Exam 2 Flashcards by porter hacking

TEA
Tetra ethyl ammonium

Blocks K+ channels

How well did you know this?

Not at all

Perfectly

TTX tetrodotoxin

Blocks na current

How well did you know this?

Not at all

Perfectly

In a normal ap vsodium vs vpotassium Chanel states

Na closed to open to inactivated to closed

K closed to open to closed

How well did you know this?

Not at all

Perfectly

INaT

Transient (NA)
Fast activate then inactivate
Axon
Upward swing of action potentials

How well did you know this?

Not at all

Perfectly

INAP

Persistent (NA)
Slow activating
Non inactive
Soma and dendrites
Enhances depolarization
Contributes to steady state firing

How well did you know this?

Not at all

Perfectly

(CA)
Long lasting
High threshold
Slow activation
Slow inactivation

Dendrites
Axon terminal
(Dendritic excitation and Ca mitigated events in dendrites)

How well did you know this?

Not at all

Perfectly

Calcium
Transient low threshold
Fast activation and
Inactivation

Dendrites
Quick depolarizing of dendrites
Causes burst firing
Ca mediated events in dendrites

How well did you know this?

Not at all

Perfectly

K
Slow activation by depol
Non inactive
Axon
Repolar of AP

How well did you know this?

Not at all

Perfectly

K
Slowly active by depolarizing
Non inactivating
Required increase in Ca

Soma and dendrites

Increases interval between action potentials

How well did you know this?

Not at all

Perfectly

K
Transient
Fast activate by depol
Fast inactive

Soma and dendrites
Delays the onset of the AP

How well did you know this?

Not at all

Perfectly

K
Slowly active by depol
Non inactive
Blocked by activation of muscarinic receptors

Soma and dendrites

Contributes to spike frequency adaptation

Blocking this current enhances cell excitability

How well did you know this?

Not at all

Perfectly

Inward cation
Activated by hyper pol
Slow activating
Non inactive but stops when no longer hyper polarizing

Soma and dendrites
Pacemaker potential

How well did you know this?

Not at all

Perfectly

What happens when Ih and It are active

You get pacemaker potential with rythmic bursting

How well did you know this?

Not at all

Perfectly

Orthodromic ap

Normal toward terminus

How well did you know this?

Not at all

Perfectly

Antidromic ap

Toward soma

How well did you know this?

Not at all

Perfectly

Sensory axons
C

Slow pain
Slow pain temp

Burning

How well did you know this?

Not at all

Perfectly

Fast pain
Fast pain temp

Pricking

Propiception
Touch

Propioception touch

Diagonal line graph changes

Lower Na shift left

Higher external K shifts right

NACH Chanel’s ions

Mixed Na K

Nachr in muscle subunits

2 alpha beta delta and then gamma(embryo) and epsilon (adult)
2 ACh one to each alpha subunit opens channel

Homo vs hetero nachrs

Homo a7 a9
Na k ca
Blocked by bugarotoxin
Desense is faster and stops current sooner

Hetero
Alpha beta or alpha alpha mix
Na and k
Not blocked by bungatotoxin

How to overcome desensitization

PKC
PKA
Calcineurin

Non specific cation Chanel’s

Na k Nicotine(ACh) AMPA( glu) Kainate (glu) 5-HT3 (serotonin) Na K Ca NMDA (glu) NACHR (ACh

PSD-95

Hold ionotropic receptors in postsynaptic membrane

Homer

Holds Metabolic receptors in perisynaptic membrane

(GluR) Glutamate receptor Chanel’s subunit

M3 gate M2 selectivity filter Have ligand binding Pac-Man (shells that close causing gate to open)

NMDA receptor overview

Permeable to Na K ca Agoníst Endo glut Exo NMDA Glycine or D serine are required conagonists Antagonists MK801 APV PCP Zinc Mg blocks pore and rmp Depolarization removes zinc that blocks it

GABAa and glycine

Are simple Cl ion channels

B and a2 for cl- channels vs B a1

Long open times long currents Short open small current

Gaba B

Is a GPCR

GABA a

Simple Cl channel GABA a agonist can be used to treat anxiety seizures sleeping disorders and help relax muscles Agonists Benzodiazepine Ethanol Barbiturate During development gaba a is depolarizing And then flips after 10 days after being born

Spine synapse Shaft Soma

Soma inhib Shaft inhib Spine excite

Atypical gpcr

MgluR GABAb Form obligatory dimers

Action of GpCR

G alpha binds GTP and the separates G beta gama complex and G alpha turn on a whole bunch is shit When g alphe hydrolysis the GTP into gdp then it turns off

Adynal cyclase Phospdiesterase

Is activated by gprotien and then turn AtP into Camp Phospho which can also be activated turns Camp into just amp

CAMP and cGMP

Can open up channels directly as well They can also activate kinases like PKA or PKG which phosphorylate thinks

PLC

Interacts with pip2 Has PLA2 which makes arachidonic acid (which breaks apart and can pass through membranes and activate neighboring cells) And plc which becomes IP3 (releases internal ca) And DAg activated PKC They can also hep form endocannabinoids note they are membrane bound

Nitric gas

Is produced by some neurons Using nNos As a gas it can easily pass through membranes and go backwards and activate GC and make CGMP

Receptor tyrosine kinases

Activated by growth factors Cross phosphorylation and activate many things Promote neurite growth Prompte cell survival Promote plasticity And stabilize memory formation