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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

1. Vary in size (EPSP, IPSP)
2. no refractory period
3. 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

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


How does PIP2 2nd messenger work

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


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
-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
-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

-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



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