Topic 2 - Neural Anatomy & Physiology Flashcards
Axon Hillock
Trigger zone
High degree of voltage gated channels here
All electrical signals converge here and once they reach threshold the potential will propogate down axon
Ranvier nodes
Spaces b/w myelin sheaths
High degree of voltage gated channels
Terminal branches
OUTPUT
Presynaptic membrane
Release neurotransmitters to communicate with other cells
Dendrites
RECEIVE INFO
post synaptic membrane
Bipolar neuron
Cell body in middle
Dendritic pole on one end, axonal pole on the other
Bipolar cells in the retina
Pseudo-unipolar neuron
Cell body off to side
Dorsal root ganglion
Peripheral sensory neurons (PNS) to spinal cord
4 mulitpolar neurons
Alpha motoneuron
Pyramidal neuron
Basket cell
Interneurons
2 types of channels important for APs
- Voltage-gated ion channels
- open in response to change in membrane potential - Ligand- or neurotransmitter-gates channels
- open in response to interaction with specific chemicals (ex. Synapses b/w neurons)
4 phases of the AP
- Resting potential -70 mV (-ve inside (Cl-), +ve outside (Na+))
- Depolarization Na+ enters so that inside becomes less -ve
- Re- and hyperpolarization (K+ leaves the cell making it more -ve)
- Re-establishment of resting potential (Na+/K+ pump bring some K+ back in and pushes Na+ out)
All or none principle
When one Na+ channel opens it fauses a riplling effect
Whats is the Refractory Period and what does it allow
Innactivation of Na+ channels once they’ve been opened
Hyperpolarization from K+ out (bc this bring cell furthher from firing potential of -70 mV)
Allows for one direction flow only
What does Ca2+ endtering the cell allow for?
Allows for vesicles with neurotransmitters to leave the cell
Temporal summation
Multiple EPSPs that occur in wuick sequence at same location, one neuron
Sparial summation
EPSPs that occur at different neurons/locations
Postsynaptic inhibition
The hyperpolarization of postsynaptic membrane (dendrites)
- this inhibits bc incoming signals will not be able to meet threshold for firing
Caused by cl- entering dendrites of post synaptic cell
-ve ion will hyperpolarze the cell (make it more -ve)
Presynaptic inhibition
Decreased neurotransmitter release from inout neuron
Caused by cl- entering presynsptic end of input neuron meaning less Ca2+ enters therefore reducing neurotransmitter release for next neuron
- w/o enough neurotransmitter released, Na+ cannot enter next cell so it cannot depolarizr
If neurotransmitters are excitatory, do they cause depolarization or hyperpolarization?
Depolarization
- they start the AP!
What is more abundant at the axon hillock, IPSPs or EPSPs?
IPSPs
Renshaw cell
Inhibitory cell — a collateral offshoot of alphamotorneurons
Sends inhibitory signals to other cell
Helps with signal-to-noise ratio by helping to activate the alpha motorneurons we actually want
Divergence
One cell providing input to many other cells
Convergence
Manys cells providing input to one cell
Disinhibition
When you send an inhibitory signal to an inhibitory cell (like a renshaw cell)
Descending inhibition
Prevents protective measures from taking place bc if so, muscle would inly extend and not be able to continue with the actual intended movement which is flexion
Disinhibition
- sends inhibitory signals to the interneurons that would normally send inhibiting signsls to the alpha motorneuron
Membrane resistance and things that influence it
⬆️ permeability = ⬇️ mem resistance
The ability of the membrane to resust things…
⬆️ diameter of axon & dendrites = ⬇️ mem residtsnce bc there are ⬆️ channels so ⬆️ membrane permeability
⬇️ diameter of cell body = ⬇️ mem resistance bc it less synaptic output is needed to cause AP
For a specific neuron, is the amplitude and duration of the AP the same?
Yes
Ex. Hard vs soft touch yields same amplitude
Does ⬆️er frequency leas to ⬆️er or ⬇️er stimulus intensity
⬆️er frequency = ⬆️er stimulus intensity
