Exam 1 Flashcards
fxn of glia
insulate support and nourish neurons
nissl stain
stains nuclei of all cells as well as a clump surrounding nuclei called a nissl body aka rough ER
Golgi stain
stains a small portion of neurons completely
golgi vs cajal views
golgi: everything is connected
cajal: no they’re not (neuron doctrine)
how many ATP per pyruvic acid
17
differentiation between axon and soma
no rough er and few ribosomes in axon. protein composition is different
parts of the axon
hillock, real axon part, and terminal
differences of an axon vs axon terminal
- MTs don’t extend into terminal
- terminal contains synaptic vesicles
- inside part of synapse has tons of proteins
- terminal has a bunch of mitochondria
purpose of dendritic spines
isolate various chemical reactions that are triggered by some types of synaptic activation
classification of neurons based on number of neurites
unipolar: 1
bipolar: 2
multipolar: more
most are multipolar
stellate vs pyramidal
in cerebral cortex, distinguished by shape of dendritic tree. all pyramidal cells are spiny, stellate cells can be aspinous
types of neurons based on connections
sensory, motor, and interneurons
golgi type I vs II
type I: long axons
II: short, local circuit neurons
astrocytes
type of glial cell, surrounds and cleans up synaptic cleft, also have nt receptors, can control other substances like potassium as well
myelinating glia
two types: oligodendroglial (in CNS) and Schwann (peripheral)
microglia
remove debris left by dead or degenerating neurons or glia
cation vs anion
cat is + an is -
electric potential aka voltage
, is the force exerted on a charged particle; it reflects the differ- ence in charge between the anode and the cathode
electrical conductance
the relative ability of an electrical charge to migrate from one point to another. depends on number of ions and the ease in which these particles can travel through space
resistance
inverse of conductance
calcium pump
pumps calcium out
pore loop
part to the 3ary structure that makes a hairpin turn, used to select by shape and r groups
what is the membrane the most sensitive to
potassium, lots of introduced extracellular potassium depolarizes the cell
blood brain barrier
limits movement of potassium and other substances into the brain
potassium spatial buffering
when one astrocyte picks up excess potassium and like shifts it everywhere
oscilloscope
special type of voltmeter used for action potentials, records rate over time
phases of an action potential
- rising phase (rapid depolarization until 0mv)
- overshoot (0-40)
- falling phase
- undershoot (to about -80) aka after-hyperpolarization
- restoration of resting potential
how long does an action potential ask
about 2ms
steps of ion channels and stuff
- na+ permeable channels. open, so na+ crosses the membrane, depolarizing it. if it goes past a threshold an action potential is triggered
- na+ channels close
- k+ channels open, so potassium rushes out
- k+ channels close
maximum firing frequency
about 1000hz
absolute refractory period
once an action potential is initiated it is impossible to initiate another for about 1ms
relative refractory period
can be difficult to initiate another action potential for several ms after end of absolute refractory period. this is because the membrane stays hyper polarized until the voltage gated potassium channels close
voltage clamp
clamps the membrane potential at any value, and then look at the changes in channels opening by looking at current
what activates/inactivates/deinactivates sodium channels
- activated by depolarization above threshold
- inactivated (closed and locked) by positive membrane potential
- deinactivated (unlocked) after membrane potential is restored
they stay open for about 1ms and cannot be opened again until membrane returns to a negative value (this causes absolute refractory)
structure of a voltage gated sodium channel
4 domains, each domain has 6 transmembrane alpha helices. these domains clump together to form a pore, which twists based on voltage. na+ ions are stripped of most of the water as they pass into the channel. there is a voltage sensor of positively charged AA residues in helix 4
patch clamp
clamp a very small patch of the membrane, hopefully one that just contains one channel. clamp the potential at a certain value and look at current
stuff about voltage gated potassium channels
they’re a delayed rectifier. also open when the membrane is depolarized but takes them about 1ms to open
how does action potential conduction velocity relate to axonal diameter
wider neurons mean faster speed
saltatory conduction
using myelin sheath to skip from node to node
spike initiation zone
area that has a bunch of voltage gated sodium channels, so the AP probably starts there
electrical synapses
- happen at gap junctions, which have a diameter of about 1-2nm and are nonselective
- very fast and failsafe, found in reflexes
- causes a postsynaptic potential
- usually bidirectional
- helps coordinate oscillations and synchrony
synaptic cleft
- 20-50nm wide
- filled with fibrous extracellular protein
two kinds of presynaptic vesicle things
- synaptic vesicles (50nm diameter)
2. secretory granules (100nm diameter) aka dense core vesicles
membrane differentiations
presynaptic: active zones
postsynaptic: postsynaptic density
differentiation of cells based on what they connect to
- axodendritic (connects to a dendrite)
- axosomatic
- axoaxonic
- axospinous
- dendrodendritic
grays type I vs II
gray's type I: -membrane differentiation is thicker on postsynaptic side -usually excitatory gray's type II -symmetrical membrane differentiation -usually inhibitory
neuromuscular junction
the synapse between a motor neuron and a skeletal muscle
3 categories of neurotransmitters
- amino acids
- amines
- peptides
which NTs are most common in fast junctions
glutamate, GABA, gly in CNS, ACh in neuromuscular
where are the different NTs made
in axon terminal: amino acid and amine, concentrated into a vesicle by transport proteins
in soma: peptides. made in rough ER, split in Golgi, one of the fragment is the NT. secretory granules bud off from Golgi and are carried to axon terminal by axoplasmic transport
role of voltage gated calcium channels
depolarization of the terminal membrane causes these two open, so Ca2+ rushes in. this causes synaptic vesicles to be exocytosed. secretory granules are a little further away and generally require multiple APs to activate
types of NT receptors
- transmitter gated ion channels (generally not as selective as voltage gated ion channels)
- G-protein-coupled receptors
EPSPs vs IPSPs
excitatory postsynaptic potential: created when a transmitter gated ion channel lets in positive ions (like ACh and glutamate)
IPSP: negative ions (gly, GABA)
how do g protein coupled receptors work
- nt binds to a receptor
- this activates G proteins, which activate effector proteins
these effector proteins can be ion channels or enzymes that synthesize second messengers, which diffuse into the cytosol and can activate other things that regulate ion channel function and cell metabolism
another name for G protein coupled receptors
metabotropic receptors
autoreceptors
presynaptic receptors. usually g-protein-coupled. allows regulation of NT production
how does synapse get cleaned up
- simple diffusion out of synapse
- reuptaken by a transporter protein and either reused or degraded
- enzymatic destruction in the synaptic cleft
receptor antagonist
binds to receptor and blocks the NT
receptor agonist
binds to receptor and mimics NT
synaptic integration
multiple synaptic potentials combine in a postsynaptic neuron. includes both spatial and temporal summation
shunting inhibition
when you have a really strong inhibitory synapse at a really late site, so earlier excitatory synapses can’t do SHIT
criteria to be a NT
- must be synthesized and stored in presynaptic neuron
- must be released upon stimulation
- must produce a response in postsynaptic cell that can be experimentally replicated
immunocytochemistry
an NT from a different animal is injected into an animal, then withdraw antibodies. these antibodies are tagged and applied to brain tissue, so you can label the cells that contain the NT
in situ hybridization
create a probe that binds to mRNA you want to look at
microiontophoresis
technique where u use a really small pipette and inject some of your NT candidate and measure postsynaptic membrane potential
rule of NTs
no two NTs bind to the same receptor, but one NT can bind to many receptors. each of these is a receptor subtype
three ways to identify NT subtypes
- neuropharmacological analysis (see how the NT affects different cells OR see how antagonists/agonists of the NT affect different cells)
- ligand binding methods (label the ligand and see if it binds to receptors on certain membranes. ligand could be NT, agonist, or antagonist)
- molecular analysis (look at structure of polypeptides and subunits that make up the receptors)
co-transmitters
when two or more transmitters are released together from one terminal. often happens with amino acid OR amine and peptide. the AA/amine are often used to differentiate neurons
production of acetylcholine
choline acetyltransferase in the soma adds an acetyl group from acetyl CoA to choline. transport of choline into the neuron is the rate limiting step. cells also released acetylcholinesterase which breaks ACh down in the cleft
catecholamine synthesis
tyr-> dopa-> dopamine-> norepinephrine -> epinephrine. all share a catechol group. regulate movement, mood, attention
serotonin synthesis
tryp-> 5-HTP -> serotonin aka 5-HT
regulates mood, emotions, sleep
GABA synthesis
comes from glutamate
retrograde messengers and a specific type of them
go from post to pre. an example is endocannabinoids, which don’t need to be packaged in vesicles bc they are made quickly and, being small lipids, diffuse across membrane. usually g-coupled and help to close Ca2+ channels
how is NMDA receptor voltage and transmitter gated
mg2+ clogs the pore and only pops out when the membrane is depolarized. but you still need glutamate to bind to it to open it
5 steps in G protein operation
- each G protein has 3 subunits, alpha beta and gamma. GDP is bound to alpha subunit. whole thing is just floating around
- if the protein bumps into a receptor that has the NT attached, then it exchanges a GDP for a GTP
- the G protein splits into alpha and beta gamma complexes
- g alpha subunit is an enzyme that breaks down gtp to gdp
- alpha and beta gamma complexes come back together
shortcut pathway
G protein to ion channel pathway. fast and requires no intermediary
second messenger cascade
the process from an NT to a g protein to several other steps to a downstream enzyme
modulation
sometimes G coupled proteins indirectly effect stuff, like they cause a protein kinase to close a potassium channel. this makes the cell more excitable
mitchell
Mitchell miya
lobes of the brain
frontal in front, parietal on top, occipital in back, and temporal on bottom
fissures of the brain
central sulcus between frontal and parietal, sylvian fissure in middle between frontal temporal and parietal
which motor protein helps anterograde transport and which is retrograde
kinesin: anterograde
dynein: retrograde
muscarinic vs nicotinic receptors
- Ach
- muscarinic is G-coupled & involved in contraction of smooth muscle
- nicotinic is ionotropic and involved in muscle contraction
nmda vs ampa
- glutamate
- AMPA: allows Na & K to flow quickly through
- NMDA: also requires depolarization, allows Ca, Na, and K to flow through
