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Psych 7 Mascolo Course Notes – Neural Conduction & Transmission – Richard Mascolo, Ph.D.
Chapter 4: Neural Conduction & Synaptic Transmission
All cells carry an electrical charge, but neurons take advantage of this
Neurons take advantage of this in order to conduct messages down their length and across
to other neurons – their basic function.
A neuron’s electrical charge is called electrochemical – like your car battery the charge is
based in chemistry – charged ions that are unequally balanced across the cell membrane –
that is, inside the cell (“intracellular”) versus outside the cell (“extracellular”) – that’s why it is
called the membrane potential.
To start, what exactly is an ion? Atoms with an unequal # of positively charged protons &
negatively charged electrons. When # of protons > # of electrons, then the ion is positively
charged. When # of protons < # of electrons, then the ion is negatively charged. Here are
some examples we’ll be studying:

Sodium (Na+) => 11 protons, 10 electrons – the “+” means 1 more proton than electron

Potassium (K+) => 19 protons, 18 electrons – again, the “+” means 1 more proton than
electron

Calcium (Ca++ or Ca2+) => 20 protons, 18 electrons -- the “++” or “2+” means 2 more
protons than electrons

Chloride (Cl-) => 17 protons, 18 electrons – the “-“ means 1 more electron than proton
Summary your text’s presentation (from the previous edition, but I like it):
Psych 7 Mascolo Course Notes – Neural Conduction & Transmission – Richard Mascolo, Ph.D.
I will focus on 2 particular ions -- Na+ & K+ -- & 4 basic factors that affect their
intracellular and extracellular distributions when the neuron is inactive – its “Resting
Potential”:
#1
Na+
K+
#2
#3
#4
Differential
Cell Membrane
Sodium/Potassium Pump
Concentration
Gradient
Electrostatic
Pressure
Hard to cross
Easy to cross
extracellular
intracellular
intracellular
extracellular
intracellular
intracellular
3 of these factors are “passive” – that is, they do not require energy:
 #1 is a characteristic of the cell membrane itself – called “semipermeable”, the
imbedded channel proteins are differentially permeable to different molecules.
 #3 is actually a physical force called diffusion – substances flow down their
concentration gradient – that is, from areas of higher concentration to areas of lower
concentration.
 #4 is also a physical force involving electrical charge – substances flow away from
areas with the same electrical charge to areas with the opposite electrical charge.
The last of these factors is “active” – that is, it does require energy:
 #2 is based on a particular channel imbedded in the cell membrane – just like #1 – but
this one does require energy. This sodium-potassium pump in fact uses up 40% of
the cell’s energy – an expensive little beast! It pumps 3 sodium ions out of the cell
(efflux) for every 2 potassium ions into the cell (influx). This ratio of 3 positive ions out
for every 2 positive ions in leads to a net negative charge of the cell.
If not for the activity of the sodium-potassium pump, the other 3 factors would even out
the distribution of sodium & potassium, and the cell would end up with no electrical
charge. The sodium-potassium pump is an energy hog – evolutionary theory suggests
there must be a big adaptive advantage to maintaining this resting potential of -70mV.
A neuron receives messages from other neurons that alter its Resting Potential.
The neuron that sends the message is called “presynaptic” – the neuron that receives the
message is called “postsynaptic”. We are focusing now on the postsynaptic neuron -- its
resting potential is altered in 1 of 2 different ways. This is called a Graded Potential (GP):
 EPSP “Excitatory Postsynaptic Potential” alters the resting potential by depolarizing the
postsynaptic cell – that is, the resting potential is reduced from -70mV to, say, -68 mV.
 IPSP “Inhibitory Postsynaptic Potential” alters the resting potential by hyperpolarizing
the postsynaptic cell – that is, the resting potential is increased from -70mV to, say, -73
mV.
Psych 7 Mascolo Course Notes – Neural Conduction & Transmission – Richard Mascolo, Ph.D.
 The reason for the terms “Excitatory” & “Inhibitory” is that depolarization moves the
postsynaptic cell closer to firing a message of its own – an explosive Action Potential
(AP) -- but hyperpolarization moves the postsynaptic cell farther from firing an AP. The
depolarization required to trigger an AP is called the “threshold of excitement” – it’s
about +5mV – so the average neuron must depolarize from its resting potential of 70mV to -65mV in order to trigger an AP.
 All GPs – EPSPs & IPSPs – have these characteristics:
 their intensity can be anywhere between very strong & very weak – they are graded
 they are conducted so rapidly they can be considered instantaneous
 they lose strength as they are conducted – so they are decremental.
The combined influences of various EPSPs and IPSPs gather at the Axon Initial
Segment & determine whether or not the Postsynaptic Neuron fires an Action Potential
 Spatial Summation: Different presynaptic neurons create Graded Potentials on
different places on the Postsynaptic Neuron -- these gather just below the Axon Hillock
–first part of the Axon – the Axon Initial Segment
 Temporal Summation: One Presynaptic Neuron creates several Graded Potentials
from one space on the Postsynaptic Neuron, & these gather at the Axon Initial Segment
Conduction of Action Potentials
Ionic Basis of Action Potentials

Your text provides a detailed description of the step-by-step process of an AP. Once
again, you can focus on the activities of 2 ions – sodium & potassium – the “voltage
activated gates” that control their flow across the cell membrane.

Basically, it is the influx of Sodium that causes the “Rising Phase” (depolarization), & it is
the efflux of Potassium that causes the “Repolarization Phase” (hyperpolarization)

Your text provides a Figure illustrating this process – including the actions of those
voltage-activated gates – study it carefully
Refractory Periods

Absolute Refractory Period – 1-2 milliseconds after the axon fires an AP, it cannot fire
another one.

Relative Refractory Period – a few milliseconds later, this portion of the axon can fire
another AP, but only if it is depolarized more intensely than usual (i.e., more than +5mV)
Psych 7 Mascolo Course Notes – Neural Conduction & Transmission – Richard Mascolo, Ph.D.
Axonal Conduction of Action Potentials
Characteristic
Voltage Activated
Channels?
Decremental
Velocity
Structures:
Graded Potential (GP)
Action Potential (AP)
No – Passive Conduction
Yes (Time & Distance)
Instantaneous
Dendrite & Soma
Yes – Active Conduction
No (Actively Regenerated)
Slow
Axon
Conduction in Myelinated Axons
The difference here is that axons with myelin sheath can conduct the AP by “skipping”
between instantaneous conduction (like GPs) & slower regeneration (why APs are
nondecremental) – the former occur under the fatty myelin, the latter occur at the Nodes of
Ranvier.
Synaptic Transmission
Structure of Synapses: they are named after the part of the presynaptic neuron (dendrite,
soma, or axon) and the part of the postsynaptic neuron that are joining together to form the
synapse. Here are 3 examples (the first 2 are the most common):
 presynaptic axon joins a postsynaptic dendrite – thus: axodendritic
 presynaptic axon joins a postsynaptic soma – thus: axosomatic
 presynaptic axon joins a postsynaptic axon – thus: axoaxonic
(this last one allows for presynaptic inhibition/facilitation—see Figure 4.8)
Nondirected Synapses – see Figure 4.9 for an example
Release of NT molecules:
Exocytosis – the process by which NTs are ejected from the axon button
• NT molecules are synthesized and packed into vesicles -- small molecule NTs right there
in the terminal button and large molecule NTs in the cell soma (they have to be
transported down the axon to the terminal button) – see your text for details – either way,
they are ready for release.
• Release is dependent upon the arrival of an AP, but neither sodium nor potassium is
involved in the actual process – research has shown that when Na+ or K+ channels are
blocked at the axon button, NT molecules are still released.
• Instead, the arrival of an AP at the axon button causes Calcium channels to open; the
influx of Ca++ is the direct cause of the exocytosis process – vesicles fuse with the cell
membrane and empty their NT molecules into the synaptic cleft. (see Figure 4.10)
Psych 7 Mascolo Course Notes – Neural Conduction & Transmission – Richard Mascolo, Ph.D.
Activation of Postsynaptic Receptors by NT molecules: 2 Types of Receptors
Ionotropic Receptors activate Ion Channels & so directly cause EPSPs or IPSPs.
These effects are simple, quick, & brief. For example:
Open Sodium Channels (Na+ influx) – EPSP
•
Open Potassium Channels (K+ efflux) – IPSP
•
Open Chloride Channels (Cl- influx) -- IPSP
•
Metabotropic Receptors are indirect – the NT cause a “2nd messenger” release
inside the cell (e.g., a G protein). These effects are complicated, slow, & long-lasting
NTs land on Postsynaptic Receptors for just a few milliseconds. After that, they are
pulled back into the Presynaptic Neuron through 1 of 2 processes
 Reuptake – most common
 Enzygmatic Degradation – less common (e.g., ACh is broken down by the enzyme
AChE)
 Recycling – either way, NTs are pulled back into the Presynaptic Neuron & are used
again
Glial Cells Revisited – there are many examples of neural structures credited with many
more functions now than when I took this course! Glial cells may actually transmit information
themselves.
Gap Junctions – Since we’re on this topic of “exceptions”, I may as well acknowledge
research showing that some synaptic junctions directly transmit electrical charges without the
use of NTs. That’s all I’m going to say about this!
Autoreceptors -- primarily Inhibitory – 1 of the 2 ways that Presynaptic Inhibition can occur
Psych 7 Mascolo Course Notes – Neural Conduction & Transmission – Richard Mascolo, Ph.D.
Types of Neurotransmitters (NTs) – listed in bold –
• Amino Acids -- simple building blocks of proteins -- earliest & most prevalent
• Glutamate -- most prevalent excitatory NT
• GABA -- most prevalent inhibitory NT
• Monoamines –
Catecholamines
(Tyrosine -- Amino Acid Precursor)
(L-Dopa -- Precursor)
Dopamine
Norepinephrine
Epinephrine
Indolamine
(Tryptophan--Amino Acid Precursor)
Serotonin (5-HT)
• Acetylcholine (ACh)
• Unconventional NTs -- gases, endocannabinoids
• Neuropeptides (Endorphins)
Neurons are named after the NT they release:
Cholinergic Neurons
Dopaminergic Neurons
Serotonergic Neurons
Adrenergic Neurons
Noradrenergic Neurons
Release
Release
Release
Release
Release
Acetylcholine
Dopamine
Serotonin
Epinephrine (Adrenaline)
Norepinephrine (Noradrenaline)
How Drugs Influence Synaptic Transmission
 Figure 4.17 summarizes the steps involved in NT activity – from synthesis to
deactivation.
 Figure 4.18 details 2 basic categories of drug action:
Agonistic -- Mimic or intensify a NT effect
•
Antagonistic -- Impede or block a NT effect (e.g., Botox is a Nicotinic
•
antagonist)