CHAPTER 12
Nervous Tissue
1
Structures of the Nervous System
• Brain
• Nerves
– bundles of axons plus their associated CT & blood
vessels
– follow defined path & innervate specific regions/structures
• Spinal cord
– connects to brain thru foramen magnum
– protected by vertebral column
• Ganglia
– masses of nervous tissue outside brain & spinal cord
– closely associated with cranial/spinal nerves
• Sensory receptors = dendrites
– monitor changes in internal/external environments
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Functions of the Nervous System
• Sensory function
– receptors sense changes in internal & external environments
– AFFerent neurons carry sensory info TO brain/spinal cord
• Integrative function
– processes sensory info by analyzing sensory information
& makes decisions regarding appropriate behaviors
– interneurons have short axons that contact neurons in
brain/spinal cord; participate in integration
• Motor function
– after integration of sensory info, nervous system elicits
appropriate response
– EFFerent neurons carry motor response away from spinal
cord to effector organs/glands
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NERVOUS SYSTEM DIVISIONS
CENTRAL NERVOUS
SYSTEM
•Brain & Spinal Cord
ONLY!!!
•Integrates sensory
input from PNS &
sends output back
to PNS
PERIPHERAL NERVOUS
SYSTEM
Autonomic
Motor
•Info from CNS
to viscera
(involuntary)
Sympathetic
●”fight or flight”
Sensory
●Input from
viscera to
CNS
Somatic
Motor
•Stimulates
skel. musc.
only
(voluntary)
Sensory
●Input from
somatic
receptors
to CNS
Parasympathetic
●“rest and digest”
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Divisions of the Nervous System
• Central nervous system (CNS) = brain & spinal cord
ONLY!
• Peripheral nervous system (PNS) = all nervous tissue
outside CNS
– Somatic (voluntary) nervous system (SNS)
• neurons from cutaneous and special sensory receptors
to the CNS
• motor neurons to skeletal muscle tissue
– Autonomic (involuntary) nervous system
• detailed in Chapter 15
• sensory neurons from visceral organs to CNS
• motor neurons to smooth & cardiac muscle and glands
– sympathetic division (speeds up heart rate)
– parasympathetic division (slow down heart rate)
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NERVOUS TISSUE HISTOLOGY
• Neurons = nerve cells
– electrically excitable  can convert stimulus to
electrical signal (action potentials)
– parts of neuron
• cell body
– nucleus surrounded by cytoplasm & organelles
– rough ER & free ribosomes for protein synthesis
• dendrites = sensory (input) portion of neuron
• axons = output portion of neuron
– carry impulses away from cell body to effector cell
– attaches to cell body @ axon hillock
– axon collaterals = branches of axon
– synapse = point of communication btwn neuron & cell
» serves as site of control of nerve impulses
» prevents “backwards” transmission of impulses
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NERVOUS TISSUE HISTOLOGY
• Neuroglia = supporting cells of nervous tissue
– actively take part in nervous tissue functions
– do not generate a.p. but can reproduce  site of brain
tumors (gliomas)
– CNS neuroglia (4)
• astrocytes
– processes contact capillaries, neurons, pia mater
– strong  support neurons by holding in place
– processes around capillaries isolate neurons from
blood-borne toxins  help establish blood/brain
barrier
• oligodendrocytes form & maintain myelin sheath
around CNS axons
• microglia function as phagocytes  remove debris
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NERVOUS TISSUE HISTOLOGY
– CNS neuroglia (c’td)
• ependemyal cells produce, monitor & circulate the
cerebrospinal fluid (CSF) which is ISF of CNS
– PNS neuroglia (2)
• Schwann cells
– surround PNS axons
– myelinate single axon
– facilitate regeneration of PNS axons
– can enclose several unmyelinated axons
• satellite cells
– surround cell bodies of PNS ganglia
– provide structural support
– regulate exchange of materials btwn neurons & ISF
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Myelination
• Some axons covered by multilayered lipid & protein covering
called myelin sheath
• Provides electrical insulation which allows nerve impulse to
travel faster
• Produced by Schwann cells in PNS & oligodendrocytes in
CNS
• Neurolemma = cytoplasm & nucleus of Schwann cell
– ***found only in PNS!
• Nodes of Ranvier = gaps in myelin sheath that appear @
intervals along axon
– one Schwann cell found between two nodes
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Myelination in the CNS
• Oligodendrocytes myelinate axons in the CNS
– one oligodendrocyte myelinates several axons
– broad, flat cell processes wrap around CNS axons
• No neurolemma is formed
– probably results in lack of regrowth after injury (because
PNS axons can regenerate)
10
Gray and White Matter
• White matter = primarily myelinated axons
• Gray matter = unmyelinated structures
– nerve cell bodies, dendrites, axon terminals, bundles of
unmyelinated axons and neuroglia
– In spinal cord, white matter surrounds inner core of gray
matter
– In brain
• thin layer of gray matter covers surface
• found in clusters called nuclei deep within CNS
***A nucleus is a mass of nerve cell bodies and dendrites
inside the CNS.***
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Electrical Signals in Neurons
• Neurons are electrically excitable due to the voltage
difference across their membrane
– graded potentials participate in localized cellular
communication
– action potentials can communicate a signal over long or
short distances
• The difference in voltage across a membrane is referred
to as the membrane potential
– resting membrane potential is the voltage difference that
exists when a cell is at rest (not being stimulated)
• Plasma membrane of neurons contains ion channels that
open/close in response to stimuli
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Ion Channels
• Allow movement of specific ions across the membrane &
down their electrochemical gradient
– positively charged ions move to a negatively charged area
(lower concentration of positive charge)
– negatively charged ions generally are too large to
leave the cell, thus the tendency is for positively
charged ions to flow into the cell
• Four types of channels
– leakage channels randomly alternate btwn open/closed
conformation
• more K+ channels than Na+  K+ is “leakier”
• membrane is more permeable to K+
– voltage-gated channels open in response to a change in
voltage across the membrane  function in generation of
action potentials
13
Ion Channels
• Channels c’td
– ligand-gated channels open/close in response to
specific chemical messenger (ligand)
• ligand can be NT, hormone or an ion
• two modes of operation
– direct activation by binding of ligand to receptor
– indirect activation of channel via 2nd msgr system
– mehanically gated channels open/close in response to
mechanical stimuli
• stretching of muscle
• vibrations within ear
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Resting Membrane Potential (RMP)
• Results from unequal distribution of ions btwn ECF & ICF
– buildup of negative ions in cytosol (PO4-3, amino acids)
– buildup of positive ions outside membrane (Na+)
• Separation of charges represents a form of potential energy
– the greater the charge difference across membrane, the
greater the potential (voltage)
– potential energy difference at rest is -70 mV (this is
RMP)
• Resting potential exists because
– concentration of ions different inside & outside
• extracellular fluid rich in Na+ and Cl• cytosol full of K+, PO4-3 & amino acids
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Resting Membrane Potential (RMP)
• Resting potential exists because
– membrane permeability differs for Na+ and K+
• 50-100x greater permeability for K+
• inward flow of Na+ can’t keep up with outward flow of
K+
• ***Na+/K+ ATPase pump maintains R. M. P.***
– w/o this pump, ion concentrations would reach
equilibrium and the membrane potential (excitability)
would be destroyed
– K+ has a natural tendency to leak out of cell and Na+
tends to flow into the cell (down their respective
gradients)
– pump returns 3 Na+ to ECF and 2 K+ to cytosol
16
Graded Potentials
• Local changes (of varying magnitudes) in membrane potential
• Any stimulus that opens a gated channel produces a graded
potential
• Make cell more or less polarized
– hyperpolarization = membrane has become more negative
– depolarization = membrane has become less negative
• “Graded” means they vary in amplitude (size), depending
upon strength of stimulus
• Are decremental because they die out as they travel further
from their origin
• Occur most often in dendrites and cell body of a neuron
• Graded potentials occurring in response to NT are called
postsynaptic potentials
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How do Graded Potentials Arise?
• Source of stimuli
– mechanical stimulation of membranes with mechanical
gated ion channels (pressure)
– chemical stimulation of membranes with ligand gated ion
channels (neurotransmitter)
• Graded/postsynaptic/receptor or generator potential
– ions flow through ion channels and change membrane
potential locally
– amount of change varies with strength of stimuli
• Flow of current (ions) is local change only
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Generation of an Action Potential
• Action potential = sequence of rapidly occurring events that
briefly reverse membrane potential due to rapid changes in
membrane permeability
– depolarization = membrane becomes less negative inside
– repolarization = restoration of RMP (-70 mV)
– threshold potential = -55 mV
• potential at which an action potential is generated
• all-or-none principle: if stimulus causes depolarization
to threshold, action potential is generated
– no “large” or “small” a.p.
– stronger stimulus will not cause a larger impulse
• Action potentials can travel over long distances w/o dying out
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Depolarizing Phase of Action Potential
• In resting membrane, Na+ inactivation (inner) gate open &
activation (outer) gate is closed (Na+ cannot get in)
• Depolarizing graded potential or some stimulus initiates
movemt of Na+ into cell (↓ potential)
• This further depolarization activates Na+-gated channels
which open & allow rapid influx of Na+ until threshold reached
• @ threshold (-55mV), both Na+ gates open & Na+ enters &
membrane becomes several hundred times more permeable
to Na+
• more channels open in adjacent regions of membrane
(positive FB)
• influx of Na+ makes inside less negative (up to +30 mV)
• @ +30 mV, Na+ inner (inactivation) gates close
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Repolarizing Phase of Action Potential
• As Na+ gates close (at +30 mV), K+ gates are activated &
membrane permeability to K+ is increased
• K+ flows out of cell (down its gradient) until RMP is reached
• If the cell “overshoots” K+ efflux, hyperpolarization results
– -90 mV  cell further from threshold no a.p. can occur
• K+ channels close and the membrane potential returns to the
resting potential of -70mV via action of Na+/ K+ ATPase pump
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Refractory Period of Action Potential
• Period of time during which neuron cannot generate another
action potential
• Absolute refractory period
– even very strong stimulus will not produce another a.p.
– inactivated Na+ channels must return to the resting state
before they can be reopened
– Na+ inner gates closed & cannot reopen
• Relative refractory period
– 2nd a.p. can be generated by very strong stimulus
– Na+ channels have been restored to resting state, but
K+ channels are still open
• Allows unidirectional transmission of impulses
• Axons w/ large diameter have greater membrane surf. area
& shorter abs. refract. periods than small-diameter axons
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Propagation of Nerve Impulses
• Continuous conduction (local current flow)
– starts @ axon hillock where membrane is most sensitive
to changes in potential
– step-by-step depolarization of adjacent segments of
membrane
– membrane polarity is reversed (out becomes (-) & in
becomes (+)
– inactive area of membrane (downstream) has resting
polarity  opposite charges attract  (+) “pulls” (–)
– this opens voltage-gated channels in adjacent regions of
membrane & a.p. moves along axon
– occurs in muscle fibers & unmyelinated axons
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Propagation of Nerve Impulses
• Saltatory conduction
– in myelinated axons only
– depolarization occurs in similar way @ nodes of Ranvier
where voltage-gated channels are concentrated
– current flows thru aqueous cytosol & ECF of Schwann cells
– nerve impulses appear to jump from node to node
– much quicker/more energy efficient
• open fewer voltage channels
• less use of Na+/K+ pump  less ATP used
• Axon diameter
– large fibers are all myelinated  fastest
– medium fibers myelinated, but slower (b/c less surf. area)
– small fibers unmyelinated & slowest (longest abs. refr. per.)
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Encoding of Stimulus Intensity
• How do we differentiate a light touch from a firmer touch?
• Perception of intensity results from frequency of impulses
(not the magnitude of an impulse)
– frequency of impulses
• firm pressure generates impulses at a higher
frequency
– number of sensory neurons activated
• firm pressure stimulates more neurons than does a
light touch
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SIGNAL TRANSMISSION AT SYNAPSES
• Presynaptic neuron = neuron sending the signal
• Postsynaptic neurono = neuron receiving chem/elec signal
• Electrical synapses
– ionic current spreads to next cell through gap junctions
– advantages
• faster transmission of impulses  a. p. jumps directly
from pre-synaptic to post-synaptic neuron
• capable of synchronizing groups of neurons as in the
contraction of cardiac & visceral smooth muscles
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SIGNAL TRANSMISSION AT SYNAPSES
• Chemical synapses
– Synaptic cleft separates pre/post-syn neurons  chem
signals can’t “jump” from one neuron to next
– Presynaptic neuron releases NT into cleft; NT binds
receptor on post-synaptic neuron
– Binding of NT produces graded (postsynaptic) potential
• Repeated binding eventually produces a.p.
– Synaptic delay = time required for events to occur @
chemical synapse
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Mechanism of Chemical Synapse
• Action potential reaches end bulb and voltage-gated Ca+2
channels open
• Ca+2 flows inward & triggers release of neurotransmitter
• NT crosses synaptic cleft & binds to ligand-gated receptors
– ligand-gated channels activated & ions flow across
membrane
• ion flow can change postsyn. potential
• If Na+ in  depolarization
• If Cl- in or K+ out  hyperpolariz
• If depolarizing potentials reach threshold, a.p. is triggered
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Excitatory & Inhibitory Potentials
• If NT causes depolarization  excitatory postsynaptic
potential (EPSP) is generated
– excitatory = a.p. generated if sum of EPSPs exceeds -55mV
– usually results from cation channels opening
– partial depolarization makes cell more excitable
• If NT causes hyperpolarization  inhibitory PSP (IPSP)
– inhibitory because membrane is further from threshold
– usually result of K+ or Cl- channels opening
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Removal of Neurotransmitter
• Diffusion: NT diffuses away from cleft & is no longer
effective
• Enzymatic degradation
– EX: acetylcholinesterase breakdown of ACh
• Cellular uptake
– Uptake by nearby neuroglia
– Re-uptake by secreting axon
– Clinical application: some drugs block uptake process
• EX: Prozac = SSRI  blocks serotonin reuptake 
serotonin’s effects are prolonged
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Summation of PSPs
• Summation = integration of synaptic inputs
• Spatial summation results when several presynaptic
neurons secrete NT that affects single postsynaptic neuron
• Temporal summation results from repeated release of NT
from single presynaptic neuron
• One postsynaptic neuron can receive numerous
excitatory/inhibitory inputs
• Sum of inputs determines postsynaptic response
– EPSP: excitatory input > inhibitory input
• above threshold  a.p. generated
• below threshold  cell more sensitive b/c partial
depolarized
– IPSP: inhibitory input > excitatory input
• membrane is hyperpolarized & no a.p. occurs
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Summation of PSPs
• Clinical relevance: strychnine poisoning
– Under normal conditions: inhibitory neurons in spinal
cord release glycine (a NT) which inhibits XS
contractions of skeletal muscle
– Strychnine binds & inactivates glycine receptors
• inhibitory effects of glycine are removed
• uncontrolled muscle contraction results
– diaphragm remains fully contracted  death
ensues via suffocation
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Small-Molecule Neurotransmitters
• Acetylcholine (ACh)
– excitatory effect @ NMJ via direct ligand-channel binding
– inhibitory @ some parasympathetic synapses
• indirect activation of receptors via G-protein
• slows heart rate
– inactivated by acetylcholinesterase
• Amino Acids
– excitatory: glutamate & aspartate
– inhibitory: GABA & glycine
• generate IPSP via opening of Cl- channels
• Valium enhances GABA effects
– prolongs effects of GABA
– acts as anti-anxiety drug
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Small-Molecule Neurotransmitters
• Biogenic Amines
– catecholamines
• norepinephrine (NE) & epinephrine (Epi)
– also act as hormones when released from adrenal
gland
• dopamine: responsible for emotions, addictive
behaviors
– Regulates skeletal muscle tone
– Parkinson’s disease result of degeneration of
dopamine-secreting neurons
• serotonin responsible for mood control, appetite, sleep
induction
– SSRIs prevent reuptake
– Zoloft, Prozac for treatment of depression
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Small-Molecule Neurotransmitters
• Nitric oxide (NO)
– potent vasodilator: increases blood flow in regions where
it is released
– unique because is formed on demand & acts immediately
– first recognized as vasodilator that helped lower blood
pressure
– extremely toxic in high quantities
– metabolic pathway = target of Viagra
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Neuropeptides
• 3-40 amino acids linked peptide bonds
• Can be excitatory or inhibitory
• Brain has receptors for binding opiate drugs
– Enkephalins have potent analgesic effect (200x morphine)
– Opiod peptides = body’s natural painkillers
• Dynorphins
• Endorphins: responsible for “runner’s high” experienced
after exercise
• Substance P transmits pain-related input from PNS to CNS
– Enhances perception of pain
– Suppressed by enkephalins & endorphins
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Modifying Effects of NTs
• NT synthesis can be stimulated or inhibited
– Parkinson’s patients benefit from L-dopa b/c it boosts
dopamine production for limited time
• NT release can be enhanced or blocked
– Amphetamines promote release of dopamine & NE
– Botulinum toxin inhibits release of Ach  paralysis
• NT receptors can be activated or blocked
– Agonists activate: Isoproterenol activates NE & Epi
receptors dilate airways during asthma attack
– Antagonists block: Zyprexa blocks dopamine/serotonin
receptors  treatment of schizophrenia
• NT removal can be stimulated or inhibited
– Cocaine blocks dopamine reuptake  euphoric feeling
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