presynaptic cell it has released too
much and should stop release
 How neurotransmitters are inactivated
1) returned back into pre-synaptic cells
via channels to be reused (uptake)

2) enzymes can inactivate/degrade

them
- Ex) Ach

3) they can diffuse out of the synaptic

cleft through the bloodstream
 Reversal potential
● Denoted as “Erev” → graded potential
● When postsynaptic ion channels open and now multiple ions move
across the membrane
● Example, both Na and K moving across postsynaptic membrane in
opposite directions establishes a new equilibrium between the two
ions’ individual equilibrium potentials
○ This is called the Equilibrium potential
● Important to distinguish between EPSP and IPSP
● When Erev is greater than the membrane potential (Vm), there is
depolarization = excitatory = AP
● When Erev is less than Vm, there is hyperpolarization = inhibitory =
no AP
● When Erev and Vm are qual, there is no change
EPSP vs IPSP
- NT binds to postsynaptic nerve and opens ligand-gated ion channel
- So EPSP is based on type of NT and what ion channels are open
- both can undergo summation, are graded responses, and do NOT have
refractory periods

Excitatory postsynaptic potential

- Na or Ca channels are opened and depolarization happens → if enough
depolarization occurs → AP
- sometimes requires summation of multiple EPSP to produce AP

Inhibitory postsynaptic potential

- K or Cl- channels are opened and hyperpolarization happens → no AP
- These counteract EPSP and stop an AP from occurring
 ACh receptors
2 types:
1) Nicotinic: binds nicotine or ACh to
open
- Ionotropic receptor
2) Muscarinic: binds muscarine or Ach
to open
- G-protein coupled receptor

- Nicotine and muscarine are both

agonist for ACh receptors
Presynaptic Inhibition
- Inhibitory synapse onto excitatory synapse which stops the
excitatory synapse from releasing its NT
- Ex) Renshaw cells which help ensure muscles aren’t overstimulated
 Overall of chemical synapses
• Can be fast or slow (but always slower than electrical synapses)
• Fast: smaller vesicles, bind to ionotropic receptors
• Slow: larger vesicles, bind to metabotropic receptors
• Can be inhibitory or excitatory
• How is this determined? Type of NT released and what receptor it
binds to
• NTs can be excitatory or inhibitory. For example…
• Acetylcholine: major excitatory NT
• GABA: major inhibitory NT
• Only flows in one direction
Chapter 7: Sensory Physiology
Pt 1: Big Picture Ideas
Sensory
• 2 major functions:
• Signal detection
• Discrimination of some aspects of sensory

• Inputted stimuli are evaluated by 4 criteria:

• Qualitative: modality – what is the stimulus?
• Quantitative: intensity
• Temporal: duration or frequency
• Spatial: location
Sensory Modalities
• Chemoreceptors
• Touch
• Taste
• Smell
• Mechanoreceptors
• Touch
• Hearing (sound)
• Photoreceptors
• Light and Vision
• Thermoreceptors
• Touch (heat)
• Electroreceptors
 Types of Receptors
• Ionotropic: faster
• Ligand gated receptors that open in response to
NT
• Mechanoreceptors: pressure
• Ex: hair cell is ear for hearing, touch
• Thermoreceptors: temperature
• Electroreceptors: electric charge
• Metabotropic: slower, coupled
• G-proteins and second messengers are used
• Chemoreceptor: molecule binds to receptor
• Ex: taste/smell receptor
• Photoreceptor: light alters receptor protein
• Ex: rod receptor (eye)
Receptive fields
• Area of skin that, when stimulated, changes
firing rate of a neuron
• Size of receptive field depends on density of
receptors in that region
• More receptors = smaller field = larger
processing area in brain
• Small receptive field = greater acuity –
sharpness of the sensation

- Acuity: ability to detect details

- Degree of convergence determines size of
receptive field
- Test this via two point test
- Small convergence = Small receptive field
which will have more primary neurons so
smaller distance between the two points can
be distinguished
Input-Output Relations
- semi-logarithmic relationship
between stimulus intensity and
receptor response

- Allows us to respond to a HUGE

range of stimulus

- Allows us to visualize the AP

frequency relationship compared
to increasing stimulus intensity
Range fractionation
- Different cells have different sensitivities that respond to different
stimulus but when you overlap all these sensitivities, you get a wide,
dynamic range
Constant stimulus- How receptors adapt

• Tonic receptors- slow adapting

• Little adaptation to stimulus
• Maintain constant firing rate with constant
stimuli
• Think when a seatbelt is stabbing you

• Phasic receptors- fast adapting

• Adapt to stimulus
• Firing rate decreases with constant stimuli
• This is why you don’t constantly sense your
clothes on your skin or shoes on your feet
Sensory Pathways
• Olfactory (smell) → cortex
• All other pathway→ Pass through thalamus before final destination

• EX: Visual → thalamus → occipital

What’s the point?

- Different types of senses get sent to different parts of the brain for
processing
The Cortex Man
• More brain area devoted to
bigger, more emphasized body
parts
• More brain area = more
information processing
 Chapter 7: Sensory Physiology
Pt 2: Chemoreceptors (Taste and smell)
Taste
• 5 basic taste qualities:
• Salty: Na+ through ion channel, depolarization, opens Ca2+
channels
• Sour: H+ through ion channel, depolarization, opens Ca2+
channels
• Sweet: binds to membrane receptors, G proteins activated,
close K+ channels
• Bitter: binds to membrane receptors, G proteins activated,
Ca2+ entry
• Umami: meaty, brothy, savory assoc. w/ MSG – same
mechanisms as sweet
 Chemosensory Coding- taste
• Labeled-Line Coding
• Specialist receptors
• Receptors are narrowly tuned to a limited
range of stimuli

• Across-Fiber Pattern or Pattern Coding

• Generalist receptors
• Receptors are able to respond to a wider
range of stimuli
Olfaction Overview
• The Olfactory epithelium is located in the roof of the nasal cavity
• The receptor cells are bipolar neurons
• The bundles of axons from the receptor cells form the olfactory nerve
• The supporting cells cushion and support the olfactory receptor cells
• Bowman's gland produces a gel forming protein that binds odorant
proteins
 Olfactory pathway
• Bipolar neurons, ciliated dendrites
• Odors bind to receptors in the cilia
• How it works:
• G-protein coupled (metabotropic receptor)
• With help of second messengers, Na+ and
Ca2+ channels are opened
• Produces graded potential → AP stimulated

• Olfactory receptor cells will then

synapse with the mitral cells in the
olfactory bulb
• These mitral cells then amplify, refine,
and relay the signals to elicit specific
responses
 Combinatorial Coding
• Information taken from a
combination of different olfactory
receptors to determine odor
• The odorants are coded by
different combinations of
olfactory receptors
• There are specific receptors that
may be part of the code for
multiple oderants
• Like the alphabet how we use 26
letters to create millions of words
Chapter 7: Sensory Physiology
Pt 3: Photoreceptors (Sight)
Human Eye
• Fovea→ this is the highest
density of photoreceptor
cells (cones and rods)
Visual Pathway
● Visual fields go to opposite LGN
○ Ex) nfo from the right visual
field projects to both eyes
but travels via left LGN
Retina
• Cones + Rods
• Optic nerve formed by fibers
from ganglion cells
• Amacrine cells, bipolar cells,
horizontal cells also part of
processing
• Bipolar cells directly connect
photoreceptors to ganglion cell
• Lightpasses to back of retina
and the signal is then sent back
to the front near the optic nerve
Photoreceptors

• Rod cells:
• more sensitive, don’t
distinguish color
• 1 type of opsin
• Black and white
• Cone cells: 3 types of opsin
• Less sensitive, distinguish color
• Red (longest), green, blue
(shortest)
Rhodopsin
• Light sensitive pigment in photoreceptors
• Retinal + Opsin protein = Rhodopsin
• Light changes shape of retinal from cis to trans which makes the
opsin active
• works with PDE and cGMP
• this closes Na+ channels
Light
- retinal in trans conformation
- Na channels are closed and
photoreceptor is hyperpolarized
- Photoreceptor can’t releases inhibitory
NT to the bipolar cell
- Bipolar cell releases its excitatory NT
- AP in ganglion cell!!!!
Dark
- retinal in cis conformation
- Na channels are open and
photoreceptor is depolarized
- Photoreceptor releases
inhibitory NT to the bipolar cell
- Nt is glutamate
- Bipolar cell can’t release its NT
- There is a smaller or no
graded potential happening
- no AP in ganglion cell
 Lateral Inhibition
- Helps enhance contrast
- Used in eye sight
- How it works:
- A primary neurons response will
be proportional to the stimulus
strength
- Then a pathway closest to the
stimulus will inhibit its neighbors
- This inhibition of the neighboring
neurons will enhance the
perception of the simulus
Neural Pathways of Light
• Direct (vertical): from receptors → bipolar → ganglion cells
• Indirect (lateral): from receptors → horizontal cells → bipolar →
amacrine cells→ to ganglion cell
 Ganglion Receptive Fields
• 2 types: ON and OFF
center field
• Depends on the type of
bipolar neurons
• ON center: Ganglion is
active when the light
shines on the center
• OFF center: Ganglion is off
when light shines on the
surrounding area
Chapter 7: Sensory Physiology
Pt 4: Mechanoreceptors (Hearing)
Sound
• Measured in Hertz (Hz) →
number of cycles per
second (frequency)
• Pitch of sound = frequency
of sound waves
• Only concerned with WHICH
hair cells are stimulated and
WHERE on the basilar
membrane these hair are
• Intensity of sound =
amplitude of sound waves.
How loud something is
Mechanoreceptors by Hair cells
- Cochlea is spiral shaped bone found in
inner ear that is important in hearing
- It contains the Organ of Corti which has
a basilar membrane with hair cells (cilia)
on it
- the location on this basilar membrane
directly correlates to the frequency we
hear
- High frequency close to base (closer end)
- Lower frequencies at apex (distal end)
- Hair location on membrane creates a code
for a sound pitch!
- The movement of these cilia causes
certain NT to be released which will
cause APs to travel to auditory cortex in
brain
 Movement of Hair cells
• Receptors are mechanoreceptors, not
voltage-gated receptors
• Movement downward of basilar membrane
→more neurotransmitter release
• Movement upward of the basilar membrane →
less neurotransmitter release
• Hair cell transduction
• Force toward → K+ channels open, depolarizing cell,
Ca2+ enters, more Nt release
• Force away→ K+ close and less NT release
• The connection between these channels are the Tip
links
• There is a role reversal of Na and K normally, so in the
ears K+ will move through the channel and get
depolarization
• Because the endolymph (cochlear duct) has a higher K+
concentration
THE END