Module 3 Lecture 1 Flashcards

1
Q

what is Ramón y Cajal’s law of dynamic polarization

A

neurons are directional; they take in input and send output

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2
Q

synapse definition

A

where two neurons come in very close proximity to communicate with each other
- any given neuron is likely both pre- and postsynaptic

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3
Q

what theory did Golgi have about neural communication

A

reticular theory; thought the nervous system was one continuous web, and not a bunch of cells communicating

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4
Q

Cajal’s neural theory

A

that there are distinct cells that talk to each other

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5
Q

two classes of synapses

A
  • chemical: one neuron secretes NT that activates receptors on another neuron
  • electrical: neurons are in electrical continuity with each other via interlocking proteins w/ ion channels
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6
Q

what forms the gap jxn in electrical synapses

A

2 connexons

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7
Q

where were gap jxns first found

A

in the crayfish lateral giant interneuron
- if you give a crayfish an aversive stimuli, they have an escape reflex that takes a tiny amount of time to execute; mediated by electrical synapses

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8
Q

gap jxn structure

A
  • each is made of 6 connexin subunits, each with 4 TM regions
  • large, non-selective pores
  • synchronization of electrical & second messenger signals
  • has binding sites for PKA, PKC, MAP kinase, calmodulin
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9
Q

how did the Long 2002 experiment impact our understanding of electrical synapses

A
  • they simultaneously patch clamped onto two neurons in the inferior olive of mice with connexin-36 KO
  • found that connexin-36 KO mice show impaired synchrony in membrane potential changes
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10
Q

where are gap jxns found in mammals

A

hippocampus

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11
Q

gap jxn function in mammalian hippocampus

A

involved in the neurons that deal with conceptual learning & memory during hippocampal sampling of features
- may be responsible for hippocampal pattern recognition

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12
Q

what did Negeshi (1980) contribute to electrical synapses

A

showed how electrical synapses can be regulated
- dye infused into horizontal cells of Eugerres plumieri usually spreads rapidly to other horizontal cells
- dopamine, through PKA activation, can reduce this spreading

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13
Q

role of PKA in gap jxns

A

phosphorylates connexins and lowers conductance

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14
Q

what did Galvani’s frog leg experiment (~1790) contribute

A

he connected spinal muscles to spinal nerve; muscles twitched when electricity was applied to either the nerve or the muscle
- called it animal electricity

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15
Q

what is a negative Schwankung

A

the AP waveform
- observed by Dubois-Reymond and Julius Bernstein

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16
Q

what was the significance of the rheotome

A

allowed Dubois-Reymond and Bernstein to compare the voltage inside a cell to the voltage outside, and quantify the difference over time
- not precise enough to show an overshoot, and they had no sense of a refractory period

17
Q

Bernstein’s breakdown theory (1902)

A

depolarization of the cell membrane above some threshold leads to a transient breakdown of the ionic barrier between inside & outside of a cell, making the cell permeable to all ions equally

18
Q

flaws of Bernstein’s breakdown theory

A
  • implies AP should peak at 0 mV
  • membrane gets a lot more permeable, but doesn’t get equally permeable to all ions
  • there are more ions involved than just 1
19
Q

what was the first human EEG

A

Hans Berger’s Edelmann String Galvanometer
- couldn’t get detailed or high resolution about electrical signals
- they were really good at picking up on seizures

20
Q

what happens when you deliver muscarine to a heart prep

A

heart slows

21
Q

what was the first theory for what is released by the vagus nerve onto the heart

A

muscarine and adrenaline

22
Q

what is actually released by the vagus nerve onto the heart

A

acetylcholine and norepinephrine
“Vagusstoff” and “accelleronstoff”

23
Q

what was the significance of the isolated heart prep

A

allowed for the study of nerve stimulation of the heart

24
Q

isolated heart experiment methods

A
  • dissect the heart, attach it to a perfusing line
  • record from the heart to observe contractions while stimulating still-attached nerves
25
Q

results of the isolated heart experiment

A

activation of parasympathetic vagus function slows the heart down
- still not known whether muscarine is what is released from the vagus nerve

26
Q

results of the perfusate heart experiment

A

the heart connected to the perfusate of the first heart showed a slowing effect
- concluded that vagus nerve is releasing some substance that has an effect on the heart

27
Q

how long does it take for vagus nerve stimulation to take effect?

A

150 ms – very slow

28
Q

methods for NMJ prep

A

patch onto the nerve in the middle of the mouse soleus muscle; stimulate or measure from the nerve, measure from the muscle to see what’s going on
- flaw: everytime the muscle twitched, the setup was destroyed

29
Q

curare function

A

inhibits ability to get an AP
- you still get EPPs after treating with curare, but you only observe depolarization

30
Q

delay time for NMJ vs cardiac

A

100x smaller than cardiac response to vagal stimulation; muscle response is within 1 ms
- Eccles now considered that this could work in CNS

31
Q

how did Eccles determine that Cl- currents mediate inhibition of motor neurons

A

he stimulated an inhibitory interneuron synapsing on a motor neuron, and observed that removing Cl- from the bath gets rid of the hyperpolarizing inhibitory synaptic input

32
Q

what would you expect from Eccles’ interneuron experiment if there was only electric synaptic transmission

A

inhibition would not cause much hyperpolarization, but would make it harder to cause depolarization
- you would not expect there to be different patterns for excitation vs inhibition due to different ion concentrations, but rather a decrease or increase in the same ion (like K+)