Nervous tissue Flashcards
neurology
study of nervous system
neurologist diagnoses/treats disorders of nervous system
nervous system 3 roles
1) sense, interpret, respond to stimuli
2) generate movement/gland secretion (“respond” to stimuli)
3) thought, emotion, memory
nervous system and homeostasis
contributes to maintaining homeostasis
3 functions/components of nervous system
sensory function
integrative function
motor function
1) sensory function
afferent neurons (sensory)
signal toward CNS
detects EXTERNAL & INTERNAL stimuli
E.g.
tapping shoulder (external)
heart-rate/GI-tract (internal)
2) integrative function
INTERNEURONS b/w afferent and efferent neurons
INTEGRATE feedback in CNS
“deciding” appropriate “response”
also involved in complex mental/psychological processes such as deliberating & consideration via memories
also involved in simple reflexes (E.g. patellar reflex – DTR)
3) motor function
“command” sent by CNS via EFFERENT neurons
activate EFFECTORS –> E.g. muscles/glands
Can be Somatic (voluntary) or Autonomic (involuntary)
two major divisions of nervous system
CNS –> brain and spinal cord
PNS –>
= cranial nerves (CN1-12),
= spinal nerves (dorsal/ventral roots/rami),
= peripheral nerves (e.g. via cervical/brachial and lumbosacral plexus)
number of neurons in different parts of nervous system
brain = 85-100 billion
spinal cord = 100 million
ENS (enteric nervous system) = 500 million
the brain (CNS)
within cranial cavity
structural areas (discussed in neurology) as follows:
= cerebral cortex, pons, medulla, cerebellum, hypothalamus, thalamus, basal ganglia, pituitary gland, etc.
3 layers of protection for brain
cranium
meninges (CT membranes)
CSF (Cerebrospinal fluid)
= Similar to Blood Plasma composition
= cushions brains
= keeps buoyant in cavities (reduces effective weight so brain not resting heavily against cranial cavity)
CSF & weight of brain (?)
CSF buoyancy plays a critical role in preventing the brain from being damaged by its own weight against the cranial cavity (???)
cerebrum
largest part of brain
TWO hemispheres
Generally, RIGHT side interacts with left side of body,
LEFT side interacts with right side of body
I.e.
Afferent/Efferent signalling
” Exceptions exist
brain weight/size vs ratio of brain to body weight
ratio of brain mass : body mass may be one of the variables indicating intelligence
other variables:
surface area
relative size of brain cortex
E.g.
mice/humans have similar ratio, but human brain is more complex
Spinal cord (CNS)
extending from brain
Within vertebral canal (of “ column)
protected via CSF & vertebral column
begins @ foramen Magnum
Ends @ L1/L2 Spinal level (to lumbar plexus & sacral plexus)
spinal cord structure (cross section)
internal GREY MATTER (nerve cell bodies)
external WHITE MATTER (nerve tracts, i.e. axons)
—-> ASCENDING & DESCENDING tracts (afferent & efferent)
PNS
nerves + sensory receptors
outside CNS
31 spinal nerves (C0 the coccygeal nerve)
12 cranial nerves
peripheral nerves (branches of spinal AND CRANIAL nerves)
spinal nerves
8 cervical spinal nerves
12 thoracic
5 lumbar
5 sacral
1 coccygeal
spinal nerves roots
ventral roots carry efferent fibres
dorsal roots carry afferent fibres
nerve plexus & spinal nerves
branching network of nerves
e.g. brachial plexus
via Ventral rami of C5-T1
(occurs via spinal nerves)
Cranial nerves
exit directly from brain or brain stem
CN 1-12 = 12 pairs
sensory & motor signals
somatic vs autonomic
see next slides
somatic
voluntary
motor control to skeletal muscles only
general/special sense
autonomic
involuntary
to smooth/cardiac muscles, & glands
sensory feedback from same areas that are innervated
SNS (somatic nervous system)
responsible for reflex arcs
ANS (autonomic) 2 (or 3) branches
Parasympathetic nervous system
sympathetic nervous system
enteric nervous system (part of parasympathetic nervous system)
sympathetic nervous system
“fight or flight” response
changes during perceived threat to survival
E.g.
increased heart rate (increase O2 supply to skeletal muscles for action)
dilation of pupils (see in dark, increase alertness/focus)
increase glucose from liver to brain/muscle (increased alertness, readiness of skeletal muscles
dilation of airways (O2 to brain/muscles via blood)
slowing of digestion (diverting blood supply & resources to musculoskeletal system)
parasympathetic
rest/digest
sexual activity
re-establish homeostasis
decreased heart rate
constriction of pupils
bronchoconstriction
increased blood flow – to GI tract & visceral organs
ENS
intrinsic to GI tract
functions independently but technically part of Parasympathetic nervous system (of ANS)
ENS includes…
sensory neurons (chemical/mechanical changes in GI tract)
motor neurons (smooth muscle contractions + gland secretion)
Enteric nervous system example
food enters stomach:
mechanoreceptors and chemoreceptors detect change (STRETCH & pH)
why?
food causes walls of stomach to stretch
food changes pH of gastric juices
In response?
stomach peristalsis
release of HCl
cells of nervous tissue
1) neurons
2) neuroglia
neurons
excitability
generate Action Potentials in response to stimuli
how fast do Action potentials travel?
1-100meters/second
neuroglia
supporting cells of nervous system
anatomy of neuron
cell body (aka PERIKARYON) – containing NUCLEUS + organelles
dendrites – projections from cell body – receive input
axon – long thin projection – conducts action potential away from cell body
perikaryon
cell body of neuron
axon hillock
where axon meets cell body
trigger zone
area within axon hillock
Action potentials generated here (begin here)
initial segment
segment of axon closest to axon hillock
note axon hillock and related terms
axon hillock + trigger zone
initial segment
axoplasm
cytoplasm of axon
axolemma
cell membrane in region of axon
axon membrane
axon terminals
axons and axon collaterals end @ AXON TERMINALS
synaptic end bulb
bulges @ end of axon terminal
END BULBS (@ axon terminal) joint w/ motor end plate of muscle fibre
I.e.
Neuromuscular junction
axon collateral
side branches
single neuron can communicate w/ many
Nissl bodies
granular bodies within cell body (perikaryon)
consist of Rough ER
make proteins
synapse
connection b/w two neurons
or b/w neuron & effector
E.g.
NMJ & synaptic cleft
note also:
presynaptic & post-synaptic membrane
Epineurium, perineurium, endoneurium (CT LAYERS)
epineurium surrounds entire peripheral nerve
perineurium surround nerve fascicles
endoneurium surrounds individual neuron
slow vs fast axonal transport
see following slides
slow axonal transport
materials in one direction:
Cell body to axon
supplies new AXOPLASM to developing/regenerating axons
slow axonal transport, rate of movement?
1-5 mm per day
fast axonal transport
materials in both directions
(to/from cell body)
including substances that are broken down / recycled
fast axonal transport, rate of movement
200-400 mm per day
structural (shape) classifications of neurons
1) pseudo-unipolar (unipolar)
2) bipolar
3) multipolar
4) Purkinje
5) pyramidal
unipolar neurons
tactile sensory neurons
dendrite and axon terminal with Axon in between – CONTINUOUS STRUCTURE
cell body connected to axon
bipolar neuron
found in retina, in olfactory area, & inner ear
(SPECIAL SENSES)
1 axon terminal and 1 dendrite on either end of cell body
multipolar
multiple dendrites @ cell body
single axon on other end
@ brain & spinal cord
@ motor neurons
Purkinje neurons
“massive, intricately branched, flat dendritic trees”
ONLY @ CEREBELLUM
—> Control motor mvmt
Purkinje fibres in heart (NOT SAME THING)
named after same scientist
role in cardiac function
pyramidal neurons
cell bodies shaped like pyramid
found @ cerebral cortex
neuroglia
support, nourish, protect neurons
neuroglia volume of CNS
about 1/2 volume of CNS
more numerous than neurons, but smaller
astrocytes
largest, most numerous neuroglia
FOUND IN CNS, not PNS (?)
astrocyte, major function
form Blood-brain barrier (BBB)
blood-brain barrier
tightly sealed lining
maintains selective permeability of capillaries
BBB prevents harmful substances entering CNS
other functions of astrocytes
regular blood flow
maintain chemical environment for neuronal signaling
help create Neurotransmitters
Assist neuron metabolism
phagocytosis of synapse
clear debris
oligodendrocytes
myelin sheath around CNS axons
facilitate speed of AP
microglia
phagocytes of CNS
remove…
–microbes
–cellular debris
–debris from damage
ependymal cells
single layer of cells
along VENTRICLES of brain
along CENTRAL CANAL (spinal cord)
Produce CSF (cerebrospinal fluid)
note about ependymal cells and ventricles of brain
FOUR major ventricles in brain (cavities)
they produce/store CSF
2 lateral ventricles –> INTERVENTRICULAR FORAMEN
–> 3rd ventricle
–> CEREBRAL AQUEDUCT
–> 4th ventricle
–> CENTRAL CANAL
Pathology: Gliomas
brain tumors arising from glial cells (neuroglia)
highly malignant/fatal
glial cells
neuroglia
examples of gliomas
astrocytomas
oligodendrogliomas
causes of gliomas
not fully understood
ionizing radiation
rare genetic conditions
satellite cells
surround cell bodies of neurons in PNS
function:
provide structural support
regulate exchange of substances b/w neuron & interstitial fluid
schwann cells
form myelin sheath of PNS neurons
similar function to Oligodendrocytes of CNS
myelination
insulation of axons via neuroglia
via oligodendrocytes in CNS
via schwann cells in PNS
why myelination
increase rate/efficiency of AP transmission
mechanism is via SALTATORY CONDUCTION via myelin sheaths
oligodendrocytes and CNS
single oligodendrocyte myelinates multiple neurons
cell body not on neuron
DOES NOT HAVE NEURILEMMA
I.e.
NO NEURILEMMA ON AXON OF CNS
schwann cells and PNS
Schwann cell found on single neuron
cell body attached to axon
has neurilemma
Neurilemma
outermost layer of axon
sheath of schwann cells
also covers nodes of ranvier
NO NEURILEMMA IN CNS axons
axolemma
underneath neurilemma
membrane of axon
nodes of ranvier
gaps in myelination
high concentration of ion channels
allows AP to “skip” along axon – increases speed of conduction
I.e.
SALTATORY CONDUCTION
unmyelinated neurons (axons)
found in a schwann cell that does not form myelin
neuron (axon) exposed to extra cellular environment
NO SALTATORY CONDUCTIONS
I.e.
Slower conduction of AP
(continuous, without jumping)
grey vs white matter
in brain & CNS
some regions lighter than others
grey matter contains
cell bodies
dendrites
axon terminals
unmyelinated axons
neuroglia cells
white matter contains
myelinated axons
white vs grey matter – location in brain vs spinal cord
brain –> grey is superficial, white is deep
spinal cord –> white is superficial, grey is deep
what is grey matter in cerebrum called?
cortex
*cerebral cortex
collections of nervous tissue
i.e.
how nervous tissue components are grouped together
e.g. of nervous tissue grouping
cell bodies typically grouped together
axons typically grouped together
the groups/collections have their own names
E.g. of clusters/groups of neuron structures
Ganglia (ganglion)
nuclei (nucleus)
nerve
tract
ganglia
neuronal cell bodies
located in PNS
E.g.
dorsal root ganglion
dorsal root ganglion
cell bodies of sensory neurons
note varicella zoster and dorsal root ganglion
varicella zoster virus remains dormant after initial infection
I.e.
in dorsal root ganglion
if dormant varicella zoster virus reactivates in dorsal root ganglion?
= herpes zoster
nuclei
neuronal cell bodies in CNS
E.g.
Lentiform nucleus
caudate nucleus
nerves
bundle of axons in PNS
either sensory or motor, or mixed
tracts
bundle of axons in CNS
E.g. (spinal cord)
ascending tracts (sensory UP)
descending tracts (motor DOWN)
tracts in brain
information/signals from one part of brain to another
E.g.
internal capsule
corpus callosum
reflex
automatic nervous system reponse to certain kinds of stimuli
only in peripheral nerves & spinal cord
preserves homeostasis & protects organism through rapid adjustment
E.g. of reflex
hand on stove
5 components of reflex arc
1) stimulate receptor
2) activate sensory neuron
3) signal processing in CNS (via interneurons)
4) activation of motor neuron
5) response of peripheral effector
e.g. Stretch reflex
“MONOSYNAPTIC” reflex
involves muscle spindles
why monosynaptic?
no interneuron
just motor/sensory neuron
regulates skeletal muscle length
stretch reflex steps
increase muscle length
sensory neuron triggers motor response (contraction)
E.g.
patellar reflex (a DTR)
E.g. postural reflex
maintains normal, upright posture
E.g.
calf/anterior leg muscles during standing
withdrawal reflex
POLYSYNAPTIC
move away from stimulus
strongest withdrawal reflex
painful stimuli
strength of response determined by location/intensity of stimulus
sometimes withdrawal reflex also triggered by touch/pressure receptors
E.g.
perceived danger
flexor reflex
type of withdrawal reflex
affects muscles of limb
E.g.
pain when touching/grabbing hot pan
1) pain
2) sensory neuron to interneuron
3) motor neuron (anterior grey horn)
I.e.
contracts flexor muscles – withdraw hand
&
RECIPROCAL INHIBITION
= extensors relax
crossed extensor reflex
contralateral reflex
coordinated with flexor reflex
flexion of affected side + extension of opposite side
E.g.
1) step on st sharp
2) extensor reflex prepares to receive/support body weight
3) flexor reflex lifts foot
DTR
stretch reflexes
E.g.
biceps, triceps, ankle-jerk, patellar reflexes
reflex response provides info about specific segment of spinal cord via respective test
note subjective response to a stimulus
(similar to but not technically same as withdrawal reflex?)
if a stimulus is subjectively seen as dangerous or threat – similar response may occur, even if touch is not painful
E.g.
abuse victim
E.g.
phobia of insects, regardless of presence of actual threat
“conscious sensation” & subjective response to stimulus
E.g.
spider on arm
varying response depending on past experience with spiders
E.g.
someone with knowledge & interest in spiders might not have withdrawal reflex, especially if they are familiar with the species, and perceive minimal threat
General sensation & Voluntary Efferent signals
in spider example –> voluntary efferent response mimics withdrawal reflex (?)
appears similar, but technically different (?)
however, the following activation of sympathetic nervous system response (fight/flight) is involuntary
relevant pathology (multiple sclerosis)
autoimmune disease
progressive degeneration of myelin sheath of CNS axons
sheaths get replaced with scar tissue
fibrous/plaque
–> I.e. SCLEROSIS
multiple sclerosis facts
idiopathic
genetic link
signs/symptoms:
fatigue
visual disturbance
paresthesia
progressive muscle weakness
“neurological deficits”
Prognosis:
5-10 years lower life expectancy
gap is steadily closing
multiple sclerosis in Canada
one of the highest multiple sclerosis rates in the world
1/400 people
over 90,000 people
possible link to vitamin D deficiency
more common in AFAB (4x)
more common in people with a relative
note upcoming terms, RMP, Graded Potential (GP), & AP (Action potentional)
see following slides
rapidly changing membrane potential
creates electrical signal
two things that create abiity to send electrical signals are…
1) (very) Negative resting membrane potential (RMP)
2) specific ion channels in cell membrane
RMP
more naegative inside than outside
RMP in neurons
-70mV in Neurons
-90mV in muscles
why RMP?
buildup of positive ions outside cell
(sodium potassium pump (?))
why RMP ? (2)
1) Na+/K+ pump
(AS WELL AS LEAK CHANNELS) (?)
2) INABILITY OF MOST ANIONS TO LEAVE CELL
unequal distribution of ions =
inside cell mostly K+
outside cell mostly Cl- & Na+
also inside cell
negatively charged proteins
Na+/K+ pump
3 Na+ out
2 K+ in
one more cation pumped out than in = inside negative relative to outside
ALSO NOTE LEAK CHANNELS
Sodium & Potassium leak channels
passive membrane channels always open
for Na+ & K+
But how do leak channels establish RMP?
There are more K+ leak channels than there are Na+ leak channels
I.e.
more K+ leaves the cell than Na+ enters
= more relatively negative internal environment
But what does Na+ /K+ pump do in response to leak channels?
Continues to work to reestablish chemical gradient
but ultimately once again, 2 K+ enters, and 3 Na+ leaves
Why INABILITY OF ANIONS TO LEAVE CELL?
“anions can’t follow K+ out the cell”
they are attached to large molecules (E.g. ATP, or large proteins)
I.e.
Do not have appropriate channels?
I.e.
inside more negative
How neurons generate AP?
reverse membrane potential via ion channels
which ion channel types allow signal to be sent?
1) mechanically gated
2) ligand gated
3) voltage gated
mechanically gated channels?
physical distortion of cell membrane
I.e.
SENSORY RECEPTORS INVOLVING TOUCH, STRETCH, PRESSURE, VIBRATION,
** & even hearing!!! **
where are these mechanically gated channels found?
dendrites of neurons
2) Ligand gated ion channels
AKA
chemically gated ion channels
Open when binding specific ligand (chemicals – NEUROTRANSMITTERS)
E.g.
ACh (acetylcholine) @ the NMJ
where ligand gated ions channels mostly found?
mostly found on
a) DENDRITES
and b) CELL BODY of neuron
I.e.
where most synaptic communication takes place
3) voltage gated ion channels
open or close in response to changes in MEMBRANE POTENTIAL
one of the classic characteristics of EXCITABLE MEMBRANE
–> I.e.
Membranes that generate/spread APs
e.g. of Voltage gated ion channels
Na+, K+, Ca2+ channels
Some notes about the SODIUM VOLTAGE GATED ION CHANNEL – what are the TWO independent gates of “ ?
sodium channels have 2 independent gates
ACTIVATION & INACTIVATION GATES
Activation & Inactivation gates – functions
activation gate opens to let sodium in
inactivation gate closes to block sodium ions
where are Na+ & K+ voltage gated ion channels?
they are on the AXON of a neuron
where are Ca2+ voltage gated ion channels in the neuron?
on the synaptic end bulbs of the AXON TERMINAL
review of where GATED CHANNEL TYPES ARE FOUND IN NEURON
chemically (ligand) gated channels are found on the NEURON CELL BODY & DENDRITES
Voltage gated channels are found on the AXON (Na+ & K+ ion channels)
Voltage gated Ca2+ channels are found at the AXON TERMINAL @ synaptic end bulbs
MECHANICALLY GATED ION CHANNELS are found on the DENDRITES of the neuron
LEAK CHANNELS found on cell body, dendrites, AND axon
orientation/configuration of most gated ion channels @ RMP
closed
opening changes membrane potential
where leak channels found?
axon, cell body, dendrites
what are two electrical signals that neurons use to communicate?
1) Graded Potentials (GP)
2) Action Potentials (AP)
what is GP
initial stimulation of neuron causes a Graded Potential (GP)
where does GP occur?
in DENDRITES & Cell Body
what are the 3 different types of outcomes when a GP occurs?
i) GP is strong enough and an AP is generated & goes down axon
ii) GP is not strong enough and an AP is not generated (GP dies out)
iii) GP INHIBITS the neuron by making the Membrane MORE NEGATIVE
Graded potentials use which channels?
LIGAND GATED
& MECHANICALLY gated
Graded potentials are _____
VARIABLE – inconsistent
I.e.
Vary in amplitude depending on strength of stimulus
I.e.
“graded”
They are small deviations from the membrane potential (-70mV)
2 opposite effects of GP, depending on type
Can be depolarizing
or can be HYPERPOLARIZING
–> depolarizing = less negative / more positive
–> hyperpolarizing = make membrane more negative
note EPSP & IPSP
excitatory & inhibitory POST-SYNAPTIC POTENTIALS
GP are ____ized
localized
effects are limited to smaller areas of neuron – @ cell body &/or dendrites
GP last a ____ time
they last a short time – unlike AP
GP & Refractory period (?)
there is no REFRACTORY PERIOD for GPs
can AP be generated without GP
no
They must occur
– AND they must adequately DEPOLARIZE the membrane @ “trigger zone”
when GP sufficiently depolarizes the membrane @ trigger zone, what is it referred to as?
reaching threshold potential
how is amplitude of GP determined?
stimulus strength
EPSP which ion channel?
usually Na+ entering cell
IPSP which ion channel?
usually Cl- entering cell
or K+ leaving cell
summation of GP – and two types
GPs added together, adding to their strength, and ability to reach THRESHOLD POTENTIAL
1) Spatial summation
2) Temporal summation
spatial summation of GPs
summation of GP
STIMULI OCCUR AT DIFFERENT PLACES @ SAME TIME
= more Na+ ligand/mech- gated channels = LARGER GP
Temporal summation of GPs
stimuli ocurring @ same place @ different times (one after another) – in quick succession
I.e.
keeps sodium channels open –> Creates larger GP
ACTION POTENTIALS
all or none
when THRESHOLD POTENTIAL REACHED
(AKA “AP threshold”)
I.e.
membrane sufficiently depolarized to activate VOLTAGE GATED ION CHANNELS @ axon
VIA the…
TRIGGER ZONE @ axon hillock
Moves towards…
axon terminals (One-directional)
all or none
all channels open. Or none open.
(voltage gated ion channels)
WHAT IS THE THRESHOLD POTENTIAL? (AP THRESHOLD) ? (in mV)
-55 mV
EPSP takes neuron closer to threshold
IPSP takes neuron farther from threshold
what is the characteristic feature of SIZE & AMPLITUDE of AP?
always same same & amplitude
the 3 phases of AP
1) depolarization
2) repolarization
3) hyperpolarization
1) depolarization
GP causes membrane of AXON to reach THRESHOLD
@ -55mV voltage-gated Na+ channels open & Na+ rushes into cell
2) repolarization
K+ channels open – K+ rushes out of cell
cell returns to -70mV standard RMP
3) hyperpolarization
voltage gated K+ channels delayed in closing
I.e.
dip below -70mV standard RMP
eventually channels close & neuron reset to standard RMP
list of steps in generating AP
1) RMP (-70mV) – both Na+ & K+ channels closed
2) depolarization to “threshold potential” –> -55mV (?) –> voltage gated ion channels open (Na+)
3) Rapid depolarization via voltage gated sodium channels –> goes from -55mV to positive value (E.g. +10)
4) @ +30mV membrane potential –> Na+ voltage gated channels close
(VIA INACTIVATION GATE**)
–> K+ voltage gated channels open
5) Repolarization via K+ channels
as RMP reaches -70mV again, voltage-gated K+ channels begin to close
—> TAKES some time to all close, so brief HYPERPOLARIZATION occurs
what mV potential does INACTIVATION gate of Na+ voltage channels close?
@ +30mV
when do K+ voltage gated channels open?
+30mV (?)
when do K+ voltage gated channels begin to close?
-70mV
why does hyperpolarization briefly occur?
takes while for K+ channels to fully close
note about inactivation & activation gate of Na+ channels (voltage gated)
inactivation gate closes @ +30mV
later on activation gate closes again, and inactivation gate opens
–> @ RMP
GP vs AP
duration, magnitude, decay?, location?
vary in duration, magnitude, and they decay, & occur @ dendrite & cell body
= GP
same duration, magnitude, long distance, only in axon
= AP
refractory period types (2)
relative refractory period
absolute refractory period
absolute refractory?
inactivation gate is closed – therefore no GP can let Na+ into cell
relative refractory
inactivation gate open, and ACTIVATION gate is closed –> HOWEVER K+ channels still open
–> therefore a STRONGER GP than usual is required to bring cell back to THRESHOLD POTENTIAL (AP threshold)
AP propagation
AP generated @ “initial segment” of axon (segment closest to “axon hillock” – where “trigger zone” is)
AP triggers adjacent units
only in one direction b/c of ABSOLUTE REFRACTORY PERIODS of voltage channels in opposite direction
continuous vs saltatory AP propagation
continuous propagation occurs in UNMYELINATED axons
–> Slower –> 1m/s
saltatory propagation occurs in myelinated axons
–> only depolarization @ nodes is necessary
–> skips internodes b/c ions can’t cross myelinated region
–> faster than “CONTINUOUS” propagation
LARGER DIAMETER AXON = less resistance to ion movement = faster propagation
axon diameter and propagation speed
LARGER DIAMETER AXON = less resistance to ion movement = faster propagation
speed of propagation via 3 factors
1) myelination amt
2) axon diameter
3) temperature
1) myelination
more myelination = faster
2) axon diameter
more diameter = faster
(less resistance to ion movement)
3) temperature
greater temperature = faster propagation
nerve fibre types (3)
based on propagation speed
1) A fibres (very fast)
2) B fibres (moderately fast)
3) C fibres (slowest)
A fibre types
alpha, beta, gamma, delta
A fibres
largest diameter
myelinated
FASTEST
(up to 130m/s)
A fibre speed
up to 130m/s
where A fibres?
Axons for AP to to skeletal muscles
what sensory impulses for A fibres?
touch, pressure, proprioception,
some pain/temperature
B fibres
moderate size diameter
myelinated
moderately fast
(up to 15m/s AP)
B fibre speed?
up to 15m/s
where B fibres?
@ ANS
& visceral organs
C fibres
smallest diameter
NO MYELIN
SLOWEST
where C fibres?
reproductive, urinary, excretory, digestive, neurons
some pain receptors
(@ skin/viscera)
I.e.
NOCICEPTORS
signal transmission b/w neurons
see following slides
what is synapse
point of interaction
b/w two neurons
or b/w neuron & effector
(e.g. muscle/gland)
synapse = info filtered/integrated
two synapse types
electrical
& chemical
some synapse terminology
pre-synaptic neuron
post-synaptic neuron
axodendritic
axo somatic
axo-dendritic synapse
synaptic end bulbs @ axon terminal
–> interact with DENDRITES
(of post-synaptic neuron)
I.e.
axodendritic SYNAPSE
axo somatic synapse
synaptic end bulbs of axon terminal
–> interact with neuron cell body itself
(of post synaptic neuron)
ELECTRICAL synapse
VIA GAP JUNCTIONS
where electrical synapses?
neocortex
smooth & cardiac muscles (NEURONS OF “ ???)
advantages of Electrical synapses
faster
synchronized
(large number of neurons / muscle fibres produce AP in unison)
coordinated
(contraction of heart muscle fibres, or visceral smooth muscle)
chemical synapse
NT across synaptic cleft (Neurotransmitters)
MOST COMMON synapse type
MOST synapses b/w neurons
ALL synapses b/w neuron & effector
speed of chemical synapse vs electrical
slight delay
advantage of chemical synapse
more control over response (?)
CAN BE EXCITATORY OR INHIBITORY
chemical synapse steps
AP arrives at synaptic end bulb of axon terminal
voltage-gated Ca2+ channel opens
Ca2+ stimulates exocytosis of synaptic vesicles containing NT (e.g. Acetylcholin)
Each vesicle containing several thousand NTs
NTs bind to LIGAND-gated ION channels on the POST-SYNAPTIC neuron (or on the effector)
I.e. “POST SYNAPTIC MEMBRANE”
ion flow generates GRADED POTENTIAL (Post-synaptic potential)
recall: When do Ion channels @ post-synaptic membrane close?
signal ends when Neurotransmitter is…
1) broken down by enzyme (recycled)
E.g.
Acetylcholinesterase for ACh
2) “Diffuses out of synaptic cleft”
3) REUPTAKE by pre-synaptic neuron
(not for ACh)
the complexity of POST-SYNAPTIC POTENTIALS
Note EPSP & IPSP
see following slides
how many synapses (pre-synaptic neurons) can a single neuron receive signal from?
Net result of all signals (integration) @ AXON HILLOCK (trigger zone)
THOUSANDS
can be both excitatory or inhibitory
Determines rate of AP @ “INITIAL SEGMENT”
synaptic fatigue
SYNAPTIC FATIGUE
E.g.
supply of NT not keeping up w/ demand (frequency of AP arriving @ Axon terminal)
Synapse unable to receive signal from Pre-synaptic neuron
–> Until NT (E.g. ACh) replenished
This inability to move AP from pre-synaptic neuron to post-synaptic neuron (b/c of NT activity)
two types of Neurotransmitter receptor
1) Ionotropic receptors
(Ligand-gated receptors)
2) Metabotropic receptors
(G-protein coupled receptors)
1) Ionotropic receptors
Ligand-gated receptors
Neurotransmitter connected DIRECTLY to ION CHANNEL
Excitatory or inhibitory
E.g.
ACh receptor @ NMJ is connected to Sodium Ion Channel
2) metabotropic receptors
G-protein coupled receptors
via messenger protein (G protein) to open Ion channel
receptor not on ion channel
USUALLY INHIBITORY
ACh excitatory @Ionotropic receptors
inhibitory @Metabotropic receptors
metabotropic receptors create ____ response usually (inhibitory or excitatory?)
usually inhibitory
2 categories of Neurotransmitters
1) Small-molecule NTs
2) Peptide NTs (larger)
E.g. of small molecule NTs
Acetylcholine
amino acids – Glutamate & Aspartate (excitatory)
GABA & Glycine (inhibitory)
Biogenic amines – Epinephrine & norepinephrine
Dopamine
Serotonin
Nitric oxide
about ACh @ responses @ different locations
excitatory NT @ NMJ
“Excitatory between pre-ganglionic and post-ganglionic neurons of the ANS”
“Inhibitory NT in cardiac muscle in response to parasympathetic NS”
about Amino Acids (as small-molecule NTs)
Glutamate & Aspartate
= excitatory AA small-molecule NTs
GABA & Glycine
= inhibitory AA small-molecule NTs
GABA = Gamma-aminobutyric Acid (CNS)
= GABA = stress-reducing, sleep enhancing
Glycine = inhibitory @ NMJ
about BIOGENIC AMINES (as small-molecule NTs)
Epinephrine & Norepinephrine (adrenaline & noradrenaline)
= can act as HORMONE when released by ADRENAL glands
= also can act as NEUROTRANSMITTER in some neurons in brain & sympathetic nerves
Epinephrine & Norepinephrine contribute to
–> Fight/flight response
–> = increase in BP, heart rate, blood sugar, etc
two other biogenic amines (as small-molecule NTs)
Dopamine (DA)
E.g.
mood & pleasure centres
Serotonin (5-HTP)
E.g.
sensory perception & mood
last example of small-molecule NT
Nitric oxide
–> potent vasodilator
–> important excitatory NT in brain
–> role in erections in males
2) PEPTIDE NEUROTRANSMITTERS
found in CNS/PNS
excitatory/inhibitory
USUALLY BIND TO METABOTROPIC RECEPTORS
many are also HORMONES (note larger size)
Peptide NTs E.g.
ENDORPHINS & ENKEPHALINS
= neuropeptide
= act as painkiller
= 200x stronger than morphine
SUBTANCE P
= neuropeptide
= enhances pain perception
discovery of first neuropeptides (i.e. peptide NTs)
neurons in brain w/ receptors for opiate drugs = discovery of first Neuropeptides
what are the ways NT effects can be modified?
1) NT synthesis increased/decreased
2) NT release increased/decreased
3) NT receptors altered (activated/blocked)
4) NT removal increased/decrease
1) NT synthesis increased/decreased
NT synthesis increased/reduced
E.g.
patient’s with Parkinson’s disease produce less dopamine
2) NT release increased/decreased
NT release increased/reduced
E.g. amphetamines enhance release of dopamine & norepinephrine
e.g. botulinum toxin blocks release of ACh from somatic motor neurons
3) NT receptors altered
NT receptors activated/blocked
E.g.
myasthenia gravis –
antibodies block ACh receptors @ NMJ
–> cause muscle weakness & fatigue
4) NT removal increased/decrease
E.g.
cocaine delays reuptake of dopamine by blocking its “active transporters”
I.e.
prevents dopamine REUPTAKE by pre-synaptic terminal/neuron
neural circuit types
neural circuits = functional groups of neurons
1) simple circuit
2) diverging circuit
3) converging circuit
4) reverberating circuit
5) parallel after-discharge circuit
simple neural circuit
simplest
single presynaptic to single post-synaptic
1:1
VERY RARE
diverging circuit
single neuron stimulates multiple neurons, which each stimulate multiple neurons
SIGNAL AMPLIFIES
E.g.
from brain to spinal cord to peripheral nerves to effector (for movement)
converging neuronal circuit
multiple neurons stimulate single neuron
facilitates SUMMATION
E.g.
single motor neuron receiving numerous signals from brain
reverberating neural circuit
similar to simple
however…
branches from later neurons synapse w/ earlier ones
(reverberate backwards)
E.g.
coordinated movements
short-term memory
breathing
parallel after-discharge neural circuit
single pre-synaptic neuron stimulating post-synaptic neuron
same neuron also stimulates parallel neurons – which all synapse back to same post-synaptic neuron
E.g.
precise activities like solving math equations
damage of nervous tissue and regenerative capabilities
see following slides
neuroplasticity
adapt/change based on experience
physical changes =
= sprouting of new dendrites
= synthesis of new proteins
= changes in synaptic contact w/ other neurons
neuroregeneration
mild-moderate damage of PNS is capable of being repaired
note role of protective sheath of NEUROLEMMA from Schwann Cells in PNS
PNS nerves have good chance of recovery
CNS nerves do NOT regenerate
neurogenesis
birth of new neurons from undifferentiated STEM CELLS
occurs during embryological development
occurs in small/specific areas of brain throughout life
processes during repair of peripheral nerve tissue
changes in cell body
also changes in axon distal to injury
CHROMATOLYSIS
= degranulation of Nissl bodies within the neuron (for repair process)
WALLERIAN DEGENERATION
= degeneration of distal portion of axon & myelin sheath
(also as a part of repair)
process of PNS repair (continued)
Schwann cells multiply via mitosis
form REGENERATION TUBE
tube guides growth/repair of axon from proximal area
axons grow 1.5mm/day from proximal area
