neuro Flashcards
oligodendrocytes
glial cells that make myelin sheath
ependymal cells
glial cell, border areas next to ventricles in brain
microglia
glial cell, cells from immune system that help 2 clear up dead material, police these areas
astrocytes
glial cell found around synapses - help regulate potassium ion levels
neurons vs glial cells- who is post- mitotic- what does that mean?
only neurons. glial cells can indeed divide. leads to brain tumors
what are schwann cells in peripheral nervous sys? what do they do?
in peripheral nervous system (outside brain/spinal cord), schwanns wraps around axon many times, forming the myelin sheath
spaces between myeline sheath name
node of ranvier
what is myelin sheath and what does it do?
The insulating envelope of myelin that surrounds the core of a nerve fiber or axon and that facilitates the transmission of nerve impulses, formed from the cell membrane of the Schwann cell in the peripheral nervous system and from oligodendroglia cells.
issues when myelin sheath malfunctions
multiple sclerosis. diabetics who have trouble with feet- myelin not properly layed down
concentration of potassium inside and outside of cell
120 mM inside, 4 mM outside
concentration sodium inside/outside cell
low inside, high outside 14, 140
concentration of Cl- inside , outside cell
low inside, high outside 4, 105 mM
permeability of potassium vs sodium
potassium has highest permeability
describe how electrical force and chemical diffusion interact with each other
as K diffuses out of cell, (diffuses down its gradient) inside of cell becomes negative. pos voltage builds up outside of cell. tends to push K + back into cell. chemical and electrical are roughly equal, but you do have positive leakage of K+ out of cell, and Na+ leakage into cell
how does the cell handle na,k leakage?
Na/K pump; pumps Na+ out of cell, K+ into cell
what happens to permeability when you stimulate a nerve?
leaves resting state, enters an active state in which cell’s membrane is more permeable to sodium than it is to potassium
Using the nernst equation, -87 mV inside the cell; why is this not the cell’s voltage?
that would be if cell was ONLY permeable to potassium. in reality it is closer to -80
Mechanism for sending electrical signal
i. The axon is normally + on outside and – on inside ii. Resting membrane potential is at -70mV (on inside of axon) iii. Our action potential begins at the axon hillock iv. Axon potential gets triggered in an “all or nothing” response in about 1msec (if we get the action potential we get it all v. Changes to +35mV on the inside of the axon and negative on the outside vi. As it increases this is depolarization and then as it drops back down it is repolarization
Resting membrane potential is ____
-70 mV inside cell. (Permeability for potassium is greater at rest and it will diffuse to outside of cell and bring + charges outside, leaving inside more negative)
what mechanism makes membrane selectively permeable to the ions?
The membrane of the cell is selectively permeable because ions have to move through special voltage gated ion channels (respond to potential difference across the membrane)
What is responsible for the ion distribution (three experiements)
- Axon at 4 celsius and the RMP is 0mV
* This suggests there is a metabolic event required - Take an axon at rest with no stimulation and put radioactive sodium 22 ion on the outside of axon. Sodium 22 ion will slowly show up on the inside of the cell
* This is the “sodium leak” which indicates the axon is not exactly impermeable to sodium at rest. This leak brings some positive charge inside the axon - Use oubain, a poison that attacks Na+/K+ pump. The resting membrane potential goes to 0mV
- Pump brings sodium outside and potassium inside to set up concentration gradient for ions. Pump is electrogenic because it puts more positive charges on the outside than inside so it helps create potential difference
- With oubain we kill the pump and we don’t have the gradient and we don’t have the potential difference in the axon
explain where you would see depolarization, repolarization and hyperpolarization on the resting membrane potential curve and what they mean
- During an action potential, permeability for sodium is greater and it diffuses into the cell and brings + charge inside, leaving the inside more positive. This is depolarization (increase conductance of sodium)
For repolarization, potassium channels open up again (even more than at rest) and let potassium leave again and take + charge outside and make – inside again
Refractory period:
a point where additional stimulus will not give u another action signal. (you already have one going on)
Its important because you only want an action potential going in ONE direction.
Refractory period has 2 parts; absolute (length of curve) and relative (outside of curve)
experimentally, if you can stimulate an axon in the middle, can you get action potentials going in both directions? can the body do this?
experiment: yes.
body: no
normally we start at axon hillock where we have only voltage gated Na channels; lets us only conduct one way. cell body does not have ion channels. only axon/axon terminal has them.
myelination has what effect on propagation of action potential?
changes electrical properties . Increases resistance, decreases capacitance- this makes local current flow go quicker. (myelinated axons are really fast)
- spaces between myelin sheaths = node of ranvier.
- In nodes of ranvier: LOTS of capacitance (lots of stored charge). Action potential jumps from node to node; called saltatory conduction
- this action is extremely fast
what 2 things affect neuron conduction velocity?
- myelination (by far most important)
- diameter (bigger is faster)
how do we get rid of Ach in the synpatic cleft?
•To turn over Ach, make it not sit indefinitely in cleft, is by using enzyme called Ach esterase . Degrades Ach. Esterase enzyme takes Ach, breaks into acetyl + choline. Acetyl group floats away. Choline taken back up by presynaptic terminal, recycled into new Ach .
why is our resting membrane potential around -70 mv?
Potassium responsible for resting membrane potential
Ek = -85
Potassium sets membrane potential bc it’s the most permeable ion. Can move toward its equilibrium potential. Therefore resting membrane potential follows K equilibrium potential.
Ek = -60 mv * log [ki]/[ko]
Membrane potential = -RT/ZF * ln ((Pk[Ki] + Pna[Nai] + Pcl [Clo])/ (P[Ko] + Pna [Nao]+ Pcl[Cli])
Take home message: must account for moth electrochemical and permeability. Goldman is the best estimate for calculating membrane potential, and gets -70 mV.
equilibrium potentials for sodium and potassium and how these determine processes in our body?
Ek = -85 mV
Ena= +65
RMP = -70 due to potassium having highest permeability
action potential: +35 mV, more permeable to Na+ during action potential
saltatory conduction
when nerve impulse jumps from node to node along myelinated axon during an action potential
(from latin saltatorius, to leap )
name an excitatroy neurotransmitter and what it does when released
Acetylcholine, Ach
*action potential triggers opening of calcium channels
calcium causes released of Ach
when released, binds to ligand gated ion channels , Ach receptors (postsynaptic membrane receptors). allows sodium through its channel. influx of na+ allows depolarization, action potential is generated
agonist vs antagonists, and examples of each
- Agonists: mimics Ach. Bind receptor and mimic action.
- Nicotine- nicotinic receptors because they can be mimicked by nicotine
- Antagonists: agent that bidns receptor and blocks action of Ach
- Curare- poison from a south american frog- blocks ach , no muscle movement. This is how you would hunt a monkey.
effect of eserine/serine
inhibits Ach esterase aka the thing that breaks down Ach. So you don’t break down Ach, it stays in synaptic cleft, you get MORE skeletal muscle contraction. but if you have a high enough dose, you get continual stimulation-
nerve gas: diaphragm goes into spasms
describe a muscarinic receptor, and agonist and antagonist for it. is nicotine always a functional agonist? why or why not?
- muscarinic: different type of Ach receptor, found in viscera. not a ligand gated ion channel- tied to and opens K+ channels. hyperpolarizes the membrane.
- agonist: muscarine
- antagonist: belladonna plant
- nicotine not a functional agent in the viscera, where there are muscarinic receptors. nicotine can’t bind to muscarinic receptor
Excitatory vs Inhibitory post synaptic potentials
EPSPS’s (excitatory post synaptic potentials.) When they bind their receptors increase conductance to sodium, potassium simultaneously.
ex: glutamate, aspartate
IPSPS Will increase conductance of chloride ions
Ex: glycine, GABA.
Both EPSP’s and IPSP’s create local current flows- when summed, if excitatory>inhibitory, reach axon hillock , fire an action potential
T/F: when ach bidns to its receptor, increases conductance to Na + and K+ simultaneously.
True!
EPSPs vs IPSP’s: what does each do to the permeability of various ions?
EPSP: increase permeability of sodium (aka depolarization)
IPSP: increase permeability of potassium + chloride ions (hyperpolarization)
if neuron is getting excitatory and inhibitory inputs, how does it do anything?
its the summation of all of those inputs; if summation of those current flows if strong enough, reach axon hillock ,will fire an action potential
adrenergic vs cholinergic receptors
Autonomic receptors are broadly divided into those for ACh (cholinergic receptors) and those for catecholamines such as NE or EPI (adrenergic receptors or adrenoceptors).
cholinergic: muscarinic, nicotinic
adrenergic: alpha causes smooth muscle contraction, beta cause smooth muscle relaxation. signal is adrenalin or epinephrine. ex: dopamine.
Generally, the PNS or cholinergic induces the ‘digest and rest’ effects while the SNS or adrenergic mimics the effect of the ‘fight or flight response’ as in the case when there is too much excitement. Inducing the digest and rest means that the gastrointestinal (GI) and genitourinary (GU) systems’ effects are increased (excited) while imitating the fight or flight response excites all other system effects except the GI and GU.
parkinsons cause and treatment
lack of dopamine. can’t give dopamine bc it wont cross blood brain barrier. DOPA treat parkinsons patients, DOES cross parkinsons patients. Load cells with more DOPA so they can then make more dopamine.
what do we mean when we say dopaminergic receptors down regulate?
pull receptors off their own membrane- harder to stimulate. Need more dopamine to get same level of stimulation. So basically if u take dopamine drugs, down regulate, takes more and more drug to get the same effect
what are endogenous cannabinoids?
Our internal cannabinoid system; free fatty acids- AEA and 2-AG: released by cells to bind receptors. System feeds back from post synaptic cell to pre synaptic cell. Released from post synaptic cell to bind a receptor on pre synaptic cell and decrease release of neurotransmitter
Really important feedback in developing nervous system
Dale’s law, and why its not always true
Neuron releases one neurotransmitter. Whether it comes out and branches, innervating different things, always releases the same neurotransmitter . (one neuron one NT)
HOWEVER:
Synpatic terminals can have co-localized things: dopamine can be paired with GABA, CCK, growth hormone releasing factor.
Have a main NT that’s released but can also release something else with it. Depends on the type of stimulation coming in.
what will happen if you remove someone’s hippocampus?
can no longer store long term memories
why? hippocamus rich in NMDA receptors; increase calcium conductance, bidn calmodulin. this increases phosphorylation of key proteins and permanently changes post synaptic function
which neurotransmitters do parasympathetic/sympathetic release?
para: Ach
symp: NE
**can also release Ach , ex- sweating**
