MCB 136 - Unit 1

3 ways molecules can enter cells

1. diffuse through phospholipid bilayer (simple or facilitated)
2. active transport
3. vesicle transport (e.g. bacteria)

factors influencing the rate/direction of flux

1. size of molecule
2. temperature
3. concentration gradient in/out of cell
4. membrane permeability
5. membrane surface area

Mechanism of Na+/K+ ATPase

1. Binding Na+
2. Phosphorylation
3. Conformational change and release of Na+
4. K+ binding -> dephosphorylation
5. Releases K+ and returns the pump

2 domains that all ion channels have

1. P loop (provides specificity)
2. Transmembrane domain

how ion channels have specificity

1. charge exclusion
2. size exclusion - determined by the strength of interactions between ion and surrounding oxygens vs. ion's propensity to dissociate back into water
3. binding sites

conserved sequence for potassium channels

-TVGYG-

SCID

-severe combined immunodeficiency disease
-caused by mutations in Orai1 (channel protein) and STIM1 (pathway protein)

What makes one cell different from another?

differential gene expression

3 functions of membranes

1. selective barrier to passage of molecules
2. detecting chemical signals from other cells
3. anchor cells to adjacent cells and extracellular matrix

rate of diffusion of molecules across membranes vs in water

1,000 to a million times slower

What is the major factor limiting diffusion across a membrane?

hydrophobic interior of lipid bilayer

What molecules can diffuse through lipid bilayer?

1. Water
2. Lipids
3. Steroids

osmotic strength

[concentration] x # ions

familial hemiplegic migraine (FHM)

-throbbing pain with nausea, vomiting, aura (visual disturbance) and light/sound sensitivity
-caused by loss-of-function mutations in Na+, K+ ATPase

Luigi Galvani

Electrical stimulation of the nerve in a frog's leg produced contraction of the leg muscle

oscilloscope

-used to measure potential across membrane
-insert electrode in cell, grounded outside

How does membrane potential vary amongst cell types?

proliferating (and cancer cells) have potentials closer to zero compared to non-proliferating cells (e.g. neurons, skeletal muscle)

K+, Na+, and protein concentration in/out cell

Intracellular: high K+, low Na+, high protein
Extracellular: low K+, high Na+, low protein

Ouabain (toxin from Acokanthera)

-shuts down Na/K ATPase
-membrane potential doesn't change instantaneously, takes time for ions to diffuse in/out of cell

What controls and maintains the resting membrane potential?

-Na+ and K+ electrochemical gradients along the membrane
-kept constant by Na+/K+ ATPase and K+ leak channels

ion hydration

In water, interactions between water molecules and ions form, making a very stable configuration. Because of Na+ small size, it has even stronger hydration. It takes energy to "break" the hydration; oxygens on amino acid residues in channels provide the e

K+ channel

-excludes Na+ (mostly) by spacing size of binding sites (more oxygens stabilize larger K+ ion)
-potential binding sites for 4 K+ ions, but repulsion between ions makes it favorable to have only 2 K+ ions

What besides electrochemical gradient drives ion permeation?

Repulsion between ions in channel

Nernst potential

equilibrium potential of one ion; the potential where electrical and chemical gradient is equal and there is no net ion flow

Goldman-Hodgkin Katz potential

membrane potential (Vm) of the cell established by relative contributions of several ions

types of stimuli that open/close ion channels

Ligand gating, voltage gating, phosphorylation gating, stretch or pressure gating

Why is membrane potential not constant?

1. ionic composition in/out of cell
2. permeability of channels changes

voltage-gated ion channels

-have S4 resting voltage sensor oriented in a V shape that blocks ion flow
-during depolarization, S4 domain rises to open channel
-charges go to S4-S5 linker to cause conformational change

batrachotoxin

a toxin, secreted by poison arrow frogs, that selectively interferes with Na+ channels causing depolarization

cell-attached patch recording

-can record a single or several channels
-glass micropipette surrounds channel

voltage-clamp recording

-apply voltage, measure current to see response
-shows channels have different rates of response

How to tell what ion is involved in a response?

Ion substitution (e.g. K+/Ca2+ replaced leads to normal physiological solution, Na+ replaced leads to no response: toxin opens sodium channel)

neuron doctrine

nervous system is an interconnected network of cells

afferent neuron

sends info from PNS (sensory receptor) to CNS

efferent neuron

sends info from CNS to PNS (muscle, gland, neuron)

steps of neuronal signaling

1. stimulate cell
2. generate electrical signal
3. signal travels through the cell
4. signal passed to next cell

Is response or perception faster?

response is faster

graded potentials

1. can be hyperpolarizing or depolarizing
2. magnitude depends on strength of stimulus
3. distance from site of stimulus affects magnitude

action potential membrane depolarization

-ligand gated channels and mechanically gated channels often serve as initial stimulus for AP
-voltage gated channels allow APs to occur by allowing rapid depolarization and repolarization

states of Na+ channels

closed<=>open->inactivated->closed; open and inactivate rapidly

states of K+ channels

closed<=>open, open and close slowly

steps of action potential

1. steady resting potential due to K+ leak channels, P(K) > P (Na)
2. depolarizing stimulus brings to threshold
3. voltage-gated Na+ channels open causing rapid depolarization
4. inactivation of Na+ channels and delayed opening of K+ channels halts depola

Do Na+/K+ concentrations change significantly during an action potential?

Na+ concentration goes from 15mM to 15.01 mM, no

Nav1.7

large protein that is a voltage-gated Na+ channel; 4 subunits that have 6 transmembrane domains each

Mutations of Nav1.7

gain of function mutations lower threshold and cause APs to fire easier; can lead to [pain in hands and feet] primary erythermalgia (PE), [pain in face] paroxysmal extreme pain disorder (PEPD), or [no pain] channelopathy-associated pain disorder (CIP)

How does the nervous system encode stimulus strength?

strong stimuli cause more action potentials

absolute refractory period

The minimum length of time after an action potential during which another action potential cannot begin; due to Na+ channels

relative refractory period

the period of time following an action potential, when it is possible, but difficult, for the neuron to fire a second action potential, due to the fact that the membrane is hyperpolarized; due to K+ channels

What is the effect of a supra-threshold stimulus?

the membrane is maintained above threshold and AP firing depends only on Na+ channels

Node of Ranvier

site of AP

myelin

wraps neuron, preventing ion leakage; greater degree of myelination leads to greater nerve conduction velocity (e.g. pain receptors not myelinated=slow)

Why do action potentials only travel in one direction?

Na+ channel inactivation

Multiple Sclerosis (MS)

-destruction of the myelin sheath on neurons in the CNS
-T cells can pass blood-brain barrier causing autoimmune response that destroys glial cells
-leads to decrease in conduction due to leakage of ions

How to diagnose MS?

1. Blood test - rule out diseases with similar symptoms
2. Lumbar puncture
3. MRI - can reveal lesion areas of MS on brain and spinal cord
4. Evoked potential test - electrical signals produced by NS in response to stimuli are recorded

How does the mouse model of MS work?

1. immunize mouse with MBP-specific peptide
2. T cell mutates and causes characteristic neuroinflammation

anatomy of chemical synapse

mechanism of neurotransmitter release

1. action potential reaches terminal
2. voltage-gated Ca2+ channels open
3. Ca2+ enters terminal
4. neurotransmitter is released and diffuses into cleft
5. neurotransmitter binds to postsynaptic receptors
6. neurotransmitter removed from cleft

inhibitory synapse

causes hyperpolarization

excitatory synapse

causes depolarization

EPSP

excitatory post synaptic potential - depolarization (towards an AP)

IPSP

inhibitory postsynaptic potential - hyperpolarization (further from AP)

temporal summation

when one presynaptic neuron releases neurotransmitter many times over a period of time

spatial summation

when multiple presynaptic neurons together release neurotransmitter

How do we know that neurotransmitter release is mediated by vesicle fusion?

1. post-synaptic cell responds in a quantal fashion: weak presynaptic signals cause tiny, quantal depolarizations corresponding to a # of vesicles
2. vesicles can be seen at the synapse with electron microscopy

What is the evidence that calcium regulates vesicle release?

1. AP evokes an increase in calcium levels at active zone between presynaptic and postsynaptic
2. Ca2+ is required for vesicle fusion (no fusion when Ca2+ removed)
3. Caged Ca2+ is sufficient to trigger vesicle fusion

Describe the caged Ca2+ experiment

Ca2+ was put in a molecular "cage." The cage would open and release Ca2+ when exposed to light (photocleavage). Vesicle fusion occurred in the light but not in the dark.

SNARE hypothesis

intertwining of v-SNARES (on vesicle) and t-SNARES (on presynaptic membrane) allows fusion of the vesicle to allow for neurotransmitter release

Which SNARE proteins are involved in fusion?

synaptobrevin (vesicle), Munc18, syntaxin (membrane)

Which protein is involved in Ca2+ triggering?

synaptotagmin - entering Ca2+ binds it and it catalyzes membrane fusion

What happens if Ca2+ cannot enter axon terminal?

No Ca2+ influx through channels -> no vesicle fusion -> no signal across synapse

What are the 2 kinds of glutamate receptors?

1. Metabotropic
2. Ionotropic (AMPA and NMDA)

What is the difference between metabotropic and ionotropic receptors?

Metabotropic receptors are indirectly linked to ion channels (e.g. G-protein coupled), while ionotropic receptors are channels themselves

mechanism of glutamate binding

1. Glutamate binds to AMPA and NMDA channels
2. Na+ enters through AMPA, causing depolarization
3. Depolarization ejects Mg2+ from the loose binding site on NMDA
4. Ca2+ enters through NMDA channel
5. Ca2+ activates second messenger pathways

Why does depolarization from AMPA R cause ejection of the Mg2+ ion in NMDA R?

accumulation of positive charge (from Na+ entering cell) causes repulsion of Mg2+ ion

What is special about dendritic spines?

they have many AMPA/NMDA receptors

What is the difference between EPSP contributions from AMPA and NMDA?

AMPA = fast and sharp
NMDA = slow and sustained

What does the hippocampus do?

consolidates short term memory to long term memory

long term potentiation

After repeated stimulation, the same stimulus leads to increased neurotransmitter release (and bigger EPSP in postsynaptic cell).

mechanism of synaptic strengthening

1. Activation of NMDA R triggers Ca2+ influx
2. Ca2+ binds calmodulin
3. Calmodulin activates CamKinase
4. CamKinase promotes phosphorylation of AMPA R and addition of more AMPA R in the membrane, leading to bigger EPSP
5. Ca2+ also activates NO synthase,

retrograde amnesia

an inability to retrieve information from one's past

anterograde amnesia

an inability to form new memories

Henry Molaison

had his hippocampus removed to control epilepsy, gave him severe anterograde amnesia

Hebb's Rule

neurons that fire together wire together

What happens to dendritic spines due to LTP?

The spine heads grow and gain more AMPA receptors, and more vesicles containing neurotransmitters are released for the same stimulus.

CT scan

computed tomography scan - a noninvasive diagnostic imaging that uses X-rays and tech to produce images of the body

What are the layers of the head (out to in)?

1. Scalp
2. Skull
3. Dura mater
4. Venous blood
5. Arachnoid mater
6. Subarachnoid space of brain
7. Pia mater
8. Brain

What is the function of the choroid plexus?

Maintains ionic balance needed for CSF production

subdural hemmorhage

Blood leaks into dural area, shows up opaque in a CT scan

subarachnoid hemmorhage

Neurons are exposed to blood in place of CSF. Blood is toxic to neurons so it kills the neurons.

positron emission tomography

Inject a positron emitting tracer that is active: fluor-deoxy-glucose. Monitor levels of FDG in terms of glucose uptake as a measure of metabolic activity.

What are symptoms of Parkinson's disease?

1) Resting tremor (shaking)
2) Slowed movement
3) Rigidity of movements of the face
4) Shuffling gait
5) Forward tilt of trunk

What is the function of Broca's area?

generating words

What is the function of Wernicke's area?

speech comprehension

fMRI

Measures haemodynamic response to neural activity: BOLD (blood oxygen level dependent) contrast. Utilizes different magnetic properties of iron when O2 is bonded and not bonded.

What causes Parkinson's disease?

degeneration of dopaminergic neurons in substantia nigra

What do colors in PET represent?

red=high, blue=low

What is the fovea's role in vision?

It is the part of the retina required for high acuity vision because of the high concentration of cones. It is depleted of other cell types so there is minimal light scattering. It also has high spatial resolution.

What is the blind spot?

Optic disc is where all nerves in eye converge to form optic nerve, creating an area where there are no photoreceptors for vision.

What does the retina create?

It makes a point-to-point map of the visual field, which is actually inverted.

What is convergence in vision?

Receiving input from multiple cells which is passed down through other types of cells.

What cell involved in vision is the first to fire an action potential?

retinal ganglion cells

Ganglion vs Nucleus

Collection of neuronal cell bodies in periphery and CNS, respectively.

visual pathway

retinal ganglion cells -> optic nerve -> optic chiasm -> optic tracts -> lateral geniculate nucleus (LGN) of thalamus -> primary visual cortex (V1)

What has to happen for something to be "seen"?

action potentials in neurons of the primary visual cortex have to fire

What is special about the outer segment of photoreceptors?

They have a special membrane that allows for enhanced protein expression.

What kind of light protein do rods have?

Rhodopsin, which is blue/green sensitive

What kinds of light protein do cones have?

S opsin - for blue light
M opsin - for green light
L opsin - for red light

What molecule absorbs light and how?

11-cis retinal, which converts to all-trans retinal when it absorbs light. There is also a conformation change in the transducin peptide.

Mechanism of phototransduction

light hits rhodopsin (visual pigment), which activates transducin (G-protein), which activates cGMP phosphodiesterase, which degrades cGMP, resulting in the closing of Na+, Ca2+ cGMP-gated channels

What does guanylyl cyclase do?

converts GTP to cGMP

How do we know channels are closed in the light?

Current in photoreceptors is decreased by light, measured through voltage-clamps

How does hyperpolarization in photoreceptors lead to depolarization of bipolar cells?

In the dark, glutamate is released from photoreceptors, which binds to metabotropic glutamate receptors in the bipolar cell. This activates phosphodiesterase so cGMP is cleaved and Na+ channels are closed in the bipolar cell. In the light, glutamate is no

How does neuron diameter effect conduction speed?

larger diameter = faster

primary erythermalgia

caused by increased Nav1.7 function, pain in feet and hands

Paroxysmal extreme pain disorder (PEPD)

caused by increased Nav1.7 function, ocular, mandibular, and rectal pain

Channelopathy-associated pain disorder

absent Nav1.7 function, experience no pain

About how long is the synaptic cleft?

~50nm

Why do axons have a lot of mitochondria?

Signal transduction requires a lot of ATP.

What is learning and what is its cellular basis?

Memory is the change in behavior after acquiring new knowledge. It is stored as the weight of synaptic connections based on experience

What is memory and what is its cellular basis?

the process by which knowledge is stored and retrieved. It is stored as the strength of synaptic circuits

The Lost Mariner

About a man from Pennsylvania who used to be in the military. He was old but thought he was young. He could remember his past clearly, but he used present tense to describe his military days. He was intelligent but struggled with tasks that took longer as

Why do sodium channels have 2 gates?

The ball and chain mechanism determines the length of time between consecutive action potentials, which encodes for stimulus strength.

How does loss of dopamine in the basal ganglia lead to the phenotypes we observe in Parkinson's patients?

The basal ganglia is involved in motor control, so when dopaminergic neurons in the basal ganglia die, control over movement is lost. Leads to shuffling gait, trembling, and rigidity.

How to measure receptive fields in the retina?

1. fix subject's gaze on some fixation point on a screen
2. record from cell in the pathway
3. shin spots of light in specific locations of screen
4. note where in space a light elicits a response

photoreceptor cell receptive fields

small and non-overlapping

retinal ganglion cell receptive fields

larger and overlapping

What happens when it is dark in the center of the receptive field?

1. cone depolarizes
2. glutamate released
3. a) on-center bipolar cell hyperpolarized
3. b) off-center bipolar cell depolarized (AMPA active)

What happens when there is light in the center of the receptive field?

1. cone hypolarized
2. less glutamate released
3. a) on-center bipolar cell depolarized
4. b) off-center bipolar cell hyperpolarized (AMPA inactive)

horizontal cells

Retinal neurons that mediate lateral interactions between photoreceptor terminals and the dendrites of bipolar cells.

retinitis pigmentosa

a progressive degeneration of the retina that affects night and peripheral vision

channelrhodopsin

A protein that, in response to light of the proper wavelength, opens a channel to admit sodium ions, which results in excitation of neurons.

neural pathway of somatosensory system

somatosensory receptors -> anterolateral column of spinal cord -(passes through medulla)-> thalamus > somatosensory cortex (in parietal lobe)
*3 total neurons
*there is an afferent pain fiber through dorsal root ganglion

A? fibers

-myelinated
-large diameter
-proprioception, light touch
-no thermal threshold

A? fibers

-lightly myelinated
-medium diameter
-nociception (mechanical)

C fibers

-unmyelinated
-small diameter
-innocuous temperature, itch
-nociception (mechanical, thermal, chemical)
- ~43 C temperature threshold

neurogenic inflammation

inflammatory peptides bind and cause Na+/Ca2+ influx, leading to action potentials

innocuous stimuli

nonpainful stimuli

noxious stimuli

painful stimuli, has S-shaped curve for pain

pain allodynia

pain to a normally innocuous stimulus

hyperalgesia

increased sensitivity to pain

voltage and current graphs for heat-evoked depolarization

voltage is normal upward "hill" shape
current is inward (a downward peak) and is faster

TRPV1

Na+/Ca2+ ion channel that opens from capsaicin or heat >43 C

heat-sensitive neuron mutations

TRPV1 and/or Nav1.7 KO's do not release NT

How can capsaicin be used to treat some conditions?

can kill sensory neurons to stop pain

TRPM8

cold sensor, menthol receptor

volt meter

a device used to measure voltage in the cell (like a thermometer)

voltage clamp

maintains a specific voltage (like a thermostat) so current/ion flow can be measured

List all the cells in the visual pathway and their locations.

1. photoreceptor - deep in retina
2. bipolar cell - medium deep in retina
3. retinal ganglion cell - least deep in retina, axon in optic nerve, and optic tract
4. interneuron - LGN (lateral geniculate nucleus) to visual cortex