Neurobio 2 Flashcards
Explain what the spike threshold is.
The amount of depolarization that a membrane potential must cross to initiate an action potential
– When crossed → action potential MUST happen!
What are 3 advantages of communicating with electrical synapses? And a disadvantage?
Fast, reliable, and allow for spike synchronization
Disadvantage: less flexible - signals cannot be modified (stronger/weaker)
If you have electrodes in two cells that are connected by a synapse. How can you determine whether the synapse is electrical or chemical?
Electrical if… spikes are synchronized in both the cells
Chemical if… there’s a millisecond delay
Where does chemical synapses delay of about 1 msec come from?
Calcium channels are opening slowly
Where does a spike start
in the axon hillock
Difference between ELECTRICAL synapses and CHEMICAL
electrical – gap junctions
chemical – neurotransmitters
Gap junctions
Direct transfer of current from one cell to the next
Spike synchronization
Causes spikes to happen at same time in both cells
Steps of chemical synapses
1- action potential depolarizes axon terminal
2- calcium channels open
3- Ca++ gushes in
4- Ca++ binds to protein
5- synaptic vesicle binds to post synaptic membrane
6- vesicle fuses with membrane
7- neurotransmitter crosses synaptic cleft
8- NT diffuses across cleft
9- NT binds to channel
10- channel opens (or closes)
11- current in or out (post-synaptic potential)
depol/hyper
PSPs
depolarization: epsp
hyperpol: ipsp
NEUROTRANSMITTERS
AMINO ACIDS (not synthesized at terminals)
- GLU: most common, excitatory NT (CNS)
- GABA, GLY: inhibition (Cl-)
AMINES
- Acetylcholine (ACh): excites muscles
- Norepinephrine (NE): symp post-ganglion
PEPTIDES (synthesized @ cell body)
- substance P: co-released along w/ other NT
- B-endorphine: binds opiate receptors
What are dense core vesicles? How do they get to the presynaptic terminal? Under what circumstances are they released?
Dense core vesicles: secretory granules that get released when they are super excitatory; vesicle full of peptide
– Co-released with transmitters
Don’t get released in active zone (full of mechanism of clear transmitters); released in terminal
What happens to the extra membrane that is added to the presynaptic terminal as vesicles fuse with the membrane?
Vesicle opens and empties its neurotransmitters into the synaptic cleft; & becomes a vesicle again (recycles)
Why is the neuromuscular junction (nmj) the most thoroughly studied vertebrate synapse? What is an important difference between the nmj and synapse in the CNS?
- motor end plate
- Easily accessible, the most powerful, and least invasive
- HUGE release of (200) vesicles released at nmj
axo-dendritic
axo-somatic
axo-axonic
axo-dendritic: more often excitatory (synapse @ dendrite of cell 2)
axo-somatic: synapse @ cell body of cell 2
axo-axonic: (pre-synaptic inhibition): synapse @ axon of another cell
Peptide neurotransmitters are generally released
with high frequency trains of spikes
Postsynaptic potentials (PSPs) generally last much longer than action potentials. Why is that adaptive, i.e. what function does that serve?
- Allow for signals to be modified (stronger/weaker)
- Action potential is a momentary event
- Principle of summation - More likely to overlap (both for temporal and spatial)
- -spatial is more likely to add together
Why does opening chloride channels, with glycine or GABA for example, inhibit a neuron even if the chloride equilibrium potential is the same as the resting potential? If a single inhibitory synapse is activated in such a neuron, would you see an ipsp?
- chloride equilibrium usually same as resting potential; will always try to go back
- if sodium depolarizes - chloride will try to balance it out
EPSP
-always depolarizing direction
ionotropic
metatrobic
iono: DIRECT action of neurotransmitter on an ion channel
meta: INDIRECT postsynaptic response, mediated by g-proteins
- direct action of g-protein: can directly act on channels or rev up an enzyme
- indirect action of g-protein: 2nd messenger
Ecl always ___ threshold
below
Synapses with post synaptic receptors that open channels that are equally permeable to sodium and K+ ions… what’s true?
Synapse would be excitatory because more current flows in than out through channels
We know that the nicotinic acetylcholine receptor opens a nonspecific cation channel (i.e. positive ion can pass through). Explain why opening this channel causes a depolarization. In other words, why is the inward sodium current greater than the outward potassium current? Which way would calcium flow, in or out?
- Depolarization caused by more sodium goes in and potassium comes out
- driving force is greater on sodium
What is meant by the term “shunting inhibition?” Describe the spatial arrangement of excitatory versus inhibitory synapses onto the neuron.
Shunting inhibition: stopping epsp from getting to soma - usually done by chloride
- Chloride CANCELS OUT EXCITATION by activating
excitatory : on periphery of dendrites
Inhibitory : cell body or basis of dendrites
What are two different ways to increase the length constant of a dendrite. Why is the length constant important functionally?
- close ion channels
- increase diameter - evolution - decreases resistance
Important because positive current leaks out / amplitude falls off with distance
Graded potentials
vary in amplitude
Spatial summation
v
Temporal summ
Spatial- different location
temporal- same location, different times
Synaptic potentials are:
LOCAL
Characteristics of synaptic potentials
- length constants vary w/ resistance (membrane and internal)
- -decrement over distance (they change)
- -positive current travels both ways (leaks out)
What would happen if activated synapse on neurons w/ GABA, which opens chloride channels?
PSP would be flat (nothing would happen)
-chloride happy at equilibrium
Explain 2 different general ways that activated G-proteins can exert their effects in a postsynaptic neuron?
- Go straight to a channel
- Go straight to an enzyme (longer turn responses/effects, more powerful, affects multiple channels)
Metatrobic
indirect postsynaptic response, mediated by g-proteins (Guanine nucleotide binding proteins)
- -GPCR: g-protein binding receptor
- -activates g-protein by trasnmitter binding to receptor: moves through cell and does something else
has BETA and ALPHA segments
GDP attached
if activates: segments fall off into 2 pieces and both get activated
What are 2 potential advantages of metabotropic synapses over ionotropic synapses? What is a disadvantage in using metabotropic synapses?
- Lasts longer & amplify the signal
- Slower to respond