NEURAL CONDUCTION

AND SYNAPTIC
TRANSMISSION
Membrane Potential
- the difference in electrical charge inside
and the outside of the cell
Microelectrodes
- used to record membrane potential
Resting Membrane Potential (Intracellular): -70
mV
- the potential inside the resting neuron is 70mV less
than outside the neuron
 IONIC BASIS OF THE RESTING POTENTIAL

POLARIZED
- to cause something to have positive and
negative charges

IONS
- positively and negatively charged particles
IONIC BASIS OF THE RESTING POTENTIAL

The resting potential is caused by the difference in the

ratio of the positive and negative charges from the
inside to the outside of a cell.
 IONIC BASIS OF THE RESTING POTENTIAL

Factors Causing Unequal Distribution of Charges

• Factors contributing to even distribution of ions (charged
particles)
– Random motion – particles tend to move down their
concentration gradient
– Electrostatic pressure – like repels like, opposites attract

• Factors contributing to uneven distribution of ions

– Selective permeability to certain ions
– Sodium-potassium pumps
 IONIC BASIS OF THE RESTING POTENTIAL

Ions Contributing to Resting Potential

• Sodium (Na+) - extracellular
• Chloride (Cl-)- extracellular
• Potassium (K+) - intracellular
• Negatively charged proteins (A-)
– Synthesized within the neuron
– Found primarily within the neuron
 IONIC BASIS OF THE RESTING POTENTIAL

Neuron at Rest
- K+ and Cl- ions pass readily
- Na+ pass with difficulty
- Negatively charged protein ions do not pass
 IONIC BASIS OF THE RESTING POTENTIAL

Equilibrium Potential (Hodgkin-Huxley

model)
• The potential at which there is no net
movement of an ion – the potential it will
move to achieve when allowed to move freely
• Na+ = 120mV
• K+ = 90mV
• Cl- = -70mV (same as resting potential)
 IONIC BASIS OF THE RESTING POTENTIAL

• Na+ is driven in by both electrostatic forces

and its concentration gradient
• K+ is driven in by electrostatic forces and out
by its concentration gradient
• Cl- is at equilibrium
• Sodium-potassium pump – active (uses ATP)
force that exchanges 3 Na+ inside for 2 K+
outside
 GENERATION AND CONDUCTION OF
POSTSYNAPTIC POTENTIALS
Firing of neurons release of
NEUROTRANSMITTERS diffuse at
synaptic clefts receptor molecules

Effects of Neurotransmitters
• Depolarize receptive membrane - resting
membrane potential

• Hyperpolarize - resting membrane potential

 GENERATION AND CONDUCTION OF
POSTSYNAPTIC POTENTIALS
Excitatory Postsynaptic Potentials (EPSPs)
- postsynaptic depolarization
- increase in the likelihood that the neuron will
fire

Inhibitory Postsynaptic Potentials (IPSPs)

- postsynaptic hyperpolarzation
- decrease the likelihood that the neuron will fire
 GENERATION AND CONDUCTION OF
POSTSYNAPTIC POTENTIALS
• Both EPSPs and IPSPs are Graded Response
• Amplitudes of EPSPs and IPSPs are
proportional to the intensity of the signals
elicited
Ex. Weak signals elicit small post synaptic
potentials
• Travel passively from their sites of generation
of synapses – dendrites or cell bodies
 GENERATION AND CONDUCTION OF
POSTSYNAPTIC POTENTIALS
• Characteristics of postsynaptic potential
transmission
- It is rapid
- it is decremental (a decrease in amplitude
as it travels)
 INTEGRATION OF POSTSYNAPTIC
POTENTIALS AND GENERATION OF ACTION
POTENTIALS
INTEGRATION OF POSTSYNAPTIC POTENTIALS
AND GENERATION OF ACTION POTENTIALS

• Excitatory or inhibitory signals must be near

the axon hillock

Threshold of Excitation
- the sum of depolarization and
hyperpolarization sufficient to depolarize the
membrane
INTEGRATION OF POSTSYNAPTIC POTENTIALS
AND GENERATION OF ACTION POTENTIALS

Action Potential (AP)

- a momentary reversal of the membrane
potential from about -70 to 50 mV
- not graded responses
- magnitude is not is not related to the intensity
of the stimuli
- “all-or-none responses”
INTEGRATION OF POSTSYNAPTIC POTENTIALS
AND GENERATION OF ACTION POTENTIALS

INTEGRATION
- adding or combining a number of individual
signals into one over all signal

SPATIAL SUMMATION
- integration of signals that occur at different
sites of the neuron
CONDUCTION OF ACTION
POTENTIALS
 IONIC BASIS OF ACTION
POTENTIALS
VOLTAGE ACTIVATED CHANNEL
- ion channels open or close in response to
changes in the voltage of the membrane period
 IONIC BASIS OF ACTION
POTENTIALS
Change in membrane potential reduced
threshold of excitation opening of
voltage-activated sodium channels
influx of Na+ ions membrane potential
becomes +50 mV from -70 mV
 IONIC BASIS OF ACTION
POTENTIALS
Change in membrane potential (influx of Na +)
opening of voltage-activated potassium
channels K+ ions near the membrane are
driven out of the membrane increase in

concentration of Na+ closure of sodium

channels
 IONIC BASIS OF ACTION
POTENTIALS

Repolarization (efflux of K+) ions closing

of
potassium channels due to hyperpolarization
IONIC BASIS OF ACTION
POTENTIALS
 REFRACTORY PERIODS
Absolute Refractory Period
- impossible to initiate another action potential

Relative Refractory Period

- possibility of firing a neuron
- application higher than normal levels of
simulation
- the amount of stimulation necessary to fire a
neuron to return to its baseline
 REFRACTORY PERIODS
Importance of Refractory Period
1. Action potentials travel in along axons in one
direction and cannot reverse direction.

2. Neural firing is related to the intensity of

stimulation.
 CONDUCTION OF ACTION
POTENTIALS
EPSPs/IPSPs Action Potentials
• Decremental • Nondecremental
• Fast • Conducted more
• Passive (energy is slowly than PSPs
not used) • Passive and active
(use ATP)
 CONDUCTION OF ACTION
POTENTIALS
Antidromic Conducion
- an action potential generated and traveling
along the axon back to the cell body

Orthodromic Conduction
- axonal conduction in the natural direction
from the cell body to terminal buttons
CONDUCTION IN MYLINATED AXONS

Nodes of Ranvier
- gaps between the adjacent myelin segments
- passage of ions through axonal membrane
- where axonal Na channels are concentrated
Nodes of Ranvier
CONDUCTION IN MYLINATED AXONS

How Action Potentials are transmitted?

Signal conducted passively instant and

decrimental 1st segment of the node
opening of Na channels ACTION
POTENTIAL NEXT NODE
CONDUCTION IN MYLINATED AXONS

Saltatory Conduction
- propagation of action of action potential in
myeleinated axons

- to skip or to jump

*Action potential only occur at the unmyelinated

nodes of Ranvier
SALTATORY CONDUCTION
SALTATORY
CONDUCTION
 VELOCITY OF AXONAL CONDUCTION

2 Properties of Axon
1. Diameter of an axon
2. Presence of myelin

Large and Myelinated: 100 meter/sec (224mi/hr)

Small and Unmyelinated: 1 meter/sec

60 meters/sec: maximum velocity of conduction in

humans
SYNAPTIC TRANSMISSION: CHEMICAL
TRANSMISSION OF SIGNALS AMONG
NEURONS
 5 Aspects of Synaptic Transmission

1. Structure of synapses
2. Packaging and transport neurotransmitters
3. Release of neurotransmitters
4. Activation of neurotransmitters
5. Reuptake, enzymatic degradation and
recycling of neurotransmitters
 STRUCTURE OF SYNAPSES
• An area of communication among neurons
• Release of neurotransmitters from buttons into the
synaptic clefts
• Induction of IPSP and EPSP

Axodendritic synapses
- synapses of axon terminals on dendrites
- termination on dendritic spines (nodules on the
surface of dendrites)
 STRUCTURE OF SYNAPSES
Axosomatic synapse
- synapse of axon terminal on somas (cell
bodies)

Dendrodendritic synapse
- capable of transmission in either direction
 STRUCTURE OF SYNAPSES
Axoaxonic synapses
- mediate presynaptic facilitation and
inhibition
- Advantage: selectively influence one
particular synapse rather than presynaptic
neuron
 STRUCTURE OF SYNAPSES
Cont. Axoaxonic synapse
- Directed synapses: synapses in which neurotransmitter
release and reception are in close proximity

- Nondirected synapse: site of release is at distance from site

of reception
• Neurotransmitter released from varicosities along axon
branches
• String-of-beads synapses
Nondirected synapse
 SYNTHESIS, PACKAGING AND
TRANSPORT OF
NEUROTRANSMITTERS
Neurotransmitter molecules
– Small
• Synthesized in the terminal button and packaged
in synaptic vesicles by the button’s Golgi bodies
– Large
• Neuropeptides – short amino acid chains (3-36
AA)
• Assembled in the cell body, packaged in vesicles,
and then transported to the axon terminal
 SYNTHESIS, PACKAGING AND
TRANSPORT OF
NEUROTRANSMITTERS
Assembly in the cytoplasm (ribosomes)
packed in vesicles by golgi complex transport
by microtubules to terminal buttons

Rate: 40 cms day

Presence of 2 neurotransmitters: Coexistence

Presence of 2 sizes of synaptic vesicles: 1 small
molecule and 1 neuropeptide
RELEASE OF NEUROTRANSMITTER

Exocytosis
- the process of neurotransmitter release
- Neuron at rest: congregation of
neurotransmitters at presynaptic membrane
- Action potentials opening of Ca2+ channels
entry of Ca2+ ions fusion of synaptic
vesicles with presynaptic membrane
emptying of contents into the synaptic clefts
EXOCYTOSIS
RELEASE OF NEUROTRANSMITTER

Exocytosis of small neurotransmitters

- pulsatile release

Exocytosis of neuropeptides
- released gradually
 ACTIVATION OF RECEPTORS BY
NEUROTRANSMITTERS
• Released NT molecules produce signals in
postsynaptic neurons by binding to receptors
• Receptors are specific for a given NT
• Ligand – a molecule that binds to another
• A neurotransmitter is a ligand of its receptor
 ACTIVATION OF RECEPTORS BY
NEUROTRANSMITTERS
Receptor Subtypes
- different types of receptors to which a
particular neurotransmitter can bind

- Advantage: transmission of different kinds of

messages to different parts of the brain by one
neurotransmitter
 ACTIVATION OF RECEPTORS BY
NEUROTRANSMITTERS

Inotropic Receptors
• NT binds and an associated ion channel
opens or closes, causing a PSP
• If Na+ channels are opened, for example, an
EPSP occurs
• If K+ channels are opened, for example, an
IPSP occurs

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 ACTIVATION OF RECEPTORS BY
NEUROTRANSMITTERS

Metabotropic
• Effects are slower, longer-lasting, more diffuse,
and more varied
• (1) NT 1st messenger binds. (2) G protein
subunit breaks away. (3) Ion channel
opened/closed OR a 2nd messenger is
synthesized. (3) 2nd messengers may have a wide
variety of effects.

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 ACTIVATION OF RECEPTORS BY
NEUROTRANSMITTERS
Autoreceptors
- bind to neuron’s own nerutransmitter
molecule
- located on presynaptic membrane
- monitor the number of nerotransmitter
molecules
 Reuptake, Enzymatic Degradation,
and Recycling
As long as NT is in the synapse, it is“active” – activity must
somehow be turned off

2 Mechanisms
• Reuptake – scoop up and recycle NT
- drawn back into presynpatic buttons by transporter
mechanisms

• Enzymatic degradation – a NT is broken down by enzymes

-
The two mechanisms for terminating neurotransmitter
action in the synapse: reuptake and enzymatic
degradation.

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Glial Function and Synaptic Transmission

Glial Cells – supporting cells

- Astrocytes: release chemical
transmitters containing receptors for
neuroreceptors
*conduct signals
* influence development of synapses
* participate in the neurotransmitter
reuptake
Glial Function and Synaptic Transmission

Gap junctions
- narrow spaces between adjacent neurons
bridged by connexins

- continuous cytoplasm of the 2 neurons

allowing electrical signals and molecules to
pass through
Glial Function and Synaptic Transmission

Cont. gap junctions

• Integral feature of local neural inhibitory circuits
• Communication between 2 astrocytes
• Less selective than synapses

Advantages
• Communication is fast
• Permit communications in either direction
THE NEUROTRANSMITTERS
 The Neurotransmitters

• Chemical messengers that enable

neurotransmission
• Transmit signals across a chemical synapse
from one neuron to another target neuron
• Produce excitation or inhibition but not both
 The Neurotransmitters
Classes of Neurotransmitters
• Amino acids
• Monoamines
• Soluble gases
• Acetylcholine
• Neuropeptides
 Amino Acid Neurotransmitters
• Usually found at fast-acting directed synapses
in the CNS
• Glutamate – Most prevalent excitatory
neurotransmitter in the CNS
• GABA
– Synthesized from glutamate
– Most prevalent inhibitory NT in the CNS
• Aspartate and Glycine (Excitatory NT)

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 Monoamines
• Synthesized from a single amino acid
• Effects tend to be diffused
• Catecholamines – synthesized from tyrosine
– Dopamine
– Norepinephrine
– Epinephrine
• Indolamines – synthesized from tryptophan
– Serotonin (5-hydroxytryptamine or 5-HT)

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 Monoamines
• Dopamine
- Excitatory and Inhibitory functions
- Inhibitory: Depression
- Excitatory: Motivation

• Norepinephrine
- Excitatory
- responsible in the stimulatory process of the body
- High levels of excretion may cause Anxiety
- Low levels: low energy, decreased focus, sleep cycle problems
 Monoamines
• Epinephrine
- Excitatory neurotransmitter
- elevated when ADHD symptoms are present
- depletion in levels can be caused by long
term stress and insomnia
- regulates heart rate and blood pressure
 Monoamines
• Serotonin
- Inhibitory neurotransmitter
- necessary for a stable mood
-  balance any excessive excitatory
neurotransmitter firing in the brain
- may regulate carbohydrate cravings, sleep cycle,
pain control, appropriate digestion
- low levels may cause decreased immune system
function
 Monoamines

Noradrenergic – neurons that release

norepinephrine

Adrenergic – neurons that release epinephrine

 Acetylcholine
• Acetylcholine (Ach)
– Acetyl group + choline
– First identified at neuromuscular junction
– Stimulates muscle movement
– Enhancement of sensory perception upon
waking up and sustaining attention

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 Unconventional Neurotransmitters

• Soluble gases – exist only briefly

– Nitric oxide and carbon monoxide
– Retrograde transmission – backwards
communication
• Endacannabinoids
– anandamide is one of the two known
endocannabinoids

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 Neuropeptides
• Large molecules
• Example – endorphins
– “Endogenous opioids”
– Produce analgesia (pain suppression)
– Receptors were identified before the natural
ligand

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Copyright © 2011 Pearson Education, Inc.
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 Pharmacology of Synaptic
Transmission
• How drugs influence synaptic activity
– Agonists – increase or facilitate activity
– Antagonists – decrease or inhibit activity
– A drug may act to alter neurotransmitter activity at
any point in its “life cycle”

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 Behavioral Pharmacology: Three
Influential Lines of Research

• Drugs selective to specific receptor subtypes may

exert different effects
– e.g. nicotinic vs. muscarinic acetylcholine
receptors
• Discovery of the endogenous opioids provided insight
into brain mechanisms of pleasure and pain
• Effects of dopamine agonists and antagonists on
psychotic symptoms led to new treatments for
schizophrenia
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FIGURE 4.19 Some mechanisms of
agonistic and antagonistic drug effects.

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