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Overview of neurophysiology Part II

FLG 327 lecture 2

Evangeline Nortje

on 17 August 2016

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Transcript of Overview of neurophysiology Part II

Overview of Neurophysiology
Part ii
axonal transport
signal conduction
repair of damaged neurons
Neurocrine molecules
Neural integration
Day 20
Day 23
Week 4
week 6
Week 11
embryological development of nervous system
in the very early embryo, cells that will become the NS lie in a flattened region called the neural plate
lateral edges of the neural plate = neural crest cells
the CNS develops from a hollow tube...
Week 40
Axons are specialized to convey chemical & electrical signals
axonal cytoplasm (axoplasm)
filled with many types of fibres & filaments BUT...
lacks ribosomes & ER
Therefore: any proteins destined for axon/ axon terminal must be synthesized in RER in cell body
Proteins are then moved down the axon by process known as:
Axonal transport
Slow axonal transport
material is moved by axoplasmic flow from cell body to axon terminal

for components not used rapidly by the cell:
cytoskeleton proteins

Fast axonal transport
neuron uses stationary microtubules along which mitochondria and vesicles are transported

"walk" along tracks with aid of motor proteins

motor proteins bind & unbind from microtubules with help of ATP

& go fashion
Moves secretory vesicles and mitochondria to axon terminal
Return old cellular components to cell body for recycling
myelinated vs unmyelinated
faster conduction
AP conduction is faster in high resistance axon
Myelin sheath provides a high resistance wall
Each node has a high [ ] of voltage gated Na+ channels

When activated they open and further depolarize the axon

Restoring the amplitude of the action potential

"jump" of AP from node to node =
Slower conduction
Have low resistance to current leak
Because the entire axon membrane is exposed to the extracellular fluid
channel opening slows conduction
channels must open sequentially all the way down the axon membrane to maintain AP

moving cursor across screen with
spacebar vs Tab key
demyelinating diseases
slows conduction of APs
current leaks out of now-uninsulated regions between the nodes
depolarisation reaching nodes may not be above threshold
If cell body dies, neuron dies
If cell body intact & axon is severed, neuron survives
section of axon separated from cell body disintegrates
1) Synaptic transmission ceases
2) Axonal degeneration (slower in CNS than PNS)
3) Myelin sheath begins to unravel
4) Debris clearance (microglia/macrophages)

somatic motor neuron
death of distal axon =
paralysis of skeletal muscles innervated by neuron
sensory neuron
death of distal axon =
loss of sensation in region innervated by neuron
Axon regeneration is not possible
= undifferentiated cell layer lines lumen of neural tube
during development some cells migrate out and differentiate into neurons and others specialize into ependymal layer
BUT some neural stem cells remain undifferentiated
correct signal = these cells are transformed into Neurons & Glial cells

What happens after injury?
Neurocine molecules
Neurocrine receptors
Act as paracrine signals
target cells located close to neuron that secretes them
some act on cells that secrete them = autocrine molecules as well

molecule acts at synapse and elicits a rapid response

act at synaptic and non-synaptic sites and are slow acting

Secreted into the blood distributed throughout the body
Receptor channels
G protein-coupled receptors
Ligand-gated ion channel
mediate rapid responses by altering the ion flow across the membrane

- mediate slower responses
- signal transduced via 2nd messenger system

Each receptor type has multiple subtypes
one NTM = different effects in different tissue
E.g. serotonin has at least 20 receptor subtypes

Neurocrines informally grouped into 7 classes according to structure
1) acetylcholine
2) amines
3) amino acids
4) peptides
5) purines
6) gases
7) lipids
lipid neurocrines = eicosannoids
receptors = cannabinoid receptors
exogenous ligand: tetrahydrocannabinoid
bind G-protein coupled receptors

Acetylcholine (Ach)

Neurons that secrete ACh & receptors that bind ACh = cholinergic

Two subtypes of cholinergic receptors:
All are active in CNS
serotonin, dopamine, norepinephrine & epinephrine
Neurons that secrete NE & receptors that bind NE= adrenergic
Adrenergic receptors divided into 2 classes:
betaα & alpha

amino acids
Glutamate, aspartate = excitatory neurotransmitters
Gamma-aminobutyric acid (GABA) = inhibitory neurotransmitter
Glycine in the spinal cord = inhibitory neurotransmitter

Substance P involved in pain pathways
Opioid peptides (enkephalins and endorphins) mediate pain relief
CCK, vasopressin & ANP

AMP adenosine monophosphate
ATP adenosine triphosphate
Bind to purinergic receptors = GPCRs
Nitric oxide (NO)
Carbon monoxide (CO)
Hydrogen sulfide (H S)
CNS neurons release many different neurocrines, including polypeptides such as:

hypothalamic releasing hormones
PNS secretes only 3 major neurocrines:

Synaptic communication by NTM
NTM release
NTM termination
Synthesis & recycling of ACh
Communication between neurons not always a one-to-one event
Synaptic plasticity
The ability of the nervous system to change activity at synapses
Short term
enhance activity at synapse = facilitation
decrease activity at synapse = depression
Long term
Long term potentiation (LTP)
Long term depression (LTD)
modification can take place on:
Modification can be:
Postsynaptic modification
Postsyaptic responses:
Fast postsynaptic responses
associated with ion channels
Neurotransmitter binds receptor-channel
Ion channel opens
Fast synaptic potential
Response is short lived

slow postsynaptic response initiated by GPCR linked to a second messenger
Slow synaptic potential
Response of second messenger takes longer than opening of ion channels
Response lasts longer
Postsynaptic potential:
Excitatory postsynaptic potential (EPSP)
caused by a DEPOLARISING synaptic potential
makes cell more likely to fire an action potential
Inhibitory postsynaptic potential (IPSP)
caused by a HYPERPOLARISING synaptic potential
Membrane potential further from threshold
Cell less likely to fire
Postsynaptic integration
When 2 or more presynaptic neurons converge on a single postsynaptic cell the response is determined by summed input
Spatial summation
almost simultaneous graded potentials originate from different locations/spaces on the neuron
Temporal summation
summation that occurs from graded potentials overlapping in time from a single presynaptic neuron
Presynaptic modification
activity of the presynaptic neurons van also be altered
Alters neurotransmitter release by the presynaptic cell

Presynaptic alteration in NTM release provides more precise control than postsynaptic modification
Pre- vs postsynaptic modification
presynaptic alteration allows for selective modulation of presynaptic collaterals & their targets

postsynaptic modulation alters the responsiveness of the entire postsynaptic neuron
Uses tracks...
saltatory conduction
IN CERTAIN CASES: Axons can regenerate their synaptic connections
Schwann cells secrete neurotrophic factors to keep cell body alive and stimulate re-growth of axon
Growing axon follows chemical signals in extracellular matrix along its former path until it makes new synapses with target cell
Degeneration is quick
Clearance is quick
Regeneration is supported
Reinnervation is supported
Schwann cells recruit macrophages by release of cytokines and chemokines
HOWEVER: the macrophages are not attracted to the region for the first few days; hence the Schwann cells take the major role in myelin cleaning until then
PNS is much faster and efficient at clearing myelin debris in comparison to CNS
Regeneration is rapid in PNS, allowing for rates of up to 1 mm a day of regrowth
- Nerve growth factor (NGF)
- Brain-derived neurotrophic factor (BDNF)
- Glial cell line-derived neurotrophic factor (GDNF)
Schwann cells provide structural guidance for reinnervation
- form a line of cells called Bands of Bungner
Favourable promoting factors in PNS
Glial cells support regeneration
Astrocytes, microglia & oligodendrocytes seal off & scar damaged region
Gliosis (Glial scar formation)
Degeneration is slow
Clearance is slow
Regeneration NOT supported
Reinnervation NOT supported
Primary causes:
In comparison to Schwann cells, oligodendrocytes require axon signals to survive
injury = oligodendrocytes programmed cell death
state of rest
Therefore, unlike Schwann cells, oligodendrocytes fail to
clean up the myelin sheaths and their debris
Oligodendrocytes fail to recruit macrophages for clean up
CNS uses Microglia for clearance, BUT...
recruitment is slower by +/- 3 days
rate of clearance is very slow among microglia in comparison to macrophages
further hinders chances for regeneration and reinnervation
Oligodendrocytes inhibit regeneration
lack of such favourable promoting factors = regeneration is stunted in CNS
= ionotropic receptors
side of the synapse
Delay in debris clearance
Myelin debris secrete inhibitory factors (axon regrowth inhibition)
excitatory inhibitory
NTM release= presynaptic inhibition
NTM release= presynaptic facilitation
Inhibitory or excitatory neuron terminates on or close to axon terminal of the presynaptic cell
Conduction is not slowed by open ion channels
Current leak out of the cell is limited
Limited membrane exposed to extracellular environment
small sections of bare membrane = nodes of ranvier
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