| Question |
Answer |
| Name the parts of the neuron |
1. body, soma, perikaryon 2. dendrites-may be apical or basal -spines 3. nucleus 4. Nissl substance (rough ER) 5. axon hillock 6. axon 7. myelin segments 8. nodes of Ranvier 9. synaptic ending, bouton, terminal 10. collaterals |
| What is located in the presynaptic terminal? |
1. contains synaptic vesicles 2. large number of mitochondria 3. active zone |
| What is the active zone of the presynaptic terminal? |
where presynaptic membrane opposes postsynaptic membrane |
| What happens when the action potential reaches the presynaptic membrane? |
when action potential reaches presynaptic membrane synaptic vesicles fuse with membrane and release neurotransmitter into synaptic cleft |
| Where is the post synaptic site located? |
dendritic spine, dendrite, soma or axon |
| What is the motor endplate region? |
at neuromuscular junction axon branches and the postsynaptic region is on the muscle |
| Where are the receptors? |
postsynaptic membrane |
| What are receptors made of? |
Protein |
| How are receptors activated? |
may be activated either by a binding (ligand-gated) or by a local change in voltage (voltage-gated channel) |
| How does an ion channel regulate receptor activation? |
because of shape, size and/or charge only permit passage of one type of ion OR may be related to second messenger system |
| Ho does a second messenger system work? |
very complex and can change cell function by increasing neurotransmitter levels or number of receptors by activating gene expression. Can also cause prolonged opening of adjacent ion channels. |
| Where is the axon hillock? What happens here? |
1. axon begins from soma 2. point of generation of the action potential |
| What is the size of an axon? |
few icrons to meters long |
| What is the function of the axon? |
transmit action potential to terminal, and can be myelenated or unmyelinated |
| Where is the action potential generated on a sensory neuron? |
action potentials are generated from receptors (modality gated) |
| Where is the action potential generated on a sensory neuron? |
peripheral and central segments of axon |
| T/F The cell body in dorsal root ganglion is unipolar. |
F, pseudounipolar |
| How does a cell membrane regulate membrane potential? |
ionic concentration |
| How is ionic concentration regulated? |
1. phospholipid bilayer 2. ion channels |
| At rest what is the voltage potential inside vs. outside the cell? |
inside -65mV to -70mV |
| What is the range of voltage potential among neurons? |
-40 to -90 |
| What concentration of ions give this voltage potential? |
1. Na is relatively low in the cell 2. K is relatively high in the cell 3. CL is relatively low in the cell 4. Ca is very low relatively inside the cell |
| What maintains the Na and K concentrations inside and outside the cell? |
Sodium potassium pump |
| What would a diffusion gradient cause with Na in relation to K? |
would favor Na to flow in and K to flow out (pump maintains resting potential) |
| Start of the action potential a the synapse |
1. neurotransmitter binds to receptor 2. causes ion channel to open 3. change in membrane permeability (flow of ions changes pot) 4. may become more neg (IPSP) or positive (EPSP) 5. graded- large or small 6. they can summate |
| What ions could the ion channel effect? |
Na, K, Ca, Cl |
| Where are action potentials generated? |
axon hillock |
| What happens when EPSPs summate to threshold? |
they can stimulate coltage gated Na and K channels to open |
| Which voltage gated channel responds more quickly? Causes what? |
1. Na channels more quickly than K 2. rapid influx od Na |
| This influx of Na causese what? |
depolarization of the membrane up to +20 to +40 |
| After the depolarization what happens? |
K channels open and repolarization occurs |
| How do Na and K return to normal? |
Na/K pump |
| What type of response is an action potential? |
all or none, stereotyped |
| What is an absolute refractory period? |
a second AP can't be generated |
| What is a relative refractory period? |
AP can be generated it the stimulus is of sufficient intensity |
| The increase in membrane potential causes what? |
conduction of the AP, the positive charge distributes along the adjacent membrane and causes voltage-gated channels in the adjacent membrane to open |
| What is the conduction velocity of AP? |
from 1-2 m/sec in unmyelinated axons to 70-120 m/sec in myelinated axons |
| What is saltatory conduction? |
the AP is propogated in a myelinated axon |
| What are the nodes of Ranvier? |
in myelinated axones these nodes have a high concentration of voltage gated Na channels |
| What is the effect of the nodes of Ranvier? |
this causes the AP to be thrust down the axon from node to node increasing conducting velocity |
| What factors influence the generation of an AP? |
1. summation of postsynaptic potentials at axon hillock 2. distance of PSP to axon hillovk 3. PSPs on distal dendrites 4. PSPs summate over tiem and area 5. sum of inhib. or excit input 6. axo-axonic synapse (presynaptic inhibition |
| How does the distance of the PSP to axon hillock influence generation of AP? |
closer the greater the influence |
| PSPs on distal dendrites have more or less of an effect? |
less |
| Process of synaptic transmission? |
1. AP reaches synaptic ending 2. voltage gated Ca open, Ca centers 3. synaptic vesicle binds to membrane 4. release neurotransmitter into synaptic cleft |
| Where are neurotransmitters synthesized? |
synaptic ending |
| Where does degradation of neurotransmitters occur? |
synaptic cleft, pre or post synaptic region or by glial cells |
| What is synaptic plasticity? |
The effect of synaptic transmission onthe postsynaptic neuron is not static, it can change overtime with repeated stimulation |
| How can synapses become more efficient and effective? |
1. increased neurotransmitter production 2. creation of more post-synaptic receptors |
| How long will these plastic changes remain? |
long term and quasi-important |
| What neurotransmitter is used with a myoneural junction? |
acetyl choline |
| Where is the motor endplate? |
where synaptic ending releases transmitter into synaptic cleft to affect muscle |
| What is Myasthenia Gravis? |
autoimmune disorder, loss of strength with repeated contractions and recovery at rest |
| What causes myasthenia gravis? |
due to decreased number of Ah receptors available |
| What decreases the number of acetyl choline receptors |
antibody against receptors as part of autoimmune response |
| How common is myasthenia gravis? |
1/10000 women>men |
| When does myasthenia gravis become life threatening? |
when it affects the respiratory muscles |
| What is the treatment |
anticholinesterase drugs and corticosteroids and other immunosupressant drugs |
| Name the four phases |
|
Vanessa Kennedy
on 2009-10-06
mr. charles11
