Physiology I: Cellular Neuro > Lectures 9 & 10: Synapses > Flashcards

Lectures 9 & 10: Synapses Flashcards

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1
Q

Synapse

A
  • Site at which an impulse is transmitted from one cell to another
  • Electrical and chemical synapses
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2
Q

Electrical synapse

A
  • Nervous system, some types of smooth muscle, cardiac muscle, embryonic cells, via gap junctions
  • Each channel is hexagonal array of 6 subunits (a connexon)
  • Each subunit is made of the protein connexin
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3
Q

Chemical synapses

A
  • Nervous system: presynaptic > postsynaptic neuron)
  • Receptor cells > sensory neuron
  • Motor neuron > muscle cell (the neuromuscular junction, NMJ)
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4
Q

Characteristics of electrical synapses

A
  • Continuous (2-5nm gap)
  • Almost no synaptic delay
  • Potential bi-directional transmission
  • Coupling ratio (ratio of sizes of presynaptic and postsynaptic potentials) does vary (<50%)
  • Not readily altered by pharmacological agents
  • Connexon channels can be modulated
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5
Q

Bi-directional transmission of electrical synapses

A
  • Can allow passage of ions and larger molecules (cAMP, IP3)
  • Rectification occurs in many places
  • Mammalian CNS reflexes pathways, conduction may be bi- directional where you want very little delay or want a number of neurons to fire together (synchrony needed)
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6
Q

Connexon channels are usually open, but can be closed by

A
  • Increased [Ca]i or [H]i

- Depolarization of one cell

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7
Q

When cell is coupled via gap junctions

A
  • Channels provide a low resistance pathway (Rc) that is much lower than Rm
  • Ions take pathway of least resistance
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8
Q

In normal cells,

A
  • No current flow, because of high rm and Ri

- Current flows away (path of least resistance) without entering next cell

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9
Q

Chemical synapse characteristics

A
  • Membranes of presynaptic cell separated by synaptic space from membrane of postsynaptic cell (20 – 50nm)
  • Synaptic delay (0.5 msec)
  • Conduction is one way, always forward (Bell-Magendie Law)
  • Synapses on dendrites, axons, or cell body
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10
Q

Chemical synapse mechanism

A
  • Chemical substance released from presynaptic cell
  • Interacts with membrane of postsynaptic cell
  • Produces a change in its membrane permeability
  • Results in an electrical or chemical response
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11
Q

Action potential conduction to axon terminal

A
  • Action potential not conducted along surface of axon terminal membrane
  • Induces it to depolarize and open voltage-dependent calcium channels (N-type)
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12
Q

Calcium enters the axon terminal

A
  • Down its electrochemical gradient
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13
Q

The increase in [Ca]i causes

A
  • Synaptic vesicles to move and fuse with the surface membrane
  • Open to release their chemicals (neurotransmitters) into the synaptic cleft
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14
Q

An increase in [Ca]i is important for the release of many secretory substances from

A
  • Cells of various types
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15
Q

Released transmitter

A
  • Diffuses across cleft to postsynaptic membrane that contains receptors
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16
Q

Transmitters must bind to

A
  • Specific receptor sites on postsynaptic membrane

- Amount of binding will be dependent on amount of transmitter released

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17
Q

Neurotransmitter binding causes

A
  • Opening of specific ion channels (for Na or K or Cl)

- Evoke a change in membrane potential (the postsynaptic potential/PSP)

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18
Q

Neurotransmitter can be removed form synaptic cleft via

A
  • Diffusion away (for all transmitters)
  • Enzymatic destruction of transmitter molecule
  • Reuptake of transmitter into terminal
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19
Q

Neurotransmitter removal processes favor

A
  • Unbinding

- Leads to restoration of Vm to resting level and termination of neurotransmission

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20
Q

Enzymatic destruction of transmitter molecule occurs in

A
  • Some molecules

- ACh

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21
Q

Reuptake of transmitter into terminal

A
  • Often a sodium dependent process

- Major for catecholamines

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22
Q

Excitatory postsynaptic potentials (EPSPs)

A
  • Chemical released when binding to postsynaptic membrane induces a non-selective increase in Pm to all small ions
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23
Q

EPSP results in

A
  • Depolarization since in resting membrane PK»>PNa
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24
Q

An increase in PK, PCl, and PNa leads to

A
  • Net movement of positive charges inside, hence depolarization
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25
EPSP depolarizing response magnitude
- Small, around 1-2 mV | - Decreases decrementally as EPSP moves away from synaptic region
26
A single EPSP
- Not large enough to reach an action potential threshold - Will take nerve membrane closer to threshold - Summation will be required
27
Presynaptic neurons that cause EPSP's in postsynaptic cells are called
- Excitatory neurons | - The neurotransmitter released is an excitatory neurotransmitter
28
Convergence is characteristic when
- Many presynaptic neurons synapse on one postsynaptic cell | - These are the most common type and are the ones that allow integration
29
Divergence
- One neuron sends branches that synapse with many postsynaptic neurons
30
Motor neuron to Renshaw cell
- Divergent | - One presynaptic action potential produces a burst of action potentials in many postsynaptic cells
31
Motor neuron to Renshaw cells are rare
- Renshaw cells in ventral horn inhibit monosynaptic reflexes (also group Ia inhibitory interneurons) - Produce recurrent inhibition (or facilitation)
32
At one-to-one synapses, such as NMJ,
- There is no integration
33
Inhibitory postsynaptic potentials (IPSPs)
- Chemical release causes a selective change in membrane permeability to K and/or Cl
34
Increase in PK causes
- Hyperpolarization | - The effect of increasing PCl depends on Vm relative to ECl
35
Usually Vm = ECl or Vm is a little less negative than ECl, so
- Net effect in the first case is to reduce the size of EPSP's if occurring - Or in the second case to cause hyperpolarization - In either case, inhibition results
36
A neuron that causes an IPSP is called
- Inhibitory neuron | - Transmitter released is an inhibitory neurotransmitter
37
In some parts of the nervous system,
- A neurotransmitter can be excitatory - In other parts inhibitory - Also, more than one neurotransmitter may be released at a synapse
38
Presynaptic inhibition
- Depolarization-dependent neurotransmitter release
39
Lowered resting Vm leads to
- Reduced AP magnitude > less transmitter release at synapse > transmission inhibition/failure at “E”
40
All of the electrical signals are integrated along the membrane, but along the dendritic and nerve cell body membrane
- No action potentials are produced
41
Axon hillock membrane has lower action potential threshold so if depolarization is sufficient,
- An action potential will be generated and propagated | - Transfers information further in the circuit
42
Modulation of calcium release
- Extracellular calcium (Cao) required for vesicle release | - Removal of Cao abolishes vesicle release
43
Increase in [Mgo]
- Also reduces the number of vesicles released | - Competes with Ca
44
Increase in [Cao] or a decrease in [Mgo]
- Increases release of vesicles
45
Synaptic transmission can be modified by
- Alterations in plasma [Ca] or [Mg]
46
Fatigue (depression) of synaptic neurotransmitter release occurs upon
- Repeated stimuli
47
Botulinus toxin
- Reduces ACh release at synapses, especially at NMJ
48
Facilitation
- Increase in amount released (short time span) | - Post-tetanic potentiation is another form of augmentation
49
By presynaptic inhibition
- Reduces the amount of transmitter released
50
Long term potentiation involves
- Protein synthesis | - Perhaps involved in memory
51
Acetylcholine (ACh)
- Found in both peripheral and central nervous system - Betz cells of cortex - Basal ganglia and movement control, senile dementia (Alzheimer's) involves cholinergic pathways
52
Catecholamines
- Epi/Norepinephrine in peripheral, also central nervous system - Dopamine synapses lost in Parkinsonism - Overactive dopamine implicated in certain psychoses
53
Excitatory
- Glutamate and aspartate | - Serotonin involved in thermoregulation, mood, behavior
54
Inhibitory
- Glycine | - GABA
55
General anesthesia
- Prolongs open time of GABA receptors-linked chloride channels - Leads to prolonged postsynaptic inhibition at GABA synapses - GABA synapses are a major target of general anesthetic
56
Nitric oxide (NO)
- Gaseous - Not packaged and released from vesicles - Short-lived - Produced as needed
57
Nitric oxide (NO) found in
- Enteric nervous system - Certain blood vessels - Skeletal muscle
58
Some neurotransmitters (peptides) are made by
- Nerve cell under control of the nucleus of the nerve cell - These neurotransmitters made on ER, packaged by the Golgi and conducted to axon terminal by a fast axoplasmic transport system - Others may be synthesized in the terminal
59
Depolarization causes
- Release of number of vesicles | - Each vesicle contains a certain amount of molecules
60
The amount/per vesicle
- Quanta
61
Besides the basic, more classical neurotransmitters, certain neurons contain
- Small neuropeptides | - Act at low concentration to excite or inhibit other neurons
62
Neuroactive peptides
- Range from two amino acids to about 40 amino acids long
63
Some neuroactive peptides may act as neuromodulators
- Modifying the release or effect of a neurotransmitter
64
Pre-synaptic events
- Arrival of action potential at terminal - Opening of voltage-gated Ca channels - Ca entry into terminal - Triggering of SNARE proteins > vesicle release - Diffusion of NT across synaptic cleft
65
Post-synaptic events
- NT binds to receptors on post-synaptic membrane - Opening of ion-specific channels > change in membrane permeability > change in Vm - Change in Vm = Post-synaptic potential (PSP)
Physiology I: Cellular Neuro
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