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Mammalian physiology > Nervous system - Lectures 1-3 > Flashcards

Nervous system - Lectures 1-3 Flashcards

1
Q

How many cells in body?
- how many neurons?, glial cells?
- how many synapses?

A
  • 37 trillion cells
  • 100 billion neurons
  • 900 billion glial cells
  • 1000 trillion synapses
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2
Q

Efferent vs afferent division

A
  • afferent –> PNS –> sends info from sensory receptors to the CNS
  • efferent –> PNS –> takes info from CNS to target cells
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3
Q

Autonomic vs somatic neurons?

A
  • autonomic –> involuntary control (heart, digestion, glands, adipose tissue)
  • somatic –> skeletal muscles
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4
Q

sympathetic vs parasympathetic

A
  • sympathetic
  • parasympathetic
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5
Q

what is the enteric nervous system?

A
  • network of neurons in the walls of the digestive tract
  • a unique part of the nervous system that can act autonomously or can be controlled by CNS through autonomic division of the PNS
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6
Q

3 functions of the nervous system

A
  1. receive signals from outside (Afferent)
  2. integration of signals
  3. output (sending out signal for action)
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7
Q

Central vs peripheral nervous system

A
  • central: brain + spinal cord
  • peripheral: sensory (afferent) neurons + efferent neurons
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8
Q

What are neurons + their function?

A

neurons = functional unit of the nervous system
- carry electrical signals

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9
Q

6 parts of a neuron + functions

A
  • cell body: nucleus + important organelles
  • axon: sending out signal
  • dendrites: receive signals
  • collaterals: axon branches out to send signal to dif. cells
  • axon terminals: interact with other neurons/target cells + store/release neurotransmitters
  • varicosities: swirl around axon + store/release neurotransmitters
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10
Q

3 types of neurons separated by function

A
  1. afferent: sends into to CNS
  2. interneuron: between sensory and efferent neurons –> integrate and send info
  3. efferent: take info from CNS to target cell
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11
Q

4 types of neurons based on structure

A
  1. multipolar: highly branched interneurons, lack long extensions
  2. peudounipolar: sdendrites and axon fused together. like bipolar but 2 “axons” exit the same place in cell body
  3. bipolar: 2 relatively equal fibers extending off central cell body (from 2 different places)
  4. anaxonic neurons: interneuron with no apparent axon
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12
Q

what is a synapse?
- 2 types?

A

region where axon terminal communicates with its postsynaptic target cell
- electrical (direct contact ish) VS chemical synapses (via neurotransmitters)

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13
Q

nucleus vs ganglion?

A

both are masses of cell bodies
- nucleus in CNS
- ganglion in PNS

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14
Q

White vs gray matter?

A
  • white: phospholipids + myelin from axons! = lots of axons
  • grey: lots of dendrites, cut into nucleus (cell bodies)
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15
Q

nerve vs tract?

A
  • nerve: collection of nerve fibers (axons, white matter) in PNS
  • tract: collection of nerve fibers (axons) (white matter) in CNS
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16
Q

Signal transfer from what to what to what for somatical motor neurons?
VS for autonomic neurons

A
  • somatical: afferent (body + axon in PNS, axon terminals in CNS) –> interneuron (CNS) –> efferent (cell body in CNS, rest in PNS)
    VS
    autonomic neurons: afferent (body + axon in PNS, axon terminals in CNS) –> interneuron (CNS) –>efferent cell (body in CNS, rest in PNS) –> another effector neuron to get to target
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17
Q

Axonal transport:
- fast (3)
- slow (2)

A

FAST:
- moves organelles and proteins at rates of up fo 400 mm/day
- anterogade transport: from cell body to axon terminal
- retrogade transport: from axon terminal to cell body
SLOW:
- moves material by axoplasmic/cytoplasmic flow at 0.2-2.5mm/day
- only 1 direction! anterogade

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18
Q

3 sizes of cytoplasmic protein fibers + examples
- associated with what?
- involved in (2)

A
  1. microfilaments –> actin fibers
  2. intermediate filaments: keratin + neurofilament
  3. microtubules –> tubulin
    - associated with accessory proteins (that carry neurotransmitters?)
    - in structural support and cell movement with motor proteins
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19
Q

what (2) allows developing neurons to find their targets?
- fixed for life?

A
  • growth cones and neurotrophic factors
  • not fixed for life –> can be rearranged
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20
Q

6 types of glial cells + where

A
  1. Schwann cells (PNS)
  2. Oligodendrocytes (CNS)
  3. Satellite cells (PNS)
  4. Astrocytes (CNS)
  5. Microglia (CNS)
  6. Ependymal cells
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21
Q

Schwann cells vs oligodendrocytes vs satellite cells

A
  • Schwann cells (PNS) and Oligodendrocytes (CNS) –> wrap around axon and form insulating myelin sheaths
  • schwann: 1 cell wraps around 1 axon vs oligo: 1 cell can warp around more than 1 axon
  • Satellite cells (PNS): non-myelinating Schwann cell + wrap around cell bodies!
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22
Q

astrocyte vs microglia vs ependymal cells

A
  • astrocyte (CNS): source of stem cell + take up water, neurotransmitters, secrete neurotrophic factors, help form blood-brain barrier, provide substrates for ATP production
  • microglia (modified immune cells): act like macrophages and eat dead cells
  • ependymal cells: creates barrier between compartments (cerebral spinal fluid) + source of neural stem cells
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23
Q

what are the spaces between the myelin sheaths/gaps in insulation called?

A

Nodes of Ranvier

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24
Q
  • if cell body dies, neuron ______
  • if axon is severed, (what) survives and (what) degenerates –> sensory vs motor neuron
  • regeneration most likley in __NS than __NS
A
  • neuron dies
  • if axon is severed, cell body and attached segment survives, severed portion degenerates
  • motor neuron: target muscle = permanent paralysis
  • sensory neuron: loss of sensation from innervated area
  • more likley in PNS than CNS
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25
Q

Do all cells have a resting membrane potential?
- at how much?
- do they all change?

A

yes!
around -70mV for neurons
- other types can have -40, -80 mV…
- RMP changed only for muscle cells and nervous tissue!

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26
Q

Resting membrane potential is created because of (2)
- en résumé: (2)

A
  1. due to unequal distribution of ions inside/outside cells –> leaking channels allow diffusion
  2. due to sodium potassium ATPase pump –> pumps 3 sodium out and 2 potassium in
    - concentration of ions + electrical gradient
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27
Q

2 types of open-channels
3 types of gated channels

A

OPEN:
- leak channels (always open!)
- pores
GATED:
- chemically gated (ligand)
- voltage gated (can be locked/inactivated)
- mechanically gated (temp, touch…)

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28
Q

Intracellular vs extracellular –> more or less of:
- potassium
- sodium
- chlorine
- calcium

A

Intracellular:
- more potassium (150 mM)
- less sodium (15 mM)
- less chlorine (10 mM)
- more calcium (1mM)
Extracellular:
- less potassium (5 mM)
- more sodium (145 mM)
- more chlorine (108 mM)
- less calcium (0.0001 mM)

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29
Q

what is:
- depolarization (3)
- repolarization
- hyperpolarization

A
  • depolarization: positive charge spread along adjacent sections of axon by local current flow –> cell becomes more positive (sodium enters cell = more positive) –> dependant on voltage-gated Na+ channels
  • repolarization: goes back to normal negative (potassium leaves cell –> becomes more negative)
  • hyperpolarization: cell becomes even more negative than normal RMP (potassium continues to exit = cell becomes super negative)
30
Q

2 types of electrical signals:
graded potential vs action potential
- over what distance?
- strength?

A

graded:
- variable strength, if exceeds threshhold, causes action potential
- over short distance communication
action potentials:
- very brief, large depolarizations
- rapid signaling over long distances

31
Q

Can graded and action potentials have summation?
2 types

A

only graded potentials can be summed!
- spatial summation = 2 or more neurons simultaneously fire and have an additive effect (ie a lot of people hit at the same time) –> cause postsynaptic inhibition: release of neurotransmitter is inhibitory instead of excitatory
- temporal summation = summation occurring when graded potentials overlap in time and having an additive effect (ie hit again and again before it comes down)

32
Q

How can graded potential cause action potential? (4 steps)

A
  1. ligand and mechanical channels open/close –> sodium and potassium move in/out of cell
  2. if it reaches threshold voltage –> voltage gated channels open (IMPORTANT!)
  3. Potassium goes out + Sodium comes in
  4. induces action potential
33
Q

Local current flow is a ______ of _______ that moves through the ______

A

wave of depolarization that moves through the cell

34
Q

graded potentials lose/gain strength as they move through the cell
- bc of 2 reasons

A

lose strength
- current leak
- cytoplasmic resistance

35
Q

if strong enough, graded potentials reach the ________ zone in the ______ ________ and initial segment

A
  • trigger zone
  • axon hillock
36
Q

what is the cell’s excitability?

A

its ability to fire and action potential

37
Q

action potential begins when?

A

when graded potential reaching trigger zone depolarizes to threshold

38
Q
  • rising phase of action potential (1)
  • falling phase of action potential (4)
A
  1. voltage gated Na+ channels open and Na+ entry depolarizes cell
  2. at peak, Na+ channels close, slower voltage gated K+ channels open
  3. K+ exit repolarizes then hyperpolarizes cell
  4. voltage-gated K+ channels close, less K+ leaks out of the cell
  5. cell returns to resting membrane potential of -70 mV
39
Q

does action potential alter ion concentration gradient?

A

no

40
Q

2 types of refractory period

A
  1. absolute refractory period are due to voltage-gated Na+ channels resetting: after sodium voltage channels open and close, they lock! (inactivated) –> even if super strong stimulus, won’t have another AP
  2. relative refractory period: some sodium channels become activated again + not all potassium channels are closed –> SO you need a stronger stimulus if you want to induce another AP
41
Q

Why are there refractory periods? (2)

A

to give cells enough time to recover! + they prevent backward conduction
- potential delay of 1-2 msec btw action potentials independent of intensity of trigger

42
Q

In the axon, each _______ of the membrane is experiencing a _________ phase of the action potential

A

section
different

43
Q

Chemical synapses occur when?
common?

A

occurs where presynaptic cells release chemical transmitters (neurotransmitters) across a tiny gap to the postsynaptic cell
- neurotransmitters bind to receptor of postsynaptic cell –> opens voltage gated channels –> induce another AP
- more common type of synapse in nervous system

44
Q

a neuron may terminate on 1 of which 3 structures?

A
  • muscle
  • gland
  • neuron
45
Q

3 types of cell junctions:
- communicating junctions
- occluding junctions
- anchoring junctions

A

Communicating junctions:
- allow direct cell to cell communication
Occluding junctions:
- block movement of material between cells
Anchoring junctions:
- hold cells to one another and to the extracellular matrix

46
Q

action potentials will NOT fire during ________ refractory periods

A

absolute

47
Q

CONDUCTION OF ACTION POTENTIAL
1. ________ potential above threshold reaches the ________ zone
2. what type of Na+ channels open?
3. ________ charge flows into adjacent sections of axon by _______ ________ ________
4. Local current flow causes new section of the membrane to ___________.
5. When that happens, positive/negative charges move by local current flow into adjacent sections of the cytoplasm.
6. On the extracellular surface, current flows towards/against depolarized region.
7. Loss of what from cytoplasm repolarizes membrane (on left side of active region)

A
  1. Graded potentials, trigger zone
  2. voltage gated Na+ channels
  3. Positive charge –> local current flow
  4. depolarize
  5. positive charges
  6. toward
  7. potassium
48
Q

Why can’t there be backward flow?

A

because the Na+ channels are inactivated –> refractory period prevents backward conduction

49
Q

2 things that make action potentials conducted faster?

A
  • larger neuron
  • myelinated neurons –> less ion leakage from axon membrane + saltatory conduction!
50
Q

why do myelinated neurons conduct action potentials faster? (2)

A
  • myelin = plasma membrane/phospholipids = insulation –> leaking of electric signal is blocked
  • action potential has saltatory conduction from one node of Ranvier to another!
51
Q

what happens if 2 action potentials/stimuli at 2 ends of axon?

A

both action potentials will die out because of absolute refractory period

52
Q

what 2 chemical factors alter electrical activity of neuron?

A
  1. variety of chemicals
  2. alterations in extracellular fluid concentration of ions (Ca+ and K+)
53
Q

hyperkalemia vs hypokalemia
- which brings neuron closer/further from threshold?

A
  • hyperkalemia = excess potassium in blood! = more positive outside = moves closer to threshold –> can cause irregular hearbeat
  • hypokalemia = low potassium in blood = more positive inside = moves neuron further from threshold
54
Q

Electrical synapses:
- pass electrical signals through what?
- signal can be single or bi-directional?
- ___________ activity of a network of cells

A
  • gap junctions
  • bi-directional
  • synchronizes
55
Q

3 types of neurocrines + differences

A
  1. neurotransmitters –> 1 neuron affects 1 neuron. mostly paracrine but can be autocrine
  2. neuromodulators –> 1 neuron can affect a group of neurons. mostly paracrine but can be autocrine
  3. Neurohormones –> circulate within blood. endrocrinology
56
Q
  • ionic receptors are also called ________-channels
  • metabotropic receptors are ____(what type)__________ receptors for ___(which type of neurocrine)____________
  • neurotransmitters bind to random/specific receptors except for ___________
A
  • receptor-channels
  • G protein coupled receptors for neuromodulators
  • specific receptors except for nitric oxide (NO)
57
Q

5 steps of classical model of neurotransmitter release

A
  1. AP depolarizes axon terminal
  2. depolarization opens voltage-gated Ca2+ channels and Ca2+ enters cell
  3. Ca2+ binds to regulatory proteins –> triggers exocytosis of synaptic vesicle contents (vesicle membrane merges with plasma membrane)
  4. Neurotransmitter diffuses across synaptic cleft and binds with receptors on postsynaptic cell
  5. neurotransmitter binding initiates a response in the postsynaptic cleft
58
Q

Difference between classical model pathway and kiss-and-run pathway for neurotransmitter release

A

Kiss and run
- vesicles fuse with presynaptic membrane to form fusion pore –> neurotransmitters pass through a channel
- vesicle membrane doesn’t become part of the plasma membrane –> closes after and can be recycled!

59
Q

where are neurotransmitters synthesized?

A

cell body and axon terminal

60
Q

3 ways to terminate neurotransmitter activity (in synaptic cleft ish)
- prozac example

A
  1. diffusion away from synaptic cleft = not binding to receptors
  2. enzymatic breakdown (ie: acetylcholinesterase)
  3. uptake into cells (presynaptic axon terminal for reuse OR into glial cells)
    - prozac: drug that blocks serotonin reuptake back into presynaptic neuron –> helps for depression
61
Q

synthesis and recycling of acetylcholine (5 steps)

A
  1. Ach is made from choline and acetyl-coa
  2. in synaptic cleft, Ach is rapidly broken down by enzyme acetylcholinesterase
  3. choline is transporte back into axon terminal by cotransport with Na+
  4. Acetate is used to provide energy
  5. recycled choline is used to make more Ach
62
Q

what 2 things impact the amount of neurotransmitter released?

A
  1. number of neurons involved (ie: if touch harder = more neurons)
  2. frequency of AP (even with refractory period)
63
Q

what is synaptic plasticity?
- occurs primarily where?
- short or long term?
- may reduce or enhance synaptic activity?

A
  • change of activity at the synapses (ie increase/decrease neurotransmitters, receptors, vesicles)
  • in CNS
  • both
  • both
64
Q

divergent vs convergent pathway

A
  • divergent: 1 presynaptic neuron branches to affect large number of postsynaptic neurons
  • convergent: many presynaptic neurons provide input to influence a smaller number of post-synaptic neurons
65
Q
  • slow synaptic potentials involve (2)
  • fast synaptic potentials involve opening of (1)
A
  • G-protein coupled receptors and second messengers
  • opening of ion channels
66
Q

EPSP vs IPSP
- depolarizing or hyperpolarizing?

A
  • excitatory postsynaptic potential (EPSP) = depolarizing –> ie Na+ goes into cell
  • inhibitory postsynaptic potential (IPSP) = hyperpolarizing –> is Cl- goes into post-synaptic neuron
67
Q

synaptic activity can be modified –> __________ neuron terminates on the ______synaptic cell and modulates the release of _______(A)___________

  • presynaptic facilitation vs inhibition favors/prevents release of (A)
A
  • modulatory neuron
  • presynaptic cell
  • release of neurotransmitters
  • facilitation –> favors release
  • inhibition –> prevents release
68
Q

how to inhibit a synapse?
- global vs selective

A

when an EPSP and IPSP sum together and cancel each other out
- global: EPSP + IPSP sum together at cell body –> no AP
- selective: EPSP fires –> AP generated –> IPSP fires at one dendrite blocking release of neurotransmitter BUT AP reaches 2 other dendrites where neurotransmitters released reached target cell

69
Q

What is long term potentiation?
- potentiation similar to ________
- depression similar to _________
- probably responsible for what?
- _________ is a key element for potentiation (2 receptors)

A

when activity at a synapse induces sustained changes in quality or quantity of connection –> will “adapt” and become more effective ish
- facilitation
- inhibittion
- probably responsible for acquired behaviour
- glutamate (AMPA and NMDA receptors)

70
Q

Parkinson’s disease, schizophrenia and some depressions are caused by disorders of _____________ ___________

A

synaptic transmission

Mammalian physiology (13 decks)

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