Synaptic Communication Flashcards

1
Q

4 benefits of electrical signaling

A
  • covers long distances with minimal loss of signal
  • rapid
  • quickly repeated
  • information can be conveyed in patterns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

4 limitations of electrical signaling

A
  • binary
  • difficult to modify
  • energy intensive
  • microenvironment dependent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the resting membrane potential?

A
  • the potential energy in the electrical gradient formed across the plasma membrane
  • caused by formation of K+ concentration gradient and permeability of the membrane to K+
  • K+ concentration high inside cell, low outside cell; Na+ opposite
  • K+ moves out of cell down concentration gradient, and is then pulled back into the cell via the electrical gradient: causes internal membrane to be negative and external membrane to be positive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Ohm’s Law

A

V = IR
V is the voltage (plasma membrane)
I is the current
R is the resistance (ion channels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Electrochemical equilibrium

A
  • When the concentration and electrical gradients for an ion are in balance
  • driven by diffusion of ions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Na+/K+ ATPase

A
  • important ion transporter
  • establishes Na+ and K+ gradients across the neuron membrane
  • actively moves Na+ and K+ against concentration gradient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ion channels

A
  • passive proteins
  • allow ions to diffuse down concentration gradient
  • K+, Na+, Ca2+, and Cl- channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Neuron membrane at rest

A
  • interior of neuron is negatively charged
  • separation and slow flow of K+ ions across plasma membrane creates membrane potential
  • Na+/K+ ATPase activity maintains electrochemical gradients
  • membrane potential allows neuron electrical activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What two equations calculate membrane potentials?

A
  • Nernst equation - equilibrium potential of an individual ion
  • Goldman equation - equilibrium potential of the entire plasma membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Neuron passive electrical state

A
  • cytoplasm is electrically resistant
  • neurons electrically inert
  • passive current rapidly decays over space and time
  • active current flow allows neuron electrical information transfer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Passive current flow

A
  • current decays
  • cytoplasm resistance
  • relative to distance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Active current flow

A
  • current repropogates
  • active process
  • relative to distance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The action potential

A
  • rapid change in membrane potential
  • caused by sequential opening of Na+ and K+ channels
  • requires Na+ and K+ gradients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

4 types of ion channels

A
  • leakage - constant ion flow along gradient
  • voltage-gated - respond to changes in membrane potential
  • ligand-gated - respond to ligand binding; NT, proteins, ions, & lipids
  • physically-gated - respond to other physical stimuli; mechanical, temperature, light
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

4 types of transporters

A
  • ATPase pumps - use ATP to move one or more substrates
  • ion exchangers - energy from moving one+ ions along concentration gradient will move other ions against gradient; opposite directions
  • co-transporters - one+ ions move another ion; same direction
  • multiple transporter systems - multiple transporters working together to move substrate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Voltage-gated ion channels

A
  • physical conformation changes with membrane polarization
  • time and charge dependent
  • ions move along concentration gradients
  • passive
  • refractory period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Ligand-gated ion channels

A
  • ligand binds, changes conformation of channel to allow ion movement along concentration gradient
  • diversity of ligands
  • passive
  • open in presence of sufficient ligand and appropriate environment state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Na+/K+ ATPase pumps

A
  • bind Na+ on inside of cell
  • phosphorylated, changing structure of transporter to open to exterior
  • Na+ released, K+ binds
  • causes dephosphorylation of transporter, allowing K+ inside
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Is the neurons resting potential positive or negative?

A
  • negative

- in an AP, membrane potential is stimulated, rapidly goes positive, and then returns to the negative state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Name the 6 phases of APs

A
  • resting phase
  • activation phase
  • rising phase
  • falling phase
  • undershoot phase
  • recovery phase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What occurs during the resting phase of an AP?

A
  • very little activity

- slow leakage of K+ out of cell through k+ channel from

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What occurs during the activation phase of an AP?

A

-stimulus is induced, opening Na+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What occurs during the rising phase of an AP?

A
  • voltage-gated Na+ channels open, causing a dramatic and rapid influx of Na+ ions
  • charge of membrane is reversed (+ in, - out)
  • voltage-gated K+ channels open
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What occurs during the falling phase of an AP?

A
  • voltage-gated Na+ channels close
  • voltage-gated K+ channels open, K+ moves out
  • leaves a more negative state on the inside of the cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What happens during the undershoot phase of an AP?

A
  • refractory period prevents voltage-gated Na+ channels from opening
  • no AP can occur
  • voltage-gated K+ channels close
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What happens during the recovery phase of an AP?

A

-leaky K+ channels re-establish the resting potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What part of the neuron is an AP initiated?

A

axon hillock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What direction is an AP conducted?

A
  • anterograde; away from cell body

- unidirectional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Two ways to increase AP conductance

A

1) increase axon caliber
- reduces internal resistance; energy intensive; physically restrictive (squid example)
2) insulate axons (myelination)
- prevents current leakage, requires glial support, oligodendrocytes (CNS), Schwann cells (PNS)
- saltatory conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

2 major classes of neurotransmitters

A

small molecules and neuropeptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

small molecule NTs

A
  • amino acids or derivatives
  • synthesized in presynaptic terminal
  • stored in small synaptic vesicles
  • released from the presynaptic terminal
  • examples are glutamate, GABA, & Acetylcholine
32
Q

neuropeptide NTs

A
  • proteins
  • synthesized in the body
  • stored in large vesicles
  • released both pre- and postsynaptically, and into extracellular environment
  • Ex. brain gut peptides, opioid peptides, etc.
33
Q

Synaptic transmission steps (8)

A
  • AP
  • Ca2+ channel depolarization
  • Ca2+ influx
  • synaptic vesicle fusion
  • NT release
  • NT receptor activation
  • NT reuptake
  • NT sequestration/metabolism
34
Q

3 distinct pools for synaptic vesicles

A
  • readily releasable pool
  • recycling pool
  • reserve pool; tethered to actin and can be released
  • these are important in stages of release
35
Q

SNARE complexes

A
  • proteins that allow vesicle release

- include synaptobrevin, syntaxin, SNAP-25, and synaptotagmin

36
Q

Steps in NT release

A
  • vesicle docks
  • SNARE complexes form to pull membranes together
  • entering Ca2+ binds to synaptotagmin
  • Ca2+-bound synaptotagmin catalyzes membrane fusion by binding to SNAREs and the plasma membrane
37
Q

2 models of membrane reuptake and vesicle reformation

A
  • classic synaptic vesicle cycle

- ultrafast synaptic vesicle cycle (more likely/ faster)

38
Q

2 NT receptor types

A
  • ionotropic

- metabotropic

39
Q

Ionotropic NT receptors

A
  • ligand binding opens ion channel
  • variable selectivity for ions
  • not necessarily uni-directional
  • directly involved in creating postsynaptic electrical current and changing membrane potential
  • excitatory (depolarizing) or inhibitory (hyperpolarizing)
40
Q

Metabotropic NT receptors

A
  • G-protein coupled intracellular signals
  • relatively slow activation time
  • prolonged signal duration
  • signals modify the activity of ionotropic receptors, ion channels, and transporters
  • signals alter terminal structure and function
41
Q

Change in post-synaptic membrane potential by NT receptors

A
  • Excitatory postsynaptic potential (EPSP) - depolarization; Na+, Ca2+
  • Inhibitory postsynaptic potential (IPSP) - hyperpolarization; Cl-, K+
42
Q

Influence of location on synaptic input strength

A
  • membrane potentials decay with space and time

- proximity to the trigger zone dictates the relative influence of a synaptic input

43
Q

Postsynaptic potential summation

A
  • the total change in membrane potential based on the spatial (location) and temporal (frequency) aggregation of postsynaptic potentials
  • sufficient depolarization triggers an AP
  • think about inhibitory and excitatory signals
44
Q

Where are emotional and abstract states mapped in the brain?

A

deep brain areas

45
Q

Where are maps overlaid and compared?

A

association cotrices

46
Q

What are spinal reflexes?

A

Sensory and motor loops that function independent of descending brain control. Example is hitting the patellar ligament with a mallet and the result is a leg kick.

47
Q

What is the Hebbian Theory?

A

Neuronal networks undergo activity-dependent plasticity throughout life, and activity drives neural network consolidation, while inactivity leads to decay.

48
Q

You are born with many more neuron than you end up with as an adult. How is this related to the Hebbian Theory?

A

Synapse pruning (loss of synapses) occurs during development as a result of the strengthening of some synapses and the subsequent loss of others.

49
Q

Name the 6 changes at synaptic terminals that drive neuronal plasticity

A

1) increased/decreased synaptic vesicle release
2) increase/decreased receptor density
3) changes in receptor sensitivity and conductance
4) changes in receptor subtype expression
5) sprouting of new synapses
6) formation of new connections

50
Q

How do networks change as a result of Long-term Potentiation (LTP) and Long-term Depression (LTD)?

A

Strength of connections and number of connections can change

51
Q

Explain the somatosensory circuit of touch

A

Three neurons communicate peripheral sensation to the brain:
1st order: mechanosensory neuron –> brainstem (medulla)
2nd order: brainstem (medulla) –> thalamus
3rd order: thalamus –> somatosensory cortex

52
Q

Explain the decussation of 2nd order neurons in touch

A

They decussate (cross the midline) at the level of the medulla; information is processed contralaterally within the brain

53
Q

What is a sensory field?

A
  • discrete areas of touch discrimination that fill dermatomes
  • sensory fields overlap
  • highly variable in size
  • -size determined by # of neurons innervation a dermatome and degree of neuronal arborization
54
Q

Characteristics of mechanosensory neurons

A
  • sense touch and pain
  • activated by physical distortion
  • pseudounipolar
  • pseudo - not unipolar; has cell body
  • has continuous dendrite to axon tree
55
Q

Name the 4 types of mechanoreceptor cell types

A

Merkel’s cells, Meissner corpuscles, Ruffini endings, and Pacinian corpuscles

56
Q

Characteristics of mechanoreceptor cells

A
  • encase mechanosensory neurons
  • detect & transfer different types of skin distortion information
  • sensitivity, response time, and duration of activation vary
  • a single neuron innervates a single mechanoreceptor cell type
57
Q

What is a nociceptor?

A

mechanosensory neuron that detects pain; has free nerve endings

58
Q

What is a thermoreceptor?

A

mechanosensory neuron that detects temperature; has free nerve endings

59
Q

What is the relationship between density of peripheral innervation and sensitivity?

A
  • the higher the density of peripheral innervation, the greater the sensitivity
  • ex. fingers have more neurons that skin on the back, so fingers are more sensitive than the back
60
Q

Name the 5 places in the brain where sensory information is passed along

A
  • secondary somatosensory cortex
  • association cortex
  • premotor cortex
  • limbic cortex
  • frontal cortex
61
Q

Where are sensory fields organized?

A

in the somatosensory cortex

62
Q

Explain how the somatosensory cortex is plastic

A
  • cortical regions expand and contract in size
  • use increases connectivity
  • disuse decreases connectivity
63
Q

Describe the 3 types of pain

A

1) somatic - pain perceived from peripheral cutaneous perception; thermal, mechanical, chemical
2) visceral - pain perceived from internal organ systems; referred, perceived as peripheral
3) neuropathic - pain caused by damage to PNS and CNS neurons; perceived as a burning or shocking pain

64
Q

Name the 4 types of nociceptors

A
  • thermal nociceptors
  • mechanical nociceptors
  • polymodal nociceptors
  • silent nociceptors
65
Q

Describe thermal nociceptors

A
  • sense temperature extremes
  • fast signals
  • separate from thermoreceptors
66
Q

Describe mechanical nociceptors

A
  • sense extreme changes in pressure or tearing

- fast signal

67
Q

Describe polymodal nociceptors

A
  • sense thermal (hot and cold), mechanical, and chemical stimuli
  • slow signal
68
Q

Describe silent nociceptors

A
  • respond to visceral disorders

- fast signal

69
Q

Describe the initiation of pain signaling

A
  • cutaneous nociceptors are activated
  • inflammation releases modulatory signals (lipids - prostaglandins, thromboxanes, leukotrines, & neuropeptides)
  • inflammatory molecules drive inflammation, sensitize nociceptors, & directly activate nociceptors
70
Q

How do NSAIDs reduce inflammation?

A

-reduce the production of prostaglandins and thromboxanes

71
Q

Describe the afferent connections in pain signaling

A
  • 1st, 2nd, and 3rd order neurons
  • somatosensory cortex destination
  • 1st order neurons synapse in the spinal cord
  • 2nd order neurons decussate in the spinal cord
  • pain can be gated at the spinal cord
72
Q

What is a function of silent nociceptors?

A
  • they refer pain
  • important because brain doesn’t have a map of internal organs, so the silent nociceptors allow our brain to process visceral pain by referring the pain
73
Q

What is a similarity between silent nociceptors and peripheral nociceptors?

A

they synapse onto the same 2nd order neurons

74
Q

What is the Gate Theory of pain?

A
  • pain is gated & regulated at the level of the spinal cord; nociceptor & second order connection
  • peripheral touch inhibits nociception
  • no descending (brain) signaling required
  • descending signals can influence spinal gating
75
Q

How do opiates help the brain gate pain at the spinal cord?

A
  • they interact with central pain receptors (brain and spinal cord) to block the transmission of nociceptive stimuli to the somatosensory cortex
  • nociceptor can’t send signal to 2nd order neuron
76
Q

Comparison of NSAIDs and opiates

A
  • both can inhibit pain
  • NSAIDs prevent pain peripherally
  • opiates prevent pain centrally