Chapter 11 Fundamentals of NS and Nervous Tissue Flashcards

1
Q

Nervous system functions

A

Master rapid control and communicating system of body

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2
Q

Nervous System:

Two major anatomical components

A

*Central Nervous System (CNS):
brain and spinal cord

*Peripheral Nervous System (PNS): 
all nerves that enter and exit from CNS
ganglia – clusters of nerve cell bodies
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3
Q

Nervous System:

Three major physiological divisions

A

Sensory division:
detects environmental changes (internal and external)

Integrative division:
processes and stores sensory information and decides if output needed

Motor division
generates movements and glandular secretions

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4
Q

PNS divided into two functional subdivisions:

  • Sensory, or afferent
  • Motor, or efferent
A

Sensory, or afferent – convey impulses into CNS

* somatic sensory nerves – from skin, skeletal muscle and joints
* visceral sensory nerves – from organs

Motor, or efferent – convey impulses from CNS
*somatic motor nerves – to skeletal muscle
*autonomic nervous system (ANS) – involuntary system:
visceral motor nerves – smooth muscle, cardiac muscle, glands
sympathetic and parasympathetic divisions

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5
Q

Neuroglia Cells:

Small support cells of nervous system

A
Astrocytes
Microglial cells 
Ependymal cells
Oligodendrocytes 
Satellite cells 
Schwann cells
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6
Q

Neuroglia Cells:

Astrocytes

A

Astrocytes – in CNS

* make exchanges between capillaries and neurons 
* control chemical environment
* guide migration of young neurons and formation of synapses
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7
Q

Neuroglia Cells:

Microglia Cells

A

Microglial cells – in CNS = resident phagocytic cells

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8
Q

Neuroglia Cells:

Ependymal Cells

A

Ependymal cells – in CNS – line central cavities and spinal cord – cilia help circulate CSF

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9
Q

Neuroglia Cells:

Oligodendrocytes

A

Oligodendrocytes – in CNS – processes wrap around fibers forming myelin sheath

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10
Q

Neuroglia Cells:

Satellite Cells

A

Satellite cells – in PNS – similar function as astrocytes in CNS

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11
Q

Neuroglia Cells:

Schwann Cells

A

Schwann cells – in PNS – surround nerve fibers forming myelin sheath – important in regeneration of damaged fibers

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12
Q

Neurons

A
•	structural units of nervous system
•	have extreme longevity
•	high metabolic rate
•	post-mitotic
•	morphology (shape) varies but contains the same basic components: 
	*Soma or cell body 
	*Processes – extend from cell body
	*Dendrites 
	*Axon
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13
Q

Neurons:

Soma or cell body

A

Soma or cell body – contains nucleus – most located within CNS:
nuclei = clusters of nerve cell bodies in CNS
ganglia = clusters of nerve cell bodies in PNS

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14
Q

Neurons:

Processes

A

Processes – extend from cell body

* tracts = bundles of processes in CNS
* nerves = bundles of processes in PNS
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15
Q

Neurons:

Dendrites

A

Dendrites – receptive or input region – carry information toward cell body

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16
Q

Neurons:

Axon

A

Axon - one per neuron - carries action potential to other nerve cells or to effectors
**axon hillock initial section of axon where axon leaves cell body
• usual site where action potential generated
**axon collaterals – occasional branch off length of axon
**axon terminals - contain neurotransmitter vesicles (chemical packets)that transmit information to other nerve cells at junctions called synapses

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17
Q

Neurons:

Morphology types

A

Multipolar – 99% of neurons – have multiple dendrites plus one axon

Bipolar – one dendrite and one axon from cell body – found in retina of eye and olfactory mucosa

Unipolar – short process from cell body into T-like central and peripheral processes – primary sensory neurons
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18
Q

Myelin Sheath

A

Myelin = lipid material formed from membranes of cells or processes of cells that covers axons

Schwann cells in PNS, oligodendrocytes in CNS

* *Acts as an insulator
* *Nodes of Ranvier = gaps that occur between myelin producing cells and only place where ion exchange can occur  
* *Increases velocity of action potential up to 50x faster than unmyelinated neurons
* *Conserves energy
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19
Q

Resting Membrane Potential (RMP)

A

Voltage = measure of potential energy generated by separated electrical charges
All cells have a negative resting membrane potential
*ICF of the cell is negatively charged with respect to the ECF
Most cells maintain resting membrane potential within a narrow range
**Excitable cells = nerve and muscle cells have a more polarized (negative) RMP than non-excitable cells
(-40 to -90 mV)

20
Q

Factors contributing to Resting Membrane Potential

A

Differences in ionic distribution and permeability of membrane to various ions
K+ high inside cell, Na+ high outside cell
conductance to K+ large - leakage of out of cells results in negative charge within cells

Large negatively-charge proteins trapped within cell - influence ion distribution

Electrogenic pump (Na+-K+ ATPase)
	pumps 3 Na+ out,  2 K+ in - produces net negative charge within cells
21
Q

Changing RMP

A

Stimulus alters ion permeability - e.g. opening ligand-gated channel

Causes local reduction in membrane potential:
**Depolarizing stimulus - cell less negative/ less polar, moves membrane potential closer to zero
**Hyperpolarizing stimulus
cell more negative/more polar, moves membrane potential more negatively

22
Q

Changing RMP:

Graded potential

A

Graded potential = stimulus that produces a local response

**produces non-propagated potential where size of potential decreases exponentially with distance from initiation site

23
Q

Action potential

A

Action potential – initiated if stimulus large enough & threshold point reached
an “all-or-none” response
**positive feedback occurs and polarity of cell reverses
self-propagating electrical impulse depolarizes adjacent membrane
AP carried along whole length of cell membrane without decrement
**constant amplitude, shape and speed for a given excitable cell type
size and shape differ from one excitable tissue to the next (e.g. neurons vs cardiac muscle)
**AP duration for neurons and skeletal muscle ~ 4 ms

24
Q

Phases of an AP

A

Phases of an AP
involves changes in conductance of Na+ and K+ ions via voltage-gated channels
**resting state - sodium gates inactive and Na+ not moving
some potassium leak channels are open and K+ moving freely according to its equilibrium
depolarizing stimulus is applied

	**depolarization – local depolarization current open voltage-gated Na+ channels
	threshold point (15 to 30 mV change from RMP) = point of no return - AP initiated
	positive feedback mechanism initiated – triggers opening of critical number of fast activating voltage-gated (fVG) Na+ channels
	Na+ entry pulls the membrane potential towards Na+ equilibrium potential (lasts ~1 ms)
	self-limiting as fVG Na+ channels have automatic  inactivation gates 
**repolarization
fVG Na+ channels closing - rapid decrease in Na+ conductance (entry)
slow activating voltage-gated (sVG) K+ channels open  
increase in K+ conductance - leaves cell 
returns membrane potential toward RMP

**hyperpolarization stage = slower phase of AP
sVG K+ channels slow to close
membrane potential  pulled toward K+ equilibrium potential 
membrane potential more negative than resting levels 
sVG K+ channels close and cellular pumps restore proper ion distribution
25
Q

Phases of an AP:

Resting state

A

Phases of an AP
involves changes in conductance of Na+ and K+ ions via **voltage-gated channels
**resting state - sodium gates inactive and Na+ not moving
some potassium leak channels are open and K+ moving freely according to its equilibrium
depolarizing stimulus is applied

26
Q

Phases of an AP:

Depolarization

A
**depolarization – local depolarization current open voltage-gated Na+ channels
	threshold point (15 to 30 mV change from RMP) = point of no return - AP initiated
	positive feedback mechanism initiated – triggers opening of critical number of fast activating voltage-gated (fVG) Na+ channels
	Na+ entry pulls the membrane potential towards Na+ equilibrium potential (lasts ~1 ms)
	self-limiting as fVG Na+ channels have automatic  inactivation gates
27
Q

Phases of an AP:

Repolarization

A

**repolarization
fVG Na+ channels closing - rapid decrease in Na+ conductance (entry)
slow activating voltage-gated (sVG) K+ channels open
increase in K+ conductance - leaves cell
returns membrane potential toward RMP

28
Q

Phases of an AP:

Hyperpolarization

A

**hyperpolarization stage = slower phase of AP
sVG K+ channels slow to close
membrane potential pulled toward K+ equilibrium potential
membrane potential more negative than resting levels
sVG K+ channels close and cellular pumps restore proper ion distribution

29
Q

Refractory Periods

A

Refractory Periods
= minimum time after an action potential has been generated before the membrane can respond again

**Absolute refractory period

**Relative refractory period

30
Q

Absolute refractory period

A

Absolute refractory period (~1 ms duration)
from beginning of action potential until repolarization is ~2/3 complete
attributable to activation state of fast activating voltage-gated sodium channel
if all open – can’t open more
once closed – have a delay period before they can re-open
no stimulus, regardless of strength, can initiate another action potential during this period

31
Q

Relative refractory period

A

Relative refractory period
follows the absolute refractory period and lasts until RMP is re-established
requires a stronger stimulus than normally required to reach threshold
sufficient number of fast-activating voltage-gated Na+ channels capable of re-opening but must overcome the hyperpolarizing effect of the still open voltage-gated K+ channels

32
Q

Propagation

A

Propagation:
nerve Impulse = wave of action potentials along an axon
an action potential is a local response occurring at one specific area on the membrane
AP initiated at one point in the membrane triggers APs in neighbouring areas
adjacent areas affected by influx of + ions during depolarization
self-propagating “domino-like effect”

33
Q

Coding of Stimulus Intensity

A

Coding of Stimulus Intensity:
once generated, AP’s independent of stimulus strength
CNS determination of stimulus strength – via **frequency of AP’s –strong stimuli generate more AP/s

34
Q

Conduction Velocity

A

Conduction Velocity
in a neuron, large diameter fibers (axons) have a faster conduction rate due to lower resistance to conduction
myelin = lipid material that covers axons:
acts as an insulator
prevents loss of current and flow of ions between ECF and ICF
Nodes of Ranvier = gaps that occur between myelin producing cells and only place where ion exchange can occur
AP appears to jump from node-to-node = saltatory conduction
increases velocity of action potential up to 50x faster than unmyelinated neurons
conserves energy (uses less ATP)
Na+-K+ ATPase activity is required to restore RMP since ions only cross membrane at the nodes, less pump activity is required
multiple sclerosis (MS) = demyelinating disease

35
Q

Synapse

A

Synapse:
place where information is transmitted from one cell to another = synaptic transmission

Electrical synapse:
allows direct passage of ions from one cell to another through structure called gap junctions
found in cardiac and smooth muscle tissues

Chemical synapse:
pre-synaptic neuron – at axon terminal converts electrical signal (action potential) to chemical signal
chemical signal = neurotransmitter (NT)
synaptic cleft = physical gap that neurotransmitter diffuses across
post-synaptic membrane – receives NT that binds to specific receptor

Types of chemical synapses based on location:
axodendritic = axon terminal to dendrite
axosomatic = axon terminal to soma
axoaxonal = axon terminal to axon

36
Q

Electrical synapse

A

Electrical synapse:
allows direct passage of ions from one cell to another through structure called gap junctions
found in cardiac and smooth muscle tissues

37
Q

Chemical synapse

A

Chemical synapse:
pre-synaptic neuron – at axon terminal converts electrical signal (action potential) to chemical signal
chemical signal = neurotransmitter (NT)
synaptic cleft = physical gap that neurotransmitter diffuses across
post-synaptic membrane – receives NT that binds to specific receptor

38
Q

Types of chemical synapse

A

Types of chemical synapses based on location:
axodendritic = axon terminal to dendrite
axosomatic = axon terminal to soma
axoaxonal = axon terminal to axon

39
Q

Chemical Synapse:

Pre-synaptic Neuron

A

Presynaptic Neuron
arriving action potential causes a depolarization of axon terminal
activates voltage-gated Ca++ channels on the plasma membrane
**Ca++ influx allows neurotransmitter vesicles to fuse with pre-synaptic membrane
exocytosis of neurotransmitter into synaptic cleft
pumps remove Ca++ from axon terminal

40
Q

Chemical Synapse:

Synaptic Cleft

A

Synaptic Cleft
neurotransmitter diffuses across cleft = synaptic delay
~0.5msec

41
Q

Chemical Synapse:

Post-synaptic membranes

A

Post-synaptic membranes
**NT binds to receptors initiating signal transduction
temporarily opens ion channels producing a graded, non-propagated post-synaptic potential
depending on neurotransmitter may be excitatory or inhibitory
**excitatory post-synaptic potential (EPSP) depolarizes membrane and increases chance of AP
**inhibitory post-synaptic potential (IPSP) hyperpolarizes membrane and decreases chance of AP

42
Q

Chemical Synapse:

NT effects are terminated

A

NT effects are terminated
reuptake of NT by astrocytes or presynaptic terminal – NT destroyed or stored
degrading enzymes - degrade NT - associated with post-synaptic membrane or in synaptic cleft
diffusion of NT away from synapse

43
Q

Modification of Synaptic Events (Fig. 11.18)

A

Modification of Synaptic Events:
a single EPSP cannot induce an AP in the postsynaptic cell
**summation – adding together postsynaptic potentials:
EPSPs and IPSPs are electrically equivalent but in opposite direction
to get AP in post-synaptic neuron, the changes from more than one stimulus must be added together
**temporal summation = summing of post-synaptic potentials arriving in rapid sequence
produces a step-wise change in the post-synaptic potential
**spatial summation adds all EPSPs + IPSPs arriving at the same time on the post-synaptic neuron
sum total of effects of NTs released from more than one pre-synaptic neuron

44
Q

Strength of individual synapses can vary as a function of their use or activity

A

Strength of individual synapses can vary as a function of their use or activity:
Patterns of synaptic activation can change the response to subsequent activation
may remain for short (millisecond) or long (min to days) duration
may result in potentiation (facilitation)
underlie learning and memory

45
Q

Neurotransmitters (NT) (Table 11.3)

A

Neurotransmitters:
over 50 postulated neurotransmitters

*Acetylcholine (ACh)- most important low mw NT and found in all motor neurons
synthesis enzyme = choline-acetyltransferase
substrates = acetyl CoA and choline
**degraded in synaptic cleft by acetylcholinesterase (AChE) bound to outside of postsynaptic membrane

*Biogenic amines = derived from amino acids
catecholamines = tyrosine derivatives
include: dopamine, norepinephrine and epinephrine
indolamines = serotonin – derived from tryptophan; histamine – derived from histidine
broadly distributed throughout most of brain and spinal cord
promotes learning and memory
controls mood (through activation of reward centers)
promotes sleep induction

46
Q

Neurotransmitters (NT)

A

Amino acids – glutamate, aspartate, glycine, GABA

Peptides – substance P, endorphins, enkephalins, dynorphins

Purines – ATP, adenosine

Gases – nitric oxide (NO) - highly permeant & diffuses out of axon terminal - increases cGMP in target cell
Function determined by receptor :
*excitatory – cause depolarization
glutamate
*inhibitory – cause hyperpolarization
GABA, glycine
*both – depending on receptor present on tissue
ACh, NE
Action: direct versus indirect
*direct – binding of NT directly gates ion channel producing rapid reponse
**inotropic receptors (Fig. 11.19)
*indirect – binding of NT promote broader, longer-lasting effects by acting through intracellular second messengers
**metabotropic receptors (Fig. 11.20) = G-protein linked receptors
NT binds receptor - G-protein becomes activated
activate/inactivate different enzymes which regulate 2nd messengers
2nd messengers (cAMP, cGMP, DAG (diacylglycerol), IP3 (inositol triphosphate), Ca++ :
gate ion channels
activate other proteins that produce physiological responses
increase ICF Ca++

47
Q

Neural integration

A

Neural integration
• organized into **neuronal pools:
postsynaptic neurons in center of discharge zone more likely to reach threshold and generate AP’s than those in the edges (they become facilitated – no AP but closer to threshold)
**serial processing – one neuron stimulates the next, which stimulates the next…
e.g. reflexes

**parallel processing – inputs segregated into many pathways
important for higher level processing (integration)

**circuits = patterns of synaptic connections in neuronal pools