intro 2 Flashcards
after NT vesicle attaches how is that new membrane delt w
Vesicles membrane coated with clathrin so they are noticed and repinched off
How does nerve to muscle contraction work
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)
How does nerve to nerve conduction work
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)
How does nerve to cardiac conduction work (what type of junctions does it use)
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)
What happens in an ESPS
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
What happens in an IPSP
will activate pot/cl channels
Cl moves into cell causing it to be more negative and hyperpolarizes cell evenn more
speed and excite/inhibitory of Ach receptors, AMPA, NMDA, GABA and glycine
Ach- fast AMPA (glutamante)- fast NMDA- slow/long duration GABA- inhibatory Glycine- inhibatory
What are PSPs and some characteristics of it
happen in dendrites
- Vary in size (EPSP, IPSP)
- no refractory period
- can degrade thru lengh of dendrite
what is a ligand gated channela and the 2 types
react to NT
ionotropic- direct connection bw receptor + channel
Metatropic- Indirect connection to receptor thru a chain of events
What happens in Myasthenia Gravis
aCH channels being destroyed compomising muscle contraction
s+s of myasthenia Gravis
- weakness (small mm affected first; occular then oropharyngeal)
- usually progressive w worst weakness in 1st year
tx of myasthenia gravis
Acetylcholinesterases allowing ach to linger longer for remaining receptors
EMG studies of people with myasthenia gravis show
fatigue after 2-3 repeated stims; marked drop in contractile strength of 25% bw each stim
what are the 4 adreno receptor 2nd messengers and what do they do
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
how does cAMP/cGMP 2nd messanger work
- Receptor activates G pro
- G pro changes GMP to GTP
- GTP activates adenolyne cyclase which produces cAMP fro AMP
- cAMP activates pro kinase which phospholylates channel
How does PIP2 2nd messenger work
- receptor activates G pro
- G pro changes GMP to GTP
- GTP actibates phosolipase c which takes PIP2 and makes DAG and IP3
- IP3 causes ca to be released and activates calmodulin
- calmodulin opens channel
What does Beta 1 do in the heart (and how does beta blockers stop it)
Beta 1 found on heart that binds norenephrine causing influx of calcium (causing stronger/harder heart beat)
Beta blockers blcok this process
What is Wallerian degeneration
if u cut a neuron there will be degeneration distal from cut.
But eventually it will start moving backwards from the cut (wallerian degeneration)
what is different in the nucleus of the soma
Chromosomes are uncloiled and are thus incapable of dividing
Fast anterograde transport- speed, how it moves, ATp requirement
new materials synthesized in cell body moving towards terminal
- Saltatory stop and go movement
- 400mm/day
- uses ATP
What does fast antergrade transport travel along
travels along microtubule tracts and kinesines line the rails which basically row the components forward
Fast retrograde transport- speed, atp requirement
moves materials back to cell body
- 200mm/day
- uses ATp (dyenine)
What signals fast retrograde transport and what does it use to move
- 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
What is slow axoplasmic transport -speed/how does it move
1mm/day
-uses flagella to move
How big are microtubules/ how are they bound together
- thickest cytoskeleton component
- used for stationary tracts for transport
- Bound together by MAPs
function of neurofilamints and disease that targets them
10nm and most abundent cytoskeleton component
- Mostly ised to shape some
- alzheimers targets this n the soma becomes disorganized causing signal to break down
Function of microfilaments
interact with membrane pros to stabalize receptors and help with dendrite structure.
What are the 2 main classes of NT
- Small molecule transmitters (derived from aa in cytosol; ach, biogenic amines)
- Neuroactive peptide
Which biogenic amines is created from tyrosine
Dopamine
norepinephrine
epinephrine
At normal levels GABA has this affect where at super high levels it has this affect
Normal- inhibitory effects
high- Excitatory effects
What deficiency does ppl with huntingtons disease have and what does it cause
- lower lvls of inhibitory GABA (especially in caudate nuc)
- leads to very hyperexcitable motor regions
- Stops MAPs from functioning properly
What are neuroactive peptides and what is its drawback
NTs make in cytosol
-since only made in cytosol if repeatedly stimed its will deplete them quickly and cause plateu to become weaker etc
How do NTs get into vesicles
Inside of NT vesicle is acidic (5.5) which attract NT to the inside
