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Biological Bases of Behaviour.
Lecture 4:
Synaptic Transmission.
Learning Outcomes.
 At the end of this lecture you should be able to:
 1. Explain what is meant by a 'reflex arc'.
 2. Describe how research on reflexes has contributed to our
understanding of synaptic events.
 3. Describe how behaviour can be related to synaptic
 4. Explain the major chemical events at the synapse.
 In the late 1800's Cajal demonstrated that neurons do not
physically touch one another - they are separated by a tiny
gap called a synapse.
 From experiments assessing reflexes (automatic responses
to stimuli) Sherrington (1906) proposed that neurons
communicated with one another via the synapse.
 In a typical leg-flexing reflex a sensory neuron excites a
second neuron (interneuron) which in turn excites a motor
neuron which triggers a muscle to contract.
 This entire process is called a reflex arc.
Reflex Arc for Leg Flexion.
Brain neuron
Motor neuron
Kalat (2001), p 53
Characteristics of the Reflex.
 Sherrington observed certain properties of the reflex which
convinced him that a specific process was happening at the
junctions between neurons:
 1. Speed: He measured the total distance that an impulse
travels from sensory receptor to spinal cord to muscle, and
calculated the speed of the impulse.
 He found that the speed of conduction through a reflex arc
was significantly slower than that along a single axon,
therefore there must be some delay at the synapses.
 2. Summation: When a weak stimulus is applied (a pinch) a
reflex may not be produced, however if several small
pinches are rapidly applied they trigger a reflex.
 This is called temporal summation.
 Sherrington’s ideas were confirmed by Eccles (1964).
 He attached stimulating electrodes to 2 axons that formed
a synapse and recorded from one neuron whilst repeatedly
stimulating the other.
 During stimulation, brief depolarizations of the membrane
potential were seen (it became more positive) such
potentials (EPSP's).
 If several EPSP’s occur within a specific time then an action
potential will be triggered in the postsynaptic cell
(temporal summation).
 Alternatively, single EPSP’s from different axons can
combine to exceed the threshold of excitation of the
postsynaptic cell - this is called spatial summation.
Temporal and Spatial Summation.
Temporal summation
(several impulses from one neuron over time)
Spatial summation
(impulses from several neurons at the same time)
Kalat (2001), p 54
Synaptic Activation.
Kalat (2001), p 54
of 2 EPSP’s
3 EPSP’s
combine to
exceed the
EPSP’s combine
spatially to exceed
the threshold
Characteristics of the Reflex
 3. Inhibition: When stimulation is applied a flexor muscle
will contract, at the same time an extensor muscle will
relax, so while one muscle is being stimulated the other is
being inhibited.
 Sherrington realised that the second neuron (interneuron)
in the reflex arc must also connect to an inhibitory motor
 Eccles (1964) showed that the input from an axon not only
depolarizes the postsynaptic neuron but can also
hyperpolarize it (making it more negative), and thus less
likely to fire.
 This temporary hyperpolarization is called an inhibitory
postsynaptic potential (IPSP).
Inhibitory Synapses.
Brain neuron
Inhibitory synapse
Motor neuron to
extensor muscle
Motor neuron
to flexor
Kalat (2001), p 55
Perceptual Experience.
 The all or none law states that an action potential is either
triggered or not, this gives the impression that our sensory
experiences are either experienced or not.
 Clearly this does not happen, e.g. muscle contractions can
be weak or intensive, a spot of light can be perceived as
being faint or very bright.
 If the action potential is pulse-like how can it represent the
intensity of a stimulus?
 The answer is that a single action potential does not act as
a specific unit of information, instead variable information
is provided by the axon's rate of firing.
 E.g a high rate of firing may single a very bright light in the
retinal receptors but a low rate of firing may signal a very
dim light.
Sensation and Neural Integration.
 The all or none law is supplemented by the Rate law which
states that the strength of a stimulus is represented by the
firing rate of an axon, despite the fact that the action
potential remains constant.
 The rate of firing of an axon is determined by whether the
sum of its connections are excitatory or inhibitory - this is
referred to as neural integration.
 The greater the number of EPSP's the greater the
probability of an action potential, the greater the number of
IPSP's the lower the likelihood of an action potential.
 If a neuron is excited or inhibited, this does not necessarily
mean that behaviour is either excited or inhibited. E.g if
inhibitory neurons are inhibited then the result will be
excitation - e.g. alcohol and prefrontal cortex.
Simple Neural Integration.
Axon A stimulated =
Stimulate axon A
Axon B stimulated =
Both axons stimulated
Inhibitory synapse
Stimulate axon B
Carlson (1994) p41
The Nature of Synaptic Transmission.
 Loewi (1920’s) stimulated the vagus nerve in a frogs heart causing
heart rate to decrease. Fluid from this heart injected into a second,
caused it to also slow down.
 Stimulating the accelerator nerve (speeds up heartbeat) and injecting
fluid from this heart into a second caused it to be also stimulated.
 Synaptic transmission was thus shown to be chemical in nature.
Events at the Synapse.
 The major events at the synapse are as follows:
 1. Synthesis: Neurotransmitters are synthesised within the
terminal button by the Golgi apparatus ensuring that
neurotransmitter turnover is rapid.
 Peptides are synthesised within the soma, which lies far from
the releasing point; so peptide turnover is much slower.
 Neurotransmitters are synthesised from precursor molecules
derived form the diet, e.g acetylcholine is synthesised from
choline found in cauliflower and milk.
 Both neurotransmitters and peptides are stored in spherical
packets called synaptic vesicles.
Events at the Synapse (continued).
 2. Transport: Synaptic vesicles are transported down the
axon to the terminal buttons. They collect in the release
zone and 'dock' against the presynaptic membrane facing
the synaptic cleft.
 3. Release: The release zone contains voltage-dependent
calcium channels and so when an action potential reaches
the terminal button, it depolarizes the presynaptic
membrane, opening the calcium channels.
 The influx of calcium opens specialised channels in the
membrane called fusion pores which allow the
neurotransmitter stored in the vesicles to be released into
the synaptic cleft.
 This whole process is called exocytosis and lasts around 1-2
Release of Neurotransmitters.
Carlson (1994) p51
Undocked vesicle
Protein molecules
Entry of calcium
opens fusion pore
Fusion pore
Transmitter molecules
leave button
Synaptic Cross-Section.
Vesicles releasing
Carlson (1994) p50
Events at the Synapse (continued).
 4. Attachment: Molecules of neurotransmitter diffuse
across the synaptic cleft to the postsynaptic membrane
where they attach to the binding sites of specialised protein
 A neurotransmitter molecule fits into a binding site like a
key in a lock so receptors only work with a specific
 To complicate matters each neurotransmitter can have
several different types of receptor each with different
 As neurotransmitters are common chemicals there are
many natural and artificial chemicals (drugs, poisons) that
mimic their effects as they also fit the same binding sites.
Any chemical that attaches to a binding site is called a
Events at the Synapse (continued).
 5. Activation: When a neurotransmitter has attached to a
binding site it can have several effects depending upon the
nature of the receptors it has attached to.
 a) Ionotropic effects: These are very rapid but short-lived.
 According to North (1989) a neurotransmitter having this
effect opens the ion channels within 10ms after its release
and keeps them open for less than 20ms.
 Such events are useful for conveying rapid information
about sensory and muscular stimulation.
 Ionotropic effects can be excitatory or inhibitory, the most
common excitatory ionotropic transmitter is glutamate,
while the most common inhibitory one is GABA.
Ionotropic Receptors.
attached to binding
Closed ion channel
Carlson (1994) p54
Open ion
b) Metabotropic Effects.
 These effects are slower and longer-lasting as they involve a
sequence of metabolic reactions relying upon a secondary
 According to North (1989) they take place 30ms or more
after the release of the neurotransmitter and may last
minutes or hours.
 In such receptors the arrival of the neurotransmitter
activates G-protein and then one of two things happen:
Metabotropic Receptors.
 1. An  subunit breaks away from the G-protein, binds directly
with the ion channel and opens it.
Carlson (1994) p55
Metabotropic Receptors (continued).
 2. An  subunit breaks away from the G-protein, activates another
enzyme which then produces a second messenger (e.g cyclic AMP)
which in turn influences the ion channel.
Carlson (1994) p55
Events at the Synapse (continued).
 6. Inactivation: Neurotransmitters are removed from the
synapse in several ways:
 Deactivation: An enzyme destroys the transmitter
molecule, e.g acetylcholine is broken down into choline and
acetate by acetylcholinesterase (AChE), the choline then
returns to the presynaptic neuron where it is recombined
with acetate to form more neurotransmitter.
 Reuptake: Other transmitter substances detach from their
receptors and are taken back to the presynaptic membrane
by carrier molecules. They enter the membrane via special
membrane proteins called transporters, where they are
Transmitter molecules
returned to button
Carlson (1994) p57
References and Bibliography
Carlson, N.R. (1994). Physiology of Behaviour.
Eccles, J.C. (1964). The Physiology of Synapses.
Kalat, J.W. (2001). Biological Psychology.
North, R.A. (1989). Neurotransmitters and their receptors:
from the clone to the clinic. Seminars in the Neurosciences,
1: 81-90.
 Soltesz, I., Smetters, D.K., & Mody, I. (1995). Tonic
inhibition originates from synapses close to the soma.
Nature, 14: 1273-1283.