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

Lectures 9 & 10: Synapses Flashcards

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
Q

EPSP depolarizing response magnitude

A
  • Small, around 1-2 mV

- Decreases decrementally as EPSP moves away from synaptic region

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26
Q

A single EPSP

A
  • Not large enough to reach an
    action potential threshold
  • Will take nerve membrane closer to threshold
  • Summation will be required
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27
Q

Presynaptic neurons that cause EPSP’s in postsynaptic cells are called

A
  • Excitatory neurons

- The neurotransmitter released is an excitatory neurotransmitter

28
Q

Convergence is characteristic when

A
  • Many presynaptic neurons synapse on one postsynaptic cell

- These are the most common type and are the ones that allow integration

29
Q

Divergence

A
  • One neuron sends branches that synapse with many postsynaptic neurons
30
Q

Motor neuron to Renshaw cell

A
  • Divergent

- One presynaptic action potential produces a burst of action potentials in many postsynaptic cells

31
Q

Motor neuron to Renshaw cells are rare

A
  • Renshaw cells in ventral horn inhibit monosynaptic reflexes (also group Ia inhibitory interneurons)
  • Produce recurrent inhibition (or facilitation)
32
Q

At one-to-one synapses, such as NMJ,

A
  • There is no integration
33
Q

Inhibitory postsynaptic potentials (IPSPs)

A
  • Chemical release causes a selective change in membrane permeability to K and/or Cl
34
Q

Increase in PK causes

A
  • Hyperpolarization

- The effect of increasing PCl depends on Vm relative to ECl

35
Q

Usually Vm = ECl or Vm is a little less negative than ECl, so

A
  • 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
Q

A neuron that causes an IPSP is called

A
  • Inhibitory neuron

- Transmitter released is an inhibitory neurotransmitter

37
Q

In some parts of the nervous system,

A
  • A neurotransmitter can be excitatory
  • In other parts inhibitory
  • Also, more than one neurotransmitter may be released at a synapse
38
Q

Presynaptic inhibition

A
  • Depolarization-dependent neurotransmitter release
39
Q

Lowered resting Vm leads to

A
  • Reduced AP magnitude > less transmitter release at synapse > transmission inhibition/failure at “E”
40
Q

All of the electrical signals are integrated along the membrane, but along the dendritic and nerve cell body membrane

A
  • No action potentials are produced
41
Q

Axon hillock membrane has lower action potential threshold so if depolarization is sufficient,

A
  • An action potential will be generated and propagated

- Transfers information further in the circuit

42
Q

Modulation of calcium release

A
  • Extracellular calcium (Cao) required for vesicle release

- Removal of Cao abolishes vesicle release

43
Q

Increase in [Mgo]

A
  • Also reduces the number of vesicles released

- Competes with Ca

44
Q

Increase in [Cao] or a decrease in [Mgo]

A
  • Increases release of vesicles
45
Q

Synaptic transmission can be modified by

A
  • Alterations in plasma [Ca] or [Mg]
46
Q

Fatigue (depression) of synaptic neurotransmitter release occurs upon

A
  • Repeated stimuli
47
Q

Botulinus toxin

A
  • Reduces ACh release at synapses, especially at NMJ
48
Q

Facilitation

A
  • Increase in amount released (short time span)

- Post-tetanic potentiation is another form of augmentation

49
Q

By presynaptic inhibition

A
  • Reduces the amount of transmitter released
50
Q

Long term potentiation involves

A
  • Protein synthesis

- Perhaps involved in memory

51
Q

Acetylcholine (ACh)

A
  • 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
Q

Catecholamines

A
  • Epi/Norepinephrine in peripheral, also central nervous system
  • Dopamine synapses lost in Parkinsonism
  • Overactive dopamine implicated in certain psychoses
53
Q

Excitatory

A
  • Glutamate and aspartate

- Serotonin involved in thermoregulation, mood, behavior

54
Q

Inhibitory

A
  • Glycine

- GABA

55
Q

General anesthesia

A
  • 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
Q

Nitric oxide (NO)

A
  • Gaseous
  • Not packaged and released from vesicles
  • Short-lived
  • Produced as needed
57
Q

Nitric oxide (NO) found in

A
  • Enteric nervous system
  • Certain blood vessels
  • Skeletal muscle
58
Q

Some neurotransmitters (peptides) are made by

A
  • 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
Q

Depolarization causes

A
  • Release of number of vesicles

- Each vesicle contains a certain amount of molecules

60
Q

The amount/per vesicle

A
  • Quanta
61
Q

Besides the basic, more classical neurotransmitters, certain neurons contain

A
  • Small neuropeptides

- Act at low concentration to excite or inhibit other neurons

62
Q

Neuroactive peptides

A
  • Range from two amino acids to about 40 amino acids long
63
Q

Some neuroactive peptides may act as neuromodulators

A
  • Modifying the release or effect of a neurotransmitter
64
Q

Pre-synaptic events

A
  • 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
Q

Post-synaptic events

A
  • 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 (8 decks)

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