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117 Cards in this Set

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Function of Na+ channels
generating and propagating action potentials in excitable cells
function of K+ channels
control of excitability and shaping of electrical signals
Function of Ca++ channels
neurotransmitter release, muscle contraction and intracellular signalling pathways
hyperkalemic periodic paralysis
an Na+ chanenelopathy revealed when extracellular K+ is raised. Channel doesn't inactivate properly and action potential can't develop.
tetrodotoxin (TTX)
neurotoxin that is highly specific blocker of voltage-gated Na+ channels. Leads to respiratory paralysis and is found in puffer fish
local anesthetics- novacain, lidocain
block voltage gated Na channels in axon and prevent conduction of nerve impulses
Lamber-eaton Myasthenic Syndrome (LEMS)
autoimmune disease that impairs calcium influx and reduces transmitter relase at neuromuscular junction resulting in muscle weakness
None
halothan
anestheic that opens the leak K+ channels
nifedipin and verapamil
drugs used in the treatment of cardiovascular disease by blocking Ca++ channels
3,4 Diaminopyridine
drug used to treat LEMS by blocking K+ channel and prolongs the action potential
acetylcholine receptors
ligand gated channels at neuromuscular junction involved in excitatory neurotransmission
glutamate receptors
ligand gated channels at CA3-CA1 hippocampal synapse
GABA receptors
ligand gated channels at hippocampal synapses
Nicotinic acetylcholine receptor
ligand gated channel at neuromuscular junction that bind Ach and allows Na+ and K+ flux and induces depolarization which increases Ca++ and results in muscle contraction
hyperpolarized
a membrane potential which becomes more negative
depolarized
a membrane potential which becomes less negative
acetylcholinesterase
breaks Ach into acetate and choline and terminates signal
congenital myasthenic syndrome
this is a slow channel syndrome present at birth that is caused by mutations on Ach receptors causing weakness, rapid fatigue, and muscle atrophy
D-Tubocurarine
competetive inhibitor of Ach that causes paralysis and death by asphyxiation
Vercoronium, Pancuronium, and Rocuronium
synthetic chemicals that cause parlaysis by competitively inhibiting Ach receptors. Used in surgical procedures
α bungarotoxin
snake toxin that binds competetively and irreversibly to Ach receptors
None
Succinycholine
Ach R agonist that binds and causes depolarization and is used as a muscle relaxant
Nicotine
Ach R agonist that binds at same sites as ACh and can cause muscle contraction
Myasthenia Gravis
autoimmune neuromuscular disease caused by the destruction of peripheral NACh receptors causing muscle weakness, movement defecit and fatigue
Picrotoxin
noncompetetive blocker of GABA
Benzodiazapine
anxiolytic drug that increases GABA activity and is used for anxiety disorders and insomnia
Barbituates
anticonvulsant and sedative drug that increases GABA activity. Used for epilepsy, anesthesia and anxiety
Hormone response elements
DNA sequences where steroid receptor complexes bind and regulate rate of transcription
Gs
G-protein that stimulates AC and activates protein kinase A
Gi
G-protein that inhibits AC and inhibits protein kinase A
Gq
G-protein that is coupled to Phospholipase C which increases DAG, and in turn IP3 and Ca++ and activates protein kinase C
Cholera toxin
bacterial toxin that stimulates Gs and causes and excess production of cAMP
Pertussis Toxin
bacterial toxin that inhibits Gi and causes excess cAMP
None
Sos
guanine nucleotide exchange factor for Ras that is attracted by Grb2 in the signaling event of tyrosine kinase receptor
GTPase activating proteint (GAP)
hydrolyzes GTP and inactivates Ras
Restriction Point
the point in G1 when the cell cycle stops being GF dependent
Oncogene
a mutated protein of the cell cycle control system that is constituitively activated, Ras, myc, fos, jun
Tumor supressor gene
protein that inhibits cell cycle progression- Rb, p53
Akt pathway
signaling effect of neurotrophins binding to receptor tyrosine kinase that prevents cell death
What passes K+ ions but not Na+ or Cl- ions?
a potassium channel
changing the cell potential from -80 to 0 mV opens a voltage gated K+ channel. When the channel opens K + ions will flow in which direction
out of the cell
a chef preparing puffer fish might find his lips becoming numb because
tetrodotoxin in the fish inhibits Na+ channels
If changing the cell potential from -80 to 0 mV opens a voltage gated Ca++ channel, calcium ions will flow in which direction?
into the cell
the voltage gated calcium channel pore is formed from:
a single α subunit consisting of 4 repeated structural units each of which has 6 transmembrane domains
Voltage gated calcium channels mediate what phase of the cardiac action potential?
the plateau phase (phase 2)
Nifedipine and Verapamil block what ion channels to treat cardiovascular disease?
Calcium channels
When recording single Na+ channel currents, why are openings only observed at the beginning of a voltage shift to 0 mV
Na+ channels inactivate after they open.
Acetylcholine-activated currents at the neuromuscular junction are terminated by
acetylcholinesterase
acetylcholine receptor ion channel is opened by
acetylcholine
what single channel property is altered in slow channel syndrome?
open time is increased
Vecuronium iss used to prepare a patient for surgery because
It produces paralysis
the binding of glutamate to NMDA receptors opens an ion channel that passes
Na+, K+ and Ca++ ions
why is NMDA current absent at hyperpolarized potentials?
Mg++ enters the channel and blocks it
If a cell's resting potential is -80 nV, but it is at -60 mV because of excitatory synaptic activity what happens if a GABA-mediated synaptic current occurs
the membrane potential will hyperpolarize slightly (become more negative)
GABA receptors are targets for
barbituates
what does ion specificity depend on
pore size and strength of interaction with pore site
what is the resting potential of an excitable cell? And are the channels open or closed?
negative. Closed
what is the nernst potential for K+
-105 mV
what will K+ normally do when the channel is opened?
move out
What is the nernst potential fo Na+
61 mV
What will Na+ normally do when the channel is opened?
move in
what are the 3 molecular configurations for ion channels
heteromer, homomer, and a single polypeptide
which channels mediate fast signalling
ligand gated
where are ligand gate channels found
central and peripheral nervous systems
what are ligand gate channels called
ionotropic receptors
3 major classes of Glutamate receptors
Kainate, AMPA, and NMDA
Which class of receptors have many coregulators
NMDA Glutamate receptors
Which class of receptors is rapid desensitization a characteristic of?
AMPA Glutamate receptors
When is NMDA current absent
at hyperpolarized potentials
Which Glu receptor allows Calcium to pass?
NMDA Glutamate receptors
What inhibits NMDA
zinc
Examples of blockers of Glutamate receptors
NBQX, D-AP5. D-AP 7, ketamine, PCP, MK 801
What is the main inhibitory neurotransmitter in the CNS
GABA
What kind of channel are GABA- receptors?
Chloride
What does GABA receptor openings cause to membrane potential?
hyperpolarization
What do GABA receptors have binding sites for
barbituates, benzodiazepines, and potentiators
Steroids bind to…
intracellular receptors that affect gene transcription
None
G-protein coupled receptors are made up of
a single subunit with 7 transmembrane domains
Gq is a heterotrimeric G protein that couples to
phospholipase C. It stimulates PLC, increases DAG, increases IP3, increases intracellular calcium and activates PKC
Once cAMP is generated its signaling effects are terminated rapidly because it is destroyed by …
phosphodiesterase
IP3 receptors are primarily located …
in the membrane of the ER
Albuterol, a bronchodilator used to treat asthma, acts at what G-protein coupled receptor
beta adrenergic receptor, as an agonist
Cholera toxin kills by dehydrating the body through massive diarrhea and vomiting. It does this by attacking the cells of the uppers section of the small intestine and…
stimulating Gs, causing an excess production of cAMP
Ligand binding to receptors eventually leads to loss of receptors. This is mediated by what process?
phosphorylation of GRK, binding of β-arrestin to the phosphorylated sites, and recruitment of β-arrestin of endocytosis proteins such as clathrin
The insulin receptor is a
tyrosine kinase receptor
the unliganded epidermal growth factor tyrosine kinase receptor is made of a
a single subunit with 1 transmembrane domain
Activation of Ras leads to the following cascade
activation of Raf, phosphorylation and activation of MAP kinase kinase, phosphorylation and activation of MAP kinase
Growth factor binding to tyrosine kinase receptors stimulates progression of the cell cycle at what stage
G1
The primary cyclin that responds to growth factor stimulation is
Cyclin D
PI3 kinase catalyzes
phosphorylation of PIP2 to form PIP3
What are the 4 major receptor signalling classes?
steroid, g-protein coupled, receptor tyrosine kinases and guanylate cyclase nitric oxide signaling
Family I steroid receptor signaling
steroid enters the PM, binds to receptor and releases heat shock proteins, enter the nucleus and binds to DNA as dimer to up or downregulate transcription of mRNA
Family II steroid receptor signaling
steroids enters the PM, enters the nucleus and binds to receptor, complex binds to DNA as hetero or homo-dimer to up or downregulate transcription
None
What facilitate the binding of steroid receptors to DNA sequences?
zinc finger
Steroid-steroid receptor examples
androgens and vitamin D
What do androgens regulate?
male sexual differentiation and pubertal changes
where can HREs of androgens be found
in laryngeal myosin, prostate specific antigen
What can agonists of androgens treat?
hypogonadism
what do antagonists of androgens treat?
prostate cancer
What does Vitamin D regulate?
bone mineralization, Ca++ and PO4 homeostatis
What causes rickets
a deficiency in vitamin D
Where are vitamin d HRE's?
calbindin
What does the binding of a ligand to G-protein couple receptor do?
facilitates the exchange of GTP for GDP and the α and βγ to dissociate
How is a G-protein couple receptor signal terminated
GTP is hydrolyzed to GDP and the α subunit dissociates
How do cells respond to persistent stimulation by a drug?
by decreasing the number of receptors available to respond to a drug
3 steps of developing tolerance
desensitization, internalization and down regulation
What does the binding of a ligand to a receptor tyrosine kinase cause?
dimerization
What is the binding site for Grb2
the P-tyrosines of the receptor tyrosine kinase
How does GTP-Ras stimulate the MAP kinase cascade?
interacting with Raf kinase (Map kinase kinase kinase)
What does MAP kinase lead to?
early gene transcription and eventual activation of cyclins to stimulate cell division
What happens to cells deprived of Growth Factor
arrest at G0
Growth factors effect on cyclin D
1) induce transcription 2) stabilize 3) promote translocation to nucleus 4) promote assembly with Cdk 4 and 6
dephosphorylated Retinoblastoma protein
binds regulatory protein that favor proliferation
phosphorylated Rb
releases proteins so the cell proliferate
What causes unregulated proliferation
expression of oncogene, loss of tumor supressor gene, Growth factors always activated
Functions of neurotrophin
stimulate axonal and dendritic outgrowth and synapse formation; potentiates synaptic function; and promotes cell migration
Where do neurotrophins bind
receptor tyrosine kinases, with 3 signaling effects