Unit 1 Flashcards
specialization
adaptaton to serve a particular function
nervous system
network of cells that transmit signals throughout the body
-organize functions of the body
-characteristic cells
-networks of myriad functions
ganglion
cluster of neurons
neurophysiology
function of neurons; similar across neurons of every species
What is meant by neuron “activation?”
change in a neuron’s electrical activity
neuron doctrine
neurons are separate cells that communicate
neurons as a computational unit
neurons are computational units that comunicate with one another to achieve complex functions
synapse
site of communication between neurons
What do 86,000,000,000 neurons buy us?
-quadrillion synapses
-more neurons/connectivity = more brain power
connection between neurons/connections and brain power
more neurons/connections means more brain power
A specialized neuron is…
-suited to a particular function
-distinct from other neurons in its morphology
-distinct from other neurons in its physiology
dynamic polarization
idea proposed by Ramon y Cajal that activity propagates through the cell
neurites
the “wires;” a projection from a neuron’s cell body; specializations for transmitting signals
either axon or dendrite
soma
neuronal cell body; contain nucleus (genetic material), house organelles, and perform transcription and some translation (some in neurites)
dendrites
neurite responsible for receiving input from synapses, like an antennae
-“primary” dendrites connect to soma
-branches fork, giving arboreal appearance
-can be spiny
axon
neurite responsible for output; when neuron decides to activate, it transmits that information downstream via the axon to synapses
-neurons have a single axon
-branches can arise at right angles, more sprawling and less arboreal than dendrite
-can appear like beads on a string
dendritic arbor
collection of dendrites of a cell
primary dendrites
connect to the soma
dendritic spines
some dendrites are spiny, and synapses can form onto spines (vs. shaft) of a dendrite; afford compartmentalization (to regulate signaling) and can be grown and eliminated
proximal neurite
closer to soma; proximal dendrites are thicker than distal dendrites
distal neurite
farther from soma; distal dendrites are thinner than proximal dendrites
collaterals
term for branches of axons
axon initial segment (AIS)
proximal region of axon, attaches to axon hillock; where electrical signal in axon is generated, it is also enriched in proteins for sending this signal down the axon
axon hillock
site where axon connects to soma
axon terminals
swollen endings of axon, called bouton; half of a synapse and the site where neural activity in transformed into neurotransmitter release
neurotransmitter
chemical released by neuron to convey neural activity
synaptic vesicles
where neurotransmitters are packed; sent across synapse from presynaptic terminal to receptors on the postsynaptic terminal
synaptic cleft
gap between 2 cells where neurotransmitter is released
types (locations) of synaptic formation
1) axo-dendritic
2) axo-somatic
3) axo-axonic
4) dendro-dendritic
neuromuscular junction
special synapse between neuron (motor neuron) and muscle; high density of receptors ensures reliable response (i.e., very sensitive)
immunohistochemistry
powerful chemical approach to label microscopic structures (histology) using antibodies of the immune system; essentially allows visualization of highly specific, fine structures in nervous system
Can be defined by the following process:
1) Primary antibodies bind to an antigen (receptor) on structure of interest
2) Labeled secondary antibodies bind to the primary antibody
3) Complex soaked in substrate and exposed to color-changing enzyme
pyramidal neuron
bipolar neuron
chandelier neuron
double bouquet neuron
starburst amacrite neuron
tufted neuron
neuroglia (glia)
“nerve glue,” originally thought to control local environment of neurons; as varied and numerous as neurons, they signal and influence neural activity
glia vs. neurons
-glia have no synapses
-glia are less excitable than neurons
-glia are not typically polarized
astrocytes
“star cells” that contact blood vessels to regulate blood flow and support the blood-brain barrier
support neurons locally by…
-providing nutrients
-balancing ions, including pH
-removing neurotransmitter and ions from cleft
ependymal cells
line cavities in nervous system; motile cilia create flow in cerebrospinal fluid, providing nutrients and removing waste
myelinating cells
wrap axons of neurons with myelin to provide insulation and help signals propagate; give white matter its white (fatty) look
in brain/spinal cord: oligodendrocytes
in PNS: Schwann cells
oligodendrocytes
the myelinating cells of the brain/spinal cord; wrap axons with myelin to provide insulation and help signals propagate
Schwann cells
the myelinating cells of the PNS; wrap axons with myelin to provide insulation and help signals propagate
microglia
immune cells of the central nervous system, move to site of injury and perform phagocytosis (clean up waste)
EEG (electroencephalography)
changes in voltage on surface of brain can be detected with sensitive electrodes on scalp
voltage
measure of capability of charge to move between two points
membrane potential (Vm)
voltage or electrical potential across a membrane; difference in electrical potential inside vs outside the cell
polarization of neuron plasma membrane
neuron plasma membrane is polarized; inside of cell tends to be negative relative to outside (potential to move positive charge inwards)
How much of our energy consumption is contributed to the brain (creating voltage)?
about 20%; pure neuronal activity can burn a significant amount of calories (i.e., requires lots of energy)
balloonist theory
ancient view that fluid in ventricles inflated muscles via hollow nerves
signaling
transmission of information from one place to another; molecular signaling is ubiquitous, potent, and often slow (hormones)
Galvani
discovered electricity could make dissected legs of frog twitch; metal conducted electricity to exposed nerves (this implied that electricity could be used as a neural signal)
fast signaling with electricity
charged particles can transmit signals quickly through electricity; selective pressure to signal fast
Hodgkin and Huxley
recorded electrical activity from squid giant axon, serving as the first direct measurement of membrane potential
resting membrane potential
primes neurons to signal electrically; Vm = -65 mV; resting membrane potential is so low because of potassium leak channels that polarize the interior of the cell
spheres of hydration
when water surround NaCl and dissolves it; demonstrates how water dissolves ions
conductance (g)
the degree to which a material conducts electricity (e.g., high conductance opens ion channels); inverse of resistance
resistance (R)
inverse of conductance; R=1/g, in ohms
current (I)
directly proportional to voltage across two points and inversely proportional to resistance; I=V/R; lower resistance means more current flows
Ohm’s law
V=IR, or Voltage=Current*Resistance; for fixed voltage, current increases as resistance decreases
Important because it tells us:
1) If current can’t flow, there is no voltage
2) How voltage and current relate at a given resistance; if R is constant, V and I are proportional
plasma membrane
made up of phospholipids with hydrophilic heads and hydrophobic tails; allows proteins to be suspended in membrane and act as channels or pumps
alpha helix in plasma membrane
helps arrange hydrophobic R groups within the membrane
sodium “leak” channel
sodium can pass, but not other ions; lower conductance than potassium leak channels, which is why resting membrane potential is negative
synthesis of transmembrane proteins
synthesized in the rough endoplasmic reticulum (RER)
synthesis of other (non-transmembrane) proteins
synthesized on free ribosomes and are often found in the cytosol
electrochemical gradient
combination of diffusion and electrical field; ions flow “down it”
equilibrium potential
membrane potential at which there is no net diffusion of ions down concentration gradient; also called reversal potential
driving force
difference between the equilibrium potential and the actual voltage; tells us which way and how strongly ions will flow
Vdf=Vm-Eion
Nernst equation
formula for calculating the equilibrium potential (Eion) of each ion
Eion = (61.5mV/Z)*log[ion]outside/[ion]inside
Tricks:
-If the signs for charge (Z) and Eion align, [ion] is greater outside the cell
-For all positive ions, if [ion] is greater outside the cell, Eion will be positive
-For all negative ions, if [ion] is greater inside the cell, Eion will be negative
sodium-potassium pump
3 Na+ ions move outside the cell and 2 K+ ions move inside the cell; pumps ions against concentration gradient
What happens to Vm when you elevate [K+] outside the neuron?
Vm moves towards 0, as K+ inside the cell is less likely to leak due to changes in the concentration gradient
permeability
ease with which ions cross membrane; proportional to that of potassium (e.g., pk=1, pNa=0.05)
Goldman equation
membrane is at equilibrium between the reversal potentials of its permeable ions; ions that are more permeable (more pores/channels) bias the membrane potential more, which is why resting membrane potential is near EK+ (-65 mV)
feedback
when output is used as input; a system running with feedback is “closed loop,” while a system running without feedback is “open loop”
Where can synapses form?
along entire length of dendrite or axon
voltage-gated ion channels
open and close depending on voltage, establishing feedback systems; there is a linked ion pore and voltage sensor
linked ion pore and voltage sensor
comprise voltage-gated ion channels; there is a positively charged transmembrane domain and 4 subunits join to form channel
Key: as voltage changes, so do the forces acting on the charged domain
How does membrane potential influence voltage-gated channels?
1) Negative resting potential causes the charged side chains of the membrane to be pulled towards the inside of the cell
2) As membrane potential depolarizes, charged segment is released and the channel opens
positive feedback from sodium flow
at rest, all Na+ voltage-gated channels are closed, but as Vm reaches threshold, Na+ channels open and action potential is initiated
action potential threshold
if membrane potential doesn’t reach threshold at which Na+ channels open, there is no positive feedback, no action potential, and the membrane returns to rest; action potentials are all-or-nothing
if membrane does reach threshold, positive feedback from sodium flow occurs, resulting in explosive depolarization
action potential
also called “spike,” “nerve impulse,” or “discharge,” the action potential is generated in the soma and travels down axon, lasting on order of 1ms, and drives communication across synapses
refers to a Vm theshold being reached, causing a flow of Na+ into the cell, resulting in rapid depolarization, followed by Na+ channel closure and K+ channels opening, repolarizing and hyperpolarizing the cell
signal amplification of the action potential
myelin ensures current upstream produces a potent depolarization and the next node depolarizes strongly (increases voltage at next node)
helps transmit information down the long, thin axon; without large depolarization due to the action potential, depolarization in the soma would affect the distal axon minimally
nodes of Ranvier
myelinating glia leave gaps in myelin where channels cluster; each node must push the next past action potential theshold in order for an action potential to propagate down an axon
saltatory conduction
action potential jumping from node to node
Why does the action potential of a neuron stop near +50mV?
1) AP involves massive increase in Na+ permeability; according to the Goldman equation, this high pNa will move Vm near ENa
2) Driving force; we use driving forcr to calculate how much current will flow, and therefore how much Vm will change when channels open; Na+ current takes Vm near ENa, so driving force (and sodium current) steadily diminishes
driving force and current (AP)
large driving force means large current; small driving force means small current
polarity
refers to the potential difference across the membrane, and depolarization reduces this potential difference
voltage clamp
maintains the membrane potential at a set point, so can directly control whether voltage-gated channels are open or closed (via a patch); tool used to measure conductance (g)
equation for measuring conductance
Iion = gion(Vm - Eion)
Note: can also used Ohm’s law equation and substitute 1/g in for R
unitary conductance
how much flow a single molecule can generate; can be measured with voltage clamp patch
measuring conductance with voltage clamp
as cell is more depolarized, Na+ conductance is greater (i.e., more sodium channels open); this is observable by holding the membrane potential constant
Why doesn’t Vm stay at ENa when voltage-gated sodium channels open?
1) Sodium channels close themselves
2) Potassium channels help return to rest
inactivation of voltage-gated Na+ channels
inactivation is different than channel being closed; rather, it is blocked by ball-and-chain of amino acids (causes refractory period)
AP undershoot phase
part of action potential where the membrane is hyperpolarized due to the speed at which K+ channels close after repolarizing the cell
delayed rectifier
refers to the opening of voltage-gated potassium channels to repolarize the cell; “delayed” because it opens after the voltage-gated sodium channels and “rectifier” because it preferentially passes outward current; negative feedback
negative feedback from potassium flow
“delayed rectifier” voltage-gated potassium channels open in response to depolarization, causing hyperpolarization
effect of stronger depolarizing input in action potentials
causes faster rate of firing and pushes Vm back to threshold quicker after each AP; i.e., AP firing rate increases as the depolarizing current increases
local translation in axons
axons locally produce proteins needed at synapse and for metabolic support; local translation often necessary for survival
growth cones in developing axons use local translation
tetrodotoxin
blocks Na+ channels; for defense
alpha- and beta-toxins
shifts opening and closing of Na+ channels; to capture prey
apamin
blocks K+ channels; for defense
dendrotoxin
blocks K+ channels; for prey capture
Can a single axon form synapses with multiple dendrites?
yes, multiple dendrites can form a postsynaptic terminal with a single axon serving as the presynaptic terminals
vagus nerve
a cranial nerve connecting brainstem (vs. spinal cord) with head/body
neuron doctrine “debunked”
neuron doctrine widely accepted until the discovery of the electrical synapse (gap junction), which is a portal connecting cytosol of two neurons that allows direct ion flow from one neuron to another
Golgi belief about neurons
single structure (reticular)
Cajal belief about neurons
connected but distinct cells
chemical synapse
synapse that signals through release of chemical (neurotransmitter)
What do chemical synapses release?
many neurotransmitters can be released, and vesicles reflect the size of what is being released in that larger molecules have “denser” vesicles
active zone
source of NT release across the synapse (site where vesicles “fuse” with membrane and dump NT); located on presynaptic terminal
How many types of neurotransmitter can be released by a single neuron?
more than one type can be released
steps in chemical synaptic transmission
1) Neurotransmitter synthesis
2) Load neurotransmitter into synaptic vesicles
3) Vesicles fuse to presynaptic terminal
4) NT spills into synaptic cleft
5) NT binds to postsynaptic receptors
6) Electrical and/or biochemical response elicited in postsynaptic cell
7) Removal of neurotransmitter from synaptic cleft by transporter proteins/reuptake or simple diffuson
three major types of neurotransmitters
1) amino acids
2) amines
3) neuropeptides
amino acid neurotransmitters
small building blocks of proteins are co-opted; neurons that release amino acids have special proteins that load them into vesicles
ex. glutamate (excitatory synapses), GABA (inhibitory synapses), glycine
monoamine neurotransmitters
small organic molecules; neurons that release monoamines have special enzymes to synthesize them
ex. dopamine (DA), acetylcholine (Ach), norepinephrine (NE), serotonin (5-HT), melatonin
peptide neurotransmitters
small proteins that are typically loaded into oblong, dense-core vesicles; tend to act in a paracrine fashion (not just across synapses but diffusing to nearby cells)
ex. dynorphin, enkephalins, oxytocin, vasopressin, substance P
noncanonical neurotransmitters
1) nitric oxide - gaseous, paracrine signal, released by postsynaptic neuron (retrograde NT) through membrane (no vesicles) in response to NT
2) anandamide - hydrocarbon chain (fatty acid) in the endocannabinoid (eCB) system, retrograde signal
retrograde signal
NT transmission from postsynaptic neuron to presynaptic neuron; carried out by nitric oxide and anandamide
amino acid neurotransmitter synthesis and storage
often packaged at the presynaptic terminal, where they are found (this makes vesicle loading efficient)
monoamine neurotransmitter synthesis and storage
most can be synthesized from amino acids; often packaged at the presynaptic terminal, where amino acids are found (this makes vesicle loading efficient)
neuropeptide neurotransmitter synthesis and storage
usually packaged early and then transported
What is required to transform an action potential into NT movement from vesicles to synaptic cleft?
1) Calcium channels (AP to calcium)
2) Calcium-sensitive SNARE complex (calcium to vesicle fusion)
calcium chelators
molecules that bind with metal ions; help remove calcium from interior of neuron by binding free calcium
relationship between mitochondria and calcium
mitochondria accumulate calcium through pumps, removing it from the cytosol
voltage-gated calcium channels
have pore-forming and voltage-sensing domains (like sodium channels), and depolarization causes them to open (i.e., if AP propogates down the axon to the synapse they open); they are part of the synapse (presynaptic terminal)
calcium at the synapse (how NTs undergo exocytosis and are released)
1) Action potential arrives at axon terminal
2) Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal
3) Upon entry, Ca2+ activates synaptotagmin, causing SNARE proteins on vesicle and plasma membrane to drive fusion. Fusion of two lipid bilayers makes contents of vesicle free to leave presynaptic terminal (exocytosis)
4) NT diffuses across cleft and binds to ligand-gated ion channels on postsynaptic membrane
synaptotagmin
a calcium sensor that is activated by Ca2+ entry into the presynaptic terminal, it causes SNARE proteins on vesicle and plasma membrane to drive fusion
SNARE proteins
located on vesicles and the plasma membrane, they are activated by synaptotagmin to drive fusion
Loewi
concluded neurons communicate with chemicals because a stimulated vagus nerve changed the surrounding solution
GluSnFR
engineered protein (can be expressed through transgenesis - transfer of foreign DNA) that reveal NT (glutamate) by flourescing when binding; this allows us to visualize synapses at dendritic spines and is especially useful because individual synapses on the same dendrite are difficult to measure and distinguish
in vivo
in live animal
GluSnFR and ferret visual area
using GluSnFR, it was determined that individual synapses in ferret visual area have preferred visual motion and that neighboring spines have different visual preference
in vitro
in culture dish
ligand
any molecule that binds a receptor
receptor specificity
receptors are specific for NTs; that is, a receptor can only bind one specific NT
neurotransmitter specificity
neurotransmitters are not specific for receptors; that is, one NT can bind various receptors (i.e., divergence)
two types of neurotransmitter receptor
1) ligand-gated ion channel (ionotropic)
2) metabotropic receptor (GPCR)
To what type of receptor do amine/amino acid neurotransmitters bind?
both ionotropic or metabotropic
To what type of receptor do peptide neurotransmitters bind?
mostly metabotropic (GCPR)
ionotropic receptor structure
usually 5 subunits (pentamer) and each subunit can be coded by a different gene (heteromeric), so subunits can be mixed and matched, creating channel diversity
ionotropic receptor conformation change
instead of having a voltage-gate, when a receptor binds, the shape changes and pore opens
postsynaptic current
caused by ionotropic receptors; a synapse can be either excitatory or inhibitory depending on action
postsynaptic potential (PSP)
can be either excitatory (EPSP) or inhibitory (IPSP); PSP changes in postsynaptic cell as a response to NT binding to an ionotropic receptor
excitatory postsynaptic potential (EPSP)
occurs when channels open and positively charged ions enter the cell (depolarization)
inhibitory postsynaptic potential (IPSP)
occurs when channels open and negatively charged ions (Cl-) enter the cell (hyperpolarization)
electrical synapses
called the gap junction, at which no NTs are needed and ions simply cross - they can move in both directions; can cause fast voltage changes postsynaptically (like chemical synapses) and help synchronize spiking across cells
connexon
channel at electrical synapse; formed by six connexins
electric coupling
cells that form a gap junction are said to be “electrically coupled”
What happens when you lose gap junctions?
lose synchronization of these neurons in the brain stem
metabotropic receptors
NT binds receptor, Galpha subunit detaches from trimer and moves to enzyme or channel or activate second messenger cascade (cAMP or IP3/DAG)
ligand-gated ion channels vs. GPCRs
ligand gated ion channels are faster, but have shorter action than GPCRs
GPCR structure
part of a 7 transmembrane domain superfamily and are coded by one gene
orphan GPCR
a GCPR with no known ligand
G-protein signaling mechanism
1) G-protein bumps into activated receptor and exchanges GDP for GTP
2) Binding of GTP releases Galpha subunit, which can be either stimulatory or inhibitory, and it influences effector proteins or triggers second messenger cascade
3) Galpha inactivates by slowly converting GTP to GDP
4) Galpha and Gbetagamma recombine to start cycle again
Galpha signaling cascade
1) Galpha activates adenylyl cyclase (AC) which converts ATP to cAMP
2) cAMP activates PKA, a kinase that phosphorylates CREB, which binds DNA to alter gene expression
3) If Galpha is stimulatory, phosphorylation causes closing of K+ channels. If Galpha is inhibitory, no phosphorylation occurs and K+ channels open
GPCR amplification
idea that 1 activated G-protein can bind hundreds of NTs and consequently activate many cAMP molecules that have profound effects on the cell (gene expression)
signaling cascade convergence
idea that different G-proteins stimulate or inhibit AC, resulting in a push-pull method
Why is neurotransmitter receptor location important?
it is key to its function
autoreceptors
located in presynaptic terminal, receive the NT released from the same neuron; provides the neuron feedback and is often used for negative feedback tht can function as a safety valve (common effect of activating autoreceptors is inhibition of neurotransmitter release)
extrasynaptic receptors
receptors on postsynaptic neuron that sit on membrane outside of synapse; detect spillover, when transmitter becomes so concentrated that it has to escape synapse
ex. NMDA, which allows Ca2+ to flow in, triggers death cascades on some cells
How can NMDA receptors (metabotropic) on one cell promote survival and on others cell death?
response depends on molecules nearby; different signaling pathways by virtue of different second messenger systmes
multiple receptors for single NT
ACh has different structures of receptors, such as nicotinic receptor (ionotropic) and muscarinic receptor (metabotropic); both receptors bind ACh, but not all ligands are shared, meaning different effects are produced
receptor agonists
mimic actions of naturally occurring neurotransmitters; receptors are often named for agonist
receptor antagonists
block actions of naturally occurring neurotransmitters
synaptic integration
-process by which multiple synaptic potentials combine within one postsynaptic neuron
-most neurons in the brain and spinal cord receive thousands of synaptic inputs
-how neurons perform synaptic integration informs their computation
spatial summation
synchronous depolarization (when EPSP); looks like singular “powerful” spike when summated as EPSP or below threshold bumps when summation as EPSP and IPSP
temporal summation
rapid spikes in succession; looks like bumpy spikes when summated
axon potential propagation in dendrites
just as the AP amplifies depolarization to help signal down axon, dendrites amplify depolarization to help it reach the soma and AIS; they do so via compartmentalization
compartmentalization
dendrites can compartmentalize synaptic inputs, allowing them to amplify PSPs to help them reach the soma
ex. helps amacrine cells encode spatial visual information
neural coding
idea that neurons represent information through their electrical activity
spike rate
rate of action potential firing; increased by stronger depolarizing current
more spikes means more signaling (more NT release), which means more receptor binding and more EPSPs
rate code
information represented by the rate or frequency of action potentials of a neuron
temporal code
information represented by the precise timing of action potentials of a neuron
ex. retinal ganglion cells and the ability to use neuronal activity to recreate image an organism sees
What influences the rate and timing of action potentials?
1) Synaptic input and integration (summation)
2) Neuron state (e.g., history of second messenger signals, such as how much cAMP)
3) Electrical properties specific to the neuron (intrinsic properties; “electrical fingerprint”)
non-spiking starburst amacrine cell
as they develop, they lose their voltage-gated sodium channels and stop firing action potentials; spikes might impair function by linking dendritic compartments
relationship between ion channels and neuronal activity profiles
a neuron’s particular response is defined by the complement of ion channels in its membrane; these unique intrinsic properties allow neurons to specialize
three neuronal activity profiles
1) transient - lasting for a short time
2) sustained - sustained spike; neurons that sustain activity allow brief events to trigger prolonged effects (compliment metabotropic signaling)
3) rhythmic - patterned spikes; neurons that are rhythmically active can keep time or “pace” (pacemakers)
sodium channels and temporal spike profile
inactivation (via ball-and-chain) creates refractory period that sets limit on spike rate; activation creates relative refractory period that further shapes spike rate
i.e., switching between active/inactive establishes a rhythm
In what ways do differences in ionic currents arise from differences in ion channel?
1) Selectivity (potassium, sodium, calcium, chloride)
2) Gating - circumstances that cause the pore to open and close
3) Kinetics - the speed of opening and closing
ion channel superfamily
ion channels with different gating (i.e., what ions they pass) are organized in families
Kv channel differences
different Kv channels within the superfamily activate very differently and have differing kinetics; some are fast and sustained, some are fast and transient, and others are slow; many also require additional depolariation to obtain the same effect
transient neurons
spike that lasts for a short time; underlying proteins are transitory excitatory channels and highly responsive inhibitory channels
again, the ultimate idea here is that ion channels can greatly influence the neuronal profile, allowing neurons to specialize
sustained neurons
spike that is sustained and complimentary to metabotropic receptors; underlying proteins are sustained excitatory channels and a lack of inhibitory channels
again, the ultimate idea here is that ion channels can greatly influence the neuronal profile, allowing neurons to specialize
spike train
cycles of calcium, sodium, and potassium channel activation; opening and closing of channels modifies rhytmic activity (this is how pacemakers work)
T-type calcium channels
drive burst-firing (rapidly repeating action potentials)
calcium-activated potassium channels (KCa)
potassium channels activated in response to calcium channels; calcium binds to binding site on KCa channels, prompting K+ to leave the cell and hyperpolarize it; common in burst-firing
neuronal pacemaking
-is important for rhythmic movement
-can be generated by intrinsic properties
-involves cycles of spiking
receptor autoradiography
deposit of radioactive isotopes at receptors to identify the location of a receptor; relies on a radioligand that binds to the receptor
radioligand
a ligand that is radiolabeled; allow us to visualize where NT receptors are available in vitro and in vivo
autoradiography vs. immunohistochemistry
in IHC, antibodies can be generated that recognize antigen on NT receptors, but antibodies don’t reveal capacity to bind ligand
radioligands are also applicable for labeling in vivo
PET scan
injection of radioactive glucose allows measurement of deposition of radioactive glucose, which is higher in tumors and epileptic foci
