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
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Phases of an AP: | Resting state
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
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Phases of an AP: | Depolarization
``` **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
Phases of an AP: | Repolarization
**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
Phases of an AP: | Hyperpolarization
**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
Refractory Periods
Refractory Periods = minimum time after an action potential has been generated before the membrane can respond again **Absolute refractory period **Relative refractory period
30
Absolute refractory period
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
Relative refractory period
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
Propagation
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”
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Coding of Stimulus Intensity
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
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Conduction Velocity
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
Synapse
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
Electrical synapse
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
Chemical synapse
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
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Types of chemical synapse
Types of chemical synapses based on location: axodendritic = axon terminal to dendrite axosomatic = axon terminal to soma axoaxonal = axon terminal to axon
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Chemical Synapse: | Pre-synaptic Neuron
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
Chemical Synapse: | Synaptic Cleft
Synaptic Cleft neurotransmitter diffuses across cleft = synaptic delay ~0.5msec
41
Chemical Synapse: | Post-synaptic membranes
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
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Chemical Synapse: | NT effects are terminated
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
Modification of Synaptic Events (Fig. 11.18)
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
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Strength of individual synapses can vary as a function of their use or activity
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
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Neurotransmitters (NT) (Table 11.3)
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
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Neurotransmitters (NT)
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++
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Neural integration
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