Flashcards in Lecture 2 - ANS Deck (63)
Briefly state the 7 steps of synaptic transmission:
1.pre-synaptic membrane depolarizes due to AP
2. NT's packed in vesicles and docked at pre-synaptic v.
3. Voltage gated CA channels open w/depolarization, calcium enters pre-synaptic t.
4. increase in calcium --> fusion of vesicle with pre-synaptic membrane
5. NT released into synaptic cleft
6. NT bind to recepts in post-syn membrane
7. Post-synaptic receptors activated and trigger event
After Ca enters the pre-synaptic terminal, what occurs?
Vesicles containing NT's released into cleft
What binds the vesicles to the membrane?
Botulinum toxins and Tetanus cut what proteins and prevent the binding of the vesicle?
- prevent synaptic vesicle fusion & NT release
What kind of paralysis does Botulinum cause? Tetanus?
1. Flaccid Paralysis
2. Spastic Paralysis
Botulinum toxin affects what fibers?
TetX is taken up by inhibitory neurons where? Causing what?
- SPASTIC paralysis
NT's released from vesicles bind what kind of receptors when propagating an electrical signal?
- AChR, GABA
- allow ion influx --> Post-synaptic current = PSC
What is PSC? PSP?
Post Synaptic Current
Post Synaptic Potential
Ionototropic receptors allow ion influx leading to what 2 events?
PSC & PSP
Is the release of NT from vesicles an AP?
- it is a PSP
- graded response propagated passively
How can one get an AP from a PSP?
integration of signals
EPSP's cause what changes in the membrane? Are these AP's? What do they increase the probability of?
1. MEMBRANE DEPOLARIZATION
- influx of cautious bring membrane to zero
2. NOT APs!!! but can generate AP if strong enough
3. increase probability of AP firing
What are some inhibitory NT's? What influx do they cause?
1. GABA, Glycine
2. Influx of Cl- (IPSC)
What two events can IPSP cause? Do ESPS do the same?
1. membrane depolarization & hyper polarization
ESPS's do NOT cause hyper polarization
Which of the two stabilizes the Em at negative potential?IPSP or EPSP?
- reduce probability of AP firing
- away from AP threshold (graph is upside down)
Synaptic integration, or the effect of EPSP's and IPSP's depends on what?
Location at the neuron
Two AP's happening a the same time in different locations are called:
Sequence of AP's in the same place, close in time are called:
What are the 2 main functions of ANS?
2. Respond to external stimuli
(light, external threat --> FIGHT OR FLIGHT)
In the ANS, what controls cardiac muscle, smooth muscle & glands? What modulates organ activity and are accompanied by visceral afferents?
- EFFERENT FIBERS (motor fibers)
What are the 8 main Autonomic NT's?
1. Acethylcholine (ACh),
2. Norepinephrine (NE).
Epinephrine is a central neurotransmitter, but in the ANS its
function is mainly hormonal.
What type of post-synaptic receptor does Neuron-Viscera use?
- neuron to neuron 7 neuron to SkM both use INOTROPIC (fast)
What type of NT effect does Neuron-Viscera have?
(the other two are direct)
Which type of muscle has adventitial (outermost) perivascular varicose nerves? (around a blood vessel)
VASCULAR SMOOTH MUSCLE
- visceral smooth muscle has them all throughout
- VASCULAR ONLY AT THE TOP!!! uses coupled cells
What is the only place using NMJ?
Neuron- Skeletal Muscle
Which of the two: vascular or visceral, contains connections and highly interconnected neurons?
- ex: better coordination of heart contraction
VASCULAR has coupled cells but NOT interconnected (synapses are found on top)
Cardiac myocytes have what type of synapses?
- junctions appear partway along an axon as it extends
Describe the following for NE:
1. Where made
3. Location of degrading enzymes
1. in Vesicles, from DOPA
2. interact with adrenergic receptors
- NE action terminated by re-uptake into cytosol & degradation (MAO, COMT)
3. Cytosol, mitochondria, circulation