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Neuron Signalling and some Transporter Stuff
Terms in this set (34)
Where are uncoupling protons found? What are their function? What is the significant of this for homeostasis?
--Mitochondria in brown fat
--Lets protons flow from mitochondrial intermembrane space to matrix, bypassing ATP synthase
--Prevents ATP buildup, which normally slows down cellular respiration. Allows heat to generated continuously (nonshivering thermogenesis).
Describe the modified muscles swordfish have around their eyes? What's their purpose?
--Nonfunctional muscles that cause release of calcium ions, which must be re-uptaken. This process requires energy, which cellular respiration provides. This releases heat, which allows the swordfish to maintain temperature near the brain area.
What is a synapse?
--Where axons join up w/ other cells, axons, or dendrites.
Where are the synapses located between cells?
Very close between cells
What structures are present in the axon terminal and why?
--Lotta mitochondria b/c much energy needed
--Lotta vesicles for neurotransmitters
--Lotta golgi cisternae (for modification and vesicle formation)
What are the two ways to transfer signals?
Electrical synapse and chemical synapse
What are the characteristics, pros, and cons of electrical synapses? Why would a cell want to use them?
--Gap junctions (form a channel between the two cell membranes)
P--Signal spreads rapidly with no delay)
C--Signal cannot be fine-tuned (can't get "gain", or ramp up of current; post-synaptic signal is lower than pre-synaptic)
--Perfect for escape responses
--Useful when cell needs signal to travel very fast
What is a key difference between chemical and electrical neurotransmitters?
--Physical gaps between cells, not like electrical synapses
--neurotransmitter diffuses rapidly across cleft
Why must the gap between cells be tiny in chemical synapses?
Chemical synapses rely on the diffusion of neurotransmitters, and diffusion is not effective over long distances
What do the neurotransmitters that travel across the synaptic cleft in a chemical synapse do?
provokes electrical signal in post-synaptic cell (depolarize that cell)
What does it mean to say that the post-synaptic cell response is graded by the amount of neurotransmitter released from the pre-synaptic cell? Why is this the case?
--graded by amount of neurotransmitter (the amount of response on the post-synaptic cell is determined by amount of neurotransmitter released from pre-synaptic terminal)
--More neurotransmitters will open more channels on the post-synaptic cell membrane
Are chemical or electrical synapses more versatile?
Name two organs where electrical synapses are seen.
Heart and brain
What do dendrites do in chemical synapses?
receive chemical message from adjoining cells
Neurotransmitters bind to receptors on the post-synaptic membrane, causing what?
The receptors become activated, activating ion channels which alter membrane potential in the post-synaptic cell
• **Look at "Overview: Transmitter Release" slide
What happens when the action potential reaches the terminal end of the axon? What is this considered?
--When action potential reaches terminal end of axon, it activates a calcium channel, which allows extracellular calcium to enter cell, which stimulates the vesicles to bind to the cell membrane and release neurotransmitter.
What is meant by "ionotropic receptors"?
Ligand-gated ion channels—Neurotransmitters in synaptic cleft bind directly to ion channel on post-synaptic membrane, opening them up.
If the ligand binding to an ionotropic receptor is excitatory, what ion channels will be opened? If the ligand binding is inhibitory, what ion channels will be opened? What happens to the cell when these are opened?
--K+, Cl-, hyperpolarization
What is meant by metabotropic receptors?
--Receptors that work through a second messenger to lead to ion channel activation
Look at metabotropic receptor slide on Canvas. Note the difference between the 2 kinds presented.
Why do we need methods for removing neurotransmitters from the synaptic cleft?
If they are left there, continuous action potentials will result, which will be extremely harmful to the receptors. Note: I don't know if hyperpolarizing channel receptors would also be damaged if NT was not removed.
What are two methods for getting rid of neurotransmitters in the synaptic cleft?
o Re-uptake of neurotransmitters—neurotransmitters taken up into presynaptic membrane.
o Enzymatic deactivation—enzyme destroys the neurotransmitter molecules.
What is the target of Sarin nerve gas? What does this target normally do?
--Breaks down acetylcholine in the synaptic cleft
What are some ways that drugs can affect neurotransmitter concentration in the synaptic cleft?
o Can increase number of impulses (more NT releasing into cleft)
o Release NT with or without impulse
o Block re-uptake receptors
o Produce more or less NT
o Prevent vesicles from releasing neurotransmitter
Check out major types of neurotransmitter slide and drug mechanisms slide.
How does alcohol affect neurotransmitter release?
Binds directly to:
• GABA (gamma-aminobutyric acid). Hyperpolarization of neurons that release GABA results in sedative effect of alcohol
How does nicotine affect neurotransmitter release? What is unique about nicotine?
Unlike many other drugs, this actually has its own receptor.
• Binding of nicotine to this receptor causes calcium channels to open, allowing vesicles to fuse with membrane, releasing more NT.
How do methamphetamines (such as ____ and ____) affect neurotransmitter release?
--Riddlin and Adderall
Cause release of more dopamine into synaptic cleft
Block dopamine re-uptake transporters
What is ketamine used for? At very low doses, what has it been newly found to be useful for? How does it do this?
Used for euthanizing animals and as a human anesthetic.
At low doses, is very useful for treating severe depression that is unresponsive to other drugs.
--Neurotransmission activates NMDA receptor, which leads to the turning on of eEF2 kinase, which phosphorylates eEF2, inactivating it. When eEF2 is inactivated, brain derived neurotrophic factor is not translated. Ketamine blocks the NMDA receptor, so eEF2 kinase does not get turned on, which means that BDNF is produced. This helps with depression.
Define active and passive transport.
Passive—doesn't require energy
Define secondary active transport. What can be used to drive it? What is commonly used to drive it in human cells?
Secondary active transport—Uses an already present gradient to drive active transport.
• Any ion that has a gradient can be utilized
• Uses energy from electrochemical gradient created by Na+/K+ pump.
List 4 general ways to cross a membrane and one detail about each.
• Ways to cross a membrane
• Based on Fick's Law
Bulk flow channels
• Things that pass through the middle of the channel flow more rapidly than things that are passing along the edges of the channel. "Poisuelle" flow.
• Follows Michaelis-Menton Kinematics
Explain the graph for simple diffusion, including the axes.
Graphed-out, simple diffusion is linear (X is conc. Of solute, Y is rate).
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