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Ph2205 > intro 2 > Flashcards

intro 2 Flashcards

1
Q

after NT vesicle attaches how is that new membrane delt w

A

Vesicles membrane coated with clathrin so they are noticed and repinched off

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2
Q

How does nerve to muscle contraction work

A

one action potential leads to a muscle twitch

-in order to fire effectively many AP must arrive at the mm in quick succession (to build a contraction)

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3
Q

How does nerve to nerve conduction work

A

receptors will have lock and key with NT released causing opening of ion channel (receptor may have direct or indirect control of the ion channel)

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4
Q

How does nerve to cardiac conduction work (what type of junctions does it use)

A

Action pot in heard have longer time of Na channels open (allows for longer squeeze of heart)

-uses gap junctions (to allow the heart beat to be better timed)

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5
Q

What happens in an ESPS

A

normal propogation of action potential happens at dendrites. The ESPS then has to travel down to the hillock where it could degrade along the way

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6
Q

What happens in an IPSP

A

will activate pot/cl channels

Cl moves into cell causing it to be more negative and hyperpolarizes cell evenn more

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7
Q

speed and excite/inhibitory of Ach receptors, AMPA, NMDA, GABA and glycine

A 
Ach- fast
AMPA (glutamante)- fast
NMDA- slow/long duration
GABA- inhibatory
Glycine- inhibatory
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8
Q

What are PSPs and some characteristics of it

A

happen in dendrites

  1. Vary in size (EPSP, IPSP)
  2. no refractory period
  3. can degrade thru lengh of dendrite
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9
Q

what is a ligand gated channela and the 2 types

A

react to NT

ionotropic- direct connection bw receptor + channel

Metatropic- Indirect connection to receptor thru a chain of events

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10
Q

What happens in Myasthenia Gravis

A

aCH channels being destroyed compomising muscle contraction

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11
Q

s+s of myasthenia Gravis

A
  • weakness (small mm affected first; occular then oropharyngeal)
  • usually progressive w worst weakness in 1st year
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12
Q

tx of myasthenia gravis

A

Acetylcholinesterases allowing ach to linger longer for remaining receptors

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13
Q

EMG studies of people with myasthenia gravis show

A

fatigue after 2-3 repeated stims; marked drop in contractile strength of 25% bw each stim

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14
Q

what are the 4 adreno receptor 2nd messengers and what do they do

A

Alpha 1- excitatory, vascular smooth mm
Alpha 2- control presynaptic stransmission
Beta 1- activate ad cyclase, found in heart
Beta 2- smooth mm of vascular, leads to relaxation

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15
Q

how does cAMP/cGMP 2nd messanger work

A
  1. Receptor activates G pro
  2. G pro changes GMP to GTP
  3. GTP activates adenolyne cyclase which produces cAMP fro AMP
  4. cAMP activates pro kinase which phospholylates channel
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16
Q

How does PIP2 2nd messenger work

A
  1. receptor activates G pro
  2. G pro changes GMP to GTP
  3. GTP actibates phosolipase c which takes PIP2 and makes DAG and IP3
  4. IP3 causes ca to be released and activates calmodulin
  5. calmodulin opens channel
17
Q

What does Beta 1 do in the heart (and how does beta blockers stop it)

A

Beta 1 found on heart that binds norenephrine causing influx of calcium (causing stronger/harder heart beat)

Beta blockers blcok this process

18
Q

What is Wallerian degeneration

A

if u cut a neuron there will be degeneration distal from cut.

But eventually it will start moving backwards from the cut (wallerian degeneration)

19
Q

what is different in the nucleus of the soma

A

Chromosomes are uncloiled and are thus incapable of dividing

20
Q

Fast anterograde transport- speed, how it moves, ATp requirement

A

new materials synthesized in cell body moving towards terminal

  • Saltatory stop and go movement
  • 400mm/day
  • uses ATP
21
Q

What does fast antergrade transport travel along

A

travels along microtubule tracts and kinesines line the rails which basically row the components forward

22
Q

Fast retrograde transport- speed, atp requirement

A

moves materials back to cell body

  • 200mm/day
  • uses ATp (dyenine)
23
Q

What signals fast retrograde transport and what does it use to move

A
  • NGF signals cell incjury further along in the cells

- Uses dyenin that attaches to vesicles of reabsorbed NT and flings them back to the cell body

24
Q

What is slow axoplasmic transport -speed/how does it move

A

1mm/day

-uses flagella to move

25
Q

How big are microtubules/ how are they bound together

A
  • thickest cytoskeleton component
  • used for stationary tracts for transport
  • Bound together by MAPs
26
Q

function of neurofilamints and disease that targets them

A

10nm and most abundent cytoskeleton component

  • Mostly ised to shape some
  • alzheimers targets this n the soma becomes disorganized causing signal to break down
27
Q

Function of microfilaments

A

interact with membrane pros to stabalize receptors and help with dendrite structure.

28
Q

What are the 2 main classes of NT

A
  • Small molecule transmitters (derived from aa in cytosol; ach, biogenic amines)
  • Neuroactive peptide
29
Q

Which biogenic amines is created from tyrosine

A

Dopamine
norepinephrine
epinephrine

30
Q

At normal levels GABA has this affect where at super high levels it has this affect

A

Normal- inhibitory effects

high- Excitatory effects

31
Q

What deficiency does ppl with huntingtons disease have and what does it cause

A
  • lower lvls of inhibitory GABA (especially in caudate nuc)
  • leads to very hyperexcitable motor regions
  • Stops MAPs from functioning properly
32
Q

What are neuroactive peptides and what is its drawback

A

NTs make in cytosol

-since only made in cytosol if repeatedly stimed its will deplete them quickly and cause plateu to become weaker etc

33
Q

How do NTs get into vesicles

A

Inside of NT vesicle is acidic (5.5) which attract NT to the inside

Ph2205 (5 decks)

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