Lecture 2 Flashcards
RMP range of cells
-65 to -85
RMP of neuron
-70
2 causes of RMP
- fixed anions and uneven concentration of ions across cell
dendrites
receive signal and transmits it to cell body
axon hillock
part of neuron cell body where axon binds - generates the action potential
cell body
metabolic center of neuron and houses nucleus
synaptic cleft
space between axon terminal and dendrites of neuron, neurotransmitters are released here
proprioreceptors
receptors in muscle or joints that sense and send information about relative body position
flow of neuron stimulation and action potential generation
Na+ LGIC opens –> Na+ depolarization wave to axon hillock –> Na+ VGIC in axon hillock opens and causes depolarization –> action potential conducts down axon
factors affecting amount of depolarization
amount of Na+ entering, how long LGIC is open, how much neurotransmitter in cleft and how long it remains
threshold of neuron
-55, after this action potential cannot be stopped
cause of graded potential
Na+ LGIC opens and Na+ comes in and causes depolarization OR Cl- LGIC opens and Cl- comes in causing hyperpolarization
cause of steep depolarization
Na+ VGIC in axon/axon hillock opens, Na+ enters
cause of repolarization
slower opening of K+ VGIC, K+ exits cells and repolarizes, Na+ VGIC also closed
cause of after hyperpolarization of action potential
hyperpolarization by K+ continually exiting cell
Na+/K+ restores RMP
graded potential
graded, 2 types EPSP and IPSP
EPSP
excitatory, graded potential, caused by LGIC for Na+ opening and depolarization
IPSP
inhibitory, graded potential, caused by LGIC Cl- openinng and Cl- enters cells and causes hyperpolarization
2 ways intensity of sitmulus is encoded
frequency of action potential
recruitment = number of neurons that are sending action potentials
why refractory period is important
otherwise action potential can go one after another and muscles in perpetual contraction = tetany, diaphragm paralyzed
cause of absolute refractory period
Na+ VGIC: closed –> open –> inactive –> open, during absolute period Na+ VGIC are inactive so cant be opened
cause of relative refractory period
Na+ VGIC going from inactive to closed, some can those go to open phase but also harder since K+ exiting cell caused hyperpolarization
convergence vs divergence
convergence = many presynaptic --> 1 postsynaptic divergence = 1 presynaptic --> many postsynaptic
spatial summation vs temporal summation
spatial = multiple presynaptic synapse at different location generate EPSP to 1 postsynaptic and they build up to reach threshold temporal = 1 presynaptic generates many EPSP close together and it builds up
EPSP vs action potential
EPSP = graded, stimulated by Na+ through LGIC, max depolarizaiton = 0, summation, no refractory period
action potential = not graded (all or nothing), stimulated b Na+ through VGIC, max depolarization = +40, refractory period
CNS vs PNS
CNS = brain and spine PNS = everything else
glial cells
support cells - umbrella term for many cells
nucleus vs ganglion
nucleus = cell bodies in CNS ganglion = cell bodies in PNS
tract vs nerve
tract = axons in CNS nerve = axons in PNS
sensory neuron
sensory receptor –> brain
somatic motor neuron
brain –> skeletal muscle, voluntary movement
LMN and UMN
lower motor neuron: body in CNS and axon goes to sketal muscle
upper motor neuron - an internneuron - brain to LMN
interneuron aka associatoin neuron
completely in CNS
autonomic motor neuron
CNS –> innervates organs, glands, smooth muscles
myelination of CNS vs PNS
CNS = oligodendrocytes, wraps around multiple axons PNS = schwann cells, wraps around 1 axon
microglia
phagocytotic cells - like macrophages
astrocytes
support / caretaker cells for neurons, dilates blood vessel so more nutrients arrive,
2 factors affecting conduction speed
myelination and large diameter increases conduction rate
SNARE complex
protein complex that docks vesicle with neurotransmitter to the side of plasma membrane preventing it from randomly releasing neurotransmitter, activated by Ca2+ synaptotagmin
synaptotagmin
protein that is able to change conformation SNARE if Ca2+ activates it
flow of neurotransmitter release
Ca2+ VGIC opens –> Ca2+ enters cell –> binds to synaptotagmin –> complex causes SNARE to release vesicle with neurotransmitter
acetylcholinesterase
breaks down ACh to acetate and choline which is taken back up by presynaptic neuron to be reused, prevents ACh from staying in synaptic cleft and overstimulating
