Molecular Bio & Modifiable Synapses Flashcards
Ionotropic vs Metabotropic receptors
(Also called ligand-gates ion channels)
Neurotransmitter activates channel, which opens pore thru membrane
- 5 receptor subunits
Neurotransmitter activates receptor, which activated G protein
- Either opens G-protein gated ion channel or activated effector enzyme
- Can:
1) convert extracellular signals into the change of molecules inside neuron
2) amplify signals
3) regulate cell functions in response to signals
Glutamate receptor
Voltage-gated ion channels
Binding of glutamate opens AMPA, kainate, or NMDA
- AMPA and Kainate allows Na+ in
- NMDA allows Ca2+ in and also relies on voltage
Opens/closes in response to membrane potentials
- Glutamate will activate it but still needs membrane potential to open it completely
Signaling cascade
First messenger
Second messenger
Process found w/ metabotropic receptors
First messenger - Usually neurotransmitter or hormone
Second messenger - Molecule that relays signal from receptor to target molecules inside cell
- Usually calcium or cAMP
cAMP dependent pathway
1) First messenger binds to receptor
- Usually acetylcholine, dopamine, serotonin
2) G protein activates and activates adenylate cyclase w/ GTP
3) Adenylate cyclase uses ATP to create cAMP as signal molecule
4) cAMP activates protein kinase A to phosphorylate proteins or initiate protein synthesis
How many phosphates in:
ATP/GTP
ADP/GDP
AMP/GMP
3
2
1
(more phosphate ions = more energy)
Where do these take place?
Transcription from DNA to RNA w/ mRNA
Translation of RNA into proteins w/ Transfer RNA
Nucleus
Ribosomes at endoplasmic reticulum
Nitrogenous bases in DNA?
Uracil in RNA is paired with what?
Adenosine - Thymine
Guanine - Cytosine
Adenosine
_ nucleotide -> _ codon -> _ amino acid
3
1
1
How many essential amino acids are there?
Structure?
20 amino acids
Contains amino group, hudrogenC carboxyl, and R-group
- R-group is hydrophobic or hydrophilic -> Determines where on cell protein will be
Membrane potential
Difference in electrical charge between the inside and outside of a cell
- Resting membrane potential = ~-70 mV
Distribution of ions inside/outside of cell:
Sodium
Potassium
Chlorine
Calcium
Protein
Na+: More outside
K+: More inside
Cl-: More outside
Ca2+: Much more outside
Proteins: More inside
Equilibrium potential
Na+, K+, Cl-, Ca2+
Value of membrane potential where electrical force = diffusion force of ion
Potassium channel allows K+ ions to move from inside to outside of cell
- Driven by concentration gradient
-> Buildup of positive charge outside causes K+ to move back in driven by electrical gradient
Na+: 56 mV (Diffusion force in, electric force in (later out))
K+: -102 mV (Diff force out, electric force in)
Cl-: -76 mV (Diff force in, electric force out)
Ca2+: 125 mV (Diff force in, electric force in (later out))
- Much higher than Na+ bcuz diff of conc between inside and outside is much greater
EPSPs vs IPSPs
Axon hillock
EPSPs: Excitatory postsynaptic potential
- Depolarization of cell membrane
IPSPs: Inhibitory postsynaptic potential
- Hyperpolarization of membrane potential
Axon hillock: Where axon comes out of cell body
- Contains many voltage-gated sodium and potassium ion channels
- Where summation of EPSPs and IPSPs happen
Speed of voltage-gated sodium channels and voltage-gated potassium channels during action potentials
V-gated Na+ channels open first
- Rapidly activate and deactivate before V-gated K+ channels open
V-gated K+ channels open more slowly
Myelin sheath at peripheral nervous system vs central nervous system
Node of ranvier
Saltatory conduction
@ PNS - Schwann cell
@ CNS - Oligodendrocyte
Node of ranvier: Gaps between myelin sheath
- Depolarizes action potentials to increase speed
Saltatory conduction: Jumping of APs between nodes to travel as fast as 120 m/s
Habituation of gill withdrawal reflex in aplysia
Gill withdrawal reflex
Gill withdrawal reflex: When siphon touched, gill withdraws
When siphon touched many times, length of withdrawal decreases over time
- EPSPs in L7 motor neuron decrease over time (synaptic depression)
- Habituation retention seen, only some recovery happens longterm
Aplysia abdominal ganglion
LE sensory neuron
L7 motor neuron
Has simple neural network w/ large neurons in stomach area
LE sensory neuron connected to siphon, signals directly to L7
L7 motor neuron connected to gill
What happens when:
L7 neuron is directly stimulated
LE neuron is weakly stimulated
LE neuron is strongly stimulated
(Aplysia)
1) Gill moves
2) Evokes EPSPs in L7 neuron
3) Evokes EPSPs in L7 neuron, which moved the gill
How does synaptic depression occur?
EPSPs are reduced bcuz not enough synaptic vesicles near active zone of presynaptic beuron
What changes in the axon terminals cause longterm habituation?
(In aplysia)
Sensory neurons retract their axon terminals from motor neurons
- Lessens synaptic connections
Sensitization in aplysia with
1) Single tail shock in 1 day
2) 4x tail shock in 1 day
3) 4x tail shock over 4 days
1) Weak sensitization for few hours
2) Weak sensitization for few days
3) Strong sensitization for 7+ days
Shock to tail causes gill to withdraw more
How does the sensory neuron signal from tail to the gill?
1) Tail sensory neuron signals to modulatory interneuron
2) Modulatory interneuron signals to axon terminal of LE sensory neuron w/ serotonin
3) Action potential occurs from LE to L7, which activates gill
How does long term potentiation occur?
Silent synapses, process based memory
Structure based memory
Silent synapses: Not all presynaptic terminals are filled w/ vesicles
Process based memory: Enhancement of previous parts to fill silent synapses
1) PKA activates in cytoplasm
2) Activates translation of existing mRNAs
3) Proteins transport synaptic vesicles into silent synapses
Structure based memory: Formation of new synapses to increase release of neurotransmitters
1) Activated PKA moves from cytoplasm to nucleus
2) Activates transcription of new mRNA + translation of new proteins
3) Proteins used to form new synaptic contacts
