Slow activating vol dep K channel

Active very close to the resting potential and some are open
Depolerie slightly near the threshold of spike youll activate them and they hyperpolarize and make
problem to reach the threwhold
Typically dont have any effect during the beginning of the depolarization and fire a little spikes and then
they shut down known as adaption
kcmQ channel have 4 subunits. Kcnq1 affect heart and cardiar qrythum. New omenculture kv7 channels .
kcmq M channet have 4 subunits. They are identical or are the same. Naturalneurons have kcnq2(2) and
kcnq3(2). All 4 subunits are involved in the pening of the channel.

Eaach subunit cross the clallel 6 times and the 4th uni is positively charged and the movement of the s4
leads to the triggering of the opening of the channel.

Conductance and selev=ctively of k

Voltage gated hae 6 subunits
Then specific kcnq channel. Menion that there is a similar channel in heart and has oger duration. In
neurons they last very briefly. Mchannel regulate No. of spikes and tends to avoid adaptation.

Sympathetic ganglia has it central neuron have it and recently found in the neuron end where it starts.
So it can regulate no. of spikes. Different that hilkin honlet channels but it is different,
Focus of different nueoromuslucar modulator. They interact with g protein and not as a ca-ion channel.
The G-protein leads to activation of secondary messenger and define second messengers, IP3,
isoglycerol. Actiates gq or g11 and that activates phospholipase and breaks down phospholipids and
breaks phospholipids into 2 parts (secnd messngrs) hyprophobic di glycerol and 2 hydrocarbon chain
and polar head ip3

Acetocolinf on muscarinic chanel whhc is hy it is calld m-channel

Cel with membrane potential -40 and most will be open between -70 and -30. WhenACh is joined they
shut which leads to thechange in the rythum of the neuroms. Either the diglycerol or IP3 shuts the
channel or bith,. After a lot of research failed to show that they lead to the closure of m channel due to
Ach. One of the first neuron modulation.Aided by cloning of the m-channel. Somebody though maye not
focus on the ip3 an lipase, but on the breakage of phospholipid. A phs[ophyidal bephostpate is needed
to be in the membrane it can associate to them channel and lead to closing and opening of the channel.
The conc drops and m-channel cannot open and close. It stays closed when Ach is attached. David
Brown in London

Summarize the m channel model but make your own model. 2-2s and 2-3s kcnq subiunit. Pip2 also there.
Sprip the phospholipid and alpha and beta gamma of the g-protien.

Descripe the g-protein differentiation. The alpa has gtp and is active as long as it is there. It can stay
active for long time a fewmilliseconds to minutes. What stops it is the replacement of the gtp to gdp. G
protein because they work as gptase and breaks gtp to gpd and retrieves the a-gama complex and then
returns. It still takes time to resynthesize the phospholipid.
Just an overview of the process and its a larg topic eventhough it is just oe type. It has a lot of
relationships ad it is uncommon and it is discovered that a lot of other channels als work on the
phospholipids.

When it is working in the neuron it shows adaptation and it chages the action potention rythum of the
neurons.

There are drgs that stop the receptors is scrystopolie because it effets memory and because anesthesia
affets the suffering the body. And they give the drug and block muscurenic receptor and dont let Ach
channel and act as a antagonist. If you block that you cannot remember important memory. In addition
there are drugs that will block the m-channel directly,like ax8a1 , they should behave like AChin a way
but in alstine disease the choline channels dont work. So to cure it we have cognitivedrugs that lead to
drugs in surgery and the disease. Mutatins in the in channel function nto at all or genital epilepsy also
caused due to the nq gene and there also cause of deafness because of the channel.

Achesteratse from the prolonged conductance of the current. Sytotoxic effect in the CNS and there are
calcium pores and leads to damage and abnormal looking channel.
Nmj are different in that a drug sees a large bed but only stick on one.