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34 Cards in this Set

  • Front
  • Back
Signal transmission can occur through two means:
1. Bridged Junctions: Cell to cell channels known as gap junctions
2. Unbridged junctions: Specialized areas of apposed but discretely separate membranes - synaptic clefts
Describe the morphological characteristics of gap junctions (4)
1. The gap bn coupled cells is 3.5 nm wide.
2. Apposing cells contribute a hemi-channel known as a connexon
3. Two connexons form an ion channel with a pore size of 1.5nm in diameter
4. Each connexon is made of 6 subunits known as connexins.
Which means of conduction is faster: via Electrical Gap Junctions or Chemical Synapses? Why?
Gap Junctions - they directly bridge the gap between pre- and post-synaptic cells. They also have low-resistance and high-conductance.
What are the 6 properties of Electrical Synapses?
1. Speed; no synaptic delay
2. Synchronization of transmission
3. Involved in stereotypic, fast reflexes
4. Transmit developmental and regulatory signals bn cells
5. All or nothing transmission since no mechanism of inhibition
6. No mechanism for long-lasting changes in effectiveness (modulation) of synaptic transmission.
What are the three types of chemical synapses? (3) (Neuro...)
1. Neuro-neuronal
2. Neuromuscular
3. Neuroeffector
What is a synonym for "pre- and post-synaptic"?
Pre- and Postjunctional
What are the three presynaptic specializations?
1. Synaptic vesicles
2. Active zones (presynaptic dense projections that release neurotrans))
3. Autoreceptors/receptors
How wide is the typical synaptic cleft?
30-50nm (which wider than the adjacent extracellular space (20nm))
What are the two postsynaptic specializations?
1. Receptors
2. Postsynaptic density - an area densed with receptors in close proximity to the active zone in presynapses
What are the four types of CNS synapses?
1. Gray's 1 - asymmetric
2. Gray's 2 - symmetric
3. Monoaminergic
4. Peptidergic
Compare Gray's Type I and II with respect to:
1. Symmetry
2. Excitatory or Inhibitory
3. Cleft distance
4. Vesicle shape
1. I's post synapse is thicker than pre- and thus considered asymmetric. II's are symmetric
2. I's are excitatory vs II's inhibitory (e.g. GABA)
3. I's cleft space is wider compared to II's
4. I's vesicles are round vs II's flattened.
Describe Monoaminergic synapse with respect to:
1. Morphology
2. Vesicle shape and contents and its coating
3. Cleft distance
1. Highly branched structure dotted with vericosities that are small synapses "En passant" - in other words, there are no prominent pre- or post-synaptic densities.
2. Dense-core vesicles contain Catacholamines (e.g. norepi and dopamine) and Endoamines (5HT)
3. Cleft distance is wide
How are peptidergic synapses similar to monoaminergic synapses?
1. They also have lg dense-core vesicles with a variety of neuropeptides
2. They act mostly as modulators
Describe neuromuscular junction with respect to:
1. What do you find in the vesicles?
2. What type of channels are found within the presynaptic dense projections?
3. How does the cleft compare to that found in the CNS?
4. Describe the the postsynaptic membrane (morph, local of/ type of receptors)
1. Acetylcholine
2. Ca++ channels
3. Cleft is wide, has a basal lamina, and includes degradative enzymes
4. Post synaptic junction has fold with acetylcholine receptors apposed to presyn active zones; troughs have voltage-gated Na+ channels
1. Myasthenia Gravis is a disease at the:
2. It is caused in two ways:
a. (most common)
b. (less common)
3. Where are symptoms most pronounced?
4. What is treatment
1. Neuromuscular junction
2. a. Autoimmune - attacking acetylcholine receptors
b. Congenital
3. Eyelid muscles, upper limbs, oropharyngeal regions
4. Treat with acetylcholinesterase so as to retard breakdown and increase acetylcholine concentration
Describe how vesicles are propelled/docked to the active zone of the presynapse (3 steps):
1. Dephosphorylated Synapsin I anchors vesicles to cytoskeletal proteins
2. Depolarizing synapse releases Ca++ which activates calmodulin-dependent protein, phosphorylating synapsin I, releasing it from cytoskeleton
3. Rab3A (neuronal-specific GTPase) binds to vesicles, propelling them to active zone.
[Warning: This might be wrong] What releases the vesicle from the complex (i.e. Rab3A)
Hint: There are two cytosolic proteins involved. How do they interact and what energy source do they use?
1. NSF (N-ethylmaleimide-sensitive factor) is a cytosolic ATPase that hydrolyzes ATP to release the Rab3A (maybe)
2. SNAP (soluble NSF attachment protein) binds to NSF
What proteins are involved with vesicle fusion to the membrane and subsequent exocytosis. What reverses this process so that the vesicular membrane can be recycled?
v-SNARE and t-SNARE associate and cause fusion with plasma membrane. Once contents are exocytosed, NSF/SNAP bind to v-/t-SNARE complex and allow it to dissociate for recycling.
What triggers vesicle exocytosis?
Synaptotagmin has 4 Ca++ binding sites that are triggered from Ca depolarizing and promotes rapid fusion of the vesicle to the membrane.
What does Tetanus toxin target and cleave in the exocytosis process? What about Botulinum toxin A, B, and C?
v-SNARE (or VAMP).
Bot A and C cleave t-SNAREs (SNAP-25 and Syntaxin) and Bot B targets v-SNARE (VAMP)
How does tetanus cause contraction? What about botulism?
It prevents inhibitory neurotransmitter GABA from being released to counteract acetylcholine. Similarly, it prevents acetylcholine from being released so causes flaccidity.
What are the two classes of receptor-gated transmission?
Direct and Indirect
Describe Direct Gating
1. What are they also known as and why?
2. Fast or slow?
3. How many subunits and transmembrane domains do these channels typically have?
1. Ionotropic receptor bc they function both as a receptor and ion channel
2. Fast
The channel both recognizes it and is opened by it (aka ionotropic receptor). Acetylcholine is an example with 5 subunits and 4 transmembrane domains.They are fast.
Describe Indirect gating.
1. What are they also known as?
2. Fast or slow?
3. What does it activate? To stimulate what?
4. Number of subunits and transmembrane domains?
1. Metabotropic Receptors
2. Slow acting
3. Activates G proteins to stimulate 2nd messenger cascade (cAMP or cGMP)
4. Typically has 1 subunit with 7 transmembrane domains.
Electrical synapses and chemical synapses have different properties of transmission. Chemical synapses have a...:
1. Synaptic response is amplified or decreases?
2. Plastic or non-plastic response
3. Specific or diverse transmitter resposibility
4. Fast or slow?
5. Neuromodulation property (yes or no?)
1. Amplified (via cascade)
2. Plastic
3. Can respond to diverse array of transmitters
4. Slow response
5. Yes
Gaseous transmission can be between: (Neuro-...; two types)
1. Neuro-neuronal
2. Neuroeffector (often smooth muscle...things viagra and NO)
NO and CO as neuorotransmitters both increase production of:
How is NOS activated in neuro-NEURONAL synapse?
1. Glutamate is released from presyn and binds to NMDA and opens channel receptors (N-methyl-D-aspartate)
2. This allows Ca++ to enter through NMDA and activate NOS via its calmodulin-binding site.
3. NOS produces NO while converting arginine to citrullin
4. NO acts in postsynaptic cell, or diffuses to neighboring neurons, glial cells, or presynaptic terminal
How is the Ca2+ used to activate NOS released differently in Neuro-neuronal vs Neuro-effector synapses?
1. Neuro-neuronal: Glutamate is released from presynapse and triggers NMDA to open and allow entry of Ca2+
2. Neuro-effector synapse release Ca2+ via action potential
What are the steps to NO production in neuro-effector synapse?
1. Action potential invades presynaptic axon varicosities
2. Ca++ entry activates NOS to produce NO
3. NO diffuses into smooth muscle cells and acts there.
What effect does NO have on smooth muscle?
It binds to iron in a heme moiety that is attached to soluble guanylate cyclase that makes cGMP - a cascade that causes relaxation (among other things).
What is the rxn that synthesizes NO?
L-Argenine ---> NO + L-Citrulline

It is mediated by NO Synthase that requires cofactors Ca2+/Calmodulin and NADPH
How does NO activate soluble guanylate cyclase? What does this activation result in?
By binding to the iron in its heme moiety. Produces 2nd messenger cGMP and activation of cGMP-dependent protein kinase. This results in altered gaiting of ion channels in postsynaptic membrane.
The table on pg 10 is straight forward. However, what is the major ultrastructural difference bn chemical synapses and gaseous synapses?
Gaseous pre- and post- synapses have cytosolic NO synthase to make NO. The postsynatpic receptor is soluble guanylate cyclase with a heme moiety.