Psychology: biological approach

Nervous system processes

The first principle of the biological approach to

behaviour stated: behaviour is the product of
physiology (the structure and function of the
nervous and endocrine (‫ )غدد درون ریز‬systems). So
far, we have considered the structure of the nervous
system- we have looked at localization of function
and neuroplasticity as structural phenomena.

The nervous system is a system of neurons, the

nervous cells. A neuron consists of three parts: the
body (soma), dendrites and axon Dendrites and
axon are filaments (‫ )رشته ها‬that extrude (‫ )بیرون می ایند‬from
the soma: typically multiple (‫ )متعدد‬dendrites but
always a single axon. The function of dendrites. (and
soma) is to receive signals from other neurons,
while the function of the axon is to transmit (‫)انتقال‬
signals further. Where the axon of one neuron
approaches a dendrite or soma of another neuron,
a synapse is formed. This means that a synapse (or a
synaptic gap) is a structure that connects two
neurons: the word "synapse" comes from the Greek
synapsis meaning "conjunction" Each neuron on
average has about 15,000 connections with other
neurons, so it is a very elaborate network.
The nature of information transmission in the
nervous system is partly electrical and partly
chemical. Every neuron has a certain threshold of
excitation received ( ‫ )آستانه تحریک دریافت شده‬from the other
neurons, and if the sum excitation exceeds this
threshold, the neuron "fires-generates a brief pulse
‫ نورون آتش می‌زند و یک پالس کوتاه تولید می‌کند‬،‫اگر مجموع برانگیختگی از این آستانه فراتر رود‬.

called action potential that travels along the axon to

other neurons, passing the excitation further. Note
that the action potential is all-or-none: it either fires
or not, and there is no such thing as "firing weakly
or "firing strongly. This might remind you of the
coding languages used in computers: essentially,
they all boil down to a sequence of Os and 1s.
The pulse reaches the end of the axon and there, at
the synaptic gap, the mechanism of transmission
becomes chemical. This happens as follows. ( When
the action potential reaches the end of the axon, a
neurotransmitter is released from the axon terminal
into the synaptic gap. )
‫انتقال دهنده عصبی از پایانه آکسون به شکاف سیناپسی آزاد می شود‬
Neurotransmitters are chemical messengers. They
are constantly synthesized in the neuron and moved
to the axon terminal to be stored there. A released
neurotransmitter is available in the synaptic gap for
a short period during which it may be destroyed
(metabolized), pulled back into the pre-synaptic
axon terminal through reuptake, or reach the post-
synaptic membrane and bind to one of the
receptors on its surface.
‫یک انتقال دهنده عصبی آزاد شده برای مدت کوتاهی در شکاف سیناپسی موجود است که در‬
‫ از طریق بازجذب به انتهای آکسون پیش‬،)‫طی آن ممکن است از بین برود (متابولیز شود‬
‫ یا به غشای پس سیناپسی برسد و به یکی از گیرنده های موجود در آن‬،‫سیناپسی کشیده شود‬
‫متصل شود‬
If the neurotransmitter binds to a receptor in the
post-synaptic membrane, this process changes the
membrane potential and so contributes to
activating an electric pulse in the post-synaptic
neuron. Here the chemical mechanism becomes
electrical again.
‫ این فرآیند پتانسیل‬،‫اگر انتقال دهنده عصبی به گیرنده ای در غشای پس سیناپسی متصل شود‬
‫غشا را تغییر می دهد و بنابراین به فعال شدن یک پالس الکتریکی در نورون پس سیناپسی‬
‫کمک می کند‬

There are many different neurotransmitters. Their

exact number is unknown but more than 100 have
been identified. All neurotransmitters are broadly
divided into two groups: excitatory ( ‫ )بازدارنده‬and
inhibitory ( ‫)تحریک کننده‬. Excitatory neurotransmitters
allow the impulse to cross the synapse. They
produce stimulating effects on the brain. Inhibitory
neurotransmitters stop the impulse, preventing it
from crossing the synapse. They produce calming
effects on the brain. These neurotransmitters are
always in a state of dynamic balance.
When excitatory or inhibitory neurotransmitters are
out of their optimal ranges in the brain, this may
cause various behavioural malfunctions such as
mental disorders.

Neurotransmitters themselves are affected by

agonists and antagonists. Agonists are chemicals
that enhance ( ‫ )تقویت‬the action of a neurotransmitter.
Antagonists are chemicals that counteract (‫)مقابله می کنند‬
a neurotransmitter and so prevent a signal from
being passed further. ‫بنابراین از ارسال بیشتر سیگنال جلوگیری می کنند‬
Many drugs function as agonists or antagonists, For
example, a class of drugs known as SSRIs (selective
serotonin reuptake inhibitors) do exactly what their
name suggests: selectively inhibit (block) the
reuptake of the neurotransmitter serotonin from
the synaptic gap. This increases the concentration of
serotonin in the synapse. SSRIS have been shown to
be effective against depression.
As you see, neurotransmission is a complex process
determined simultaneously by multiple factors.
Imagine we have artificially increased the level of
neurotransmitter X in the brain and this resulted in
a change of behaviour Z (for example, elevated
mood). Can we say that neurotransmitter X
influences elevated mood? Yes, to a certain extent,
but with a lot of limitations to be kept in mind
X may function as an agonist for neurotransmitter Y,
which in turn may affect behaviour Z. In other
words, the effects of neurotransmitters may be
indirect, sometimes with many links between the
"cause" and the "effect".
X may serve as a trigger for a long-lasting process of
change in a system of interconnected variables. In
other words, the effects of X on Z may be
postponed. ‫به تعویق افتاد‬
X is usually not the only factor affecting Z. X is never
the only factor that changes. As you artificially
increase the level of X, this may result in various
side effects.
Research into the influence of neurotransmission
on behaviour will therefore always be reductionist
in the sense that we need to manipulate one
variable (X) and assume that it is the only variable
that changes. Nevertheless, with all the limitations
in mind, research into the influence of
neurotransmission on behaviour is highly intriguing,
partly because it gives us a key to influencing
human behaviour through intake of chemicals.

Areas that have been shown to be affected by

neurotransmitters have included mood, memory,
sexual arousal and mental illness, among many
others. Let's look at some of the effects of specific
neurotransmitters.
Effect of serotonin on prosocial behaviour Crockett
et al (2010) investigated the effect of serotonin on
prosocial behaviour. Serotonin is A
sample of volunteers was recruited for the study. It
included 30 healthy subjects (mean age 26). The
experiment followed a repeated measures design
with two conditions. In condition 1 participants
were given a dose of citalopram. This drug is a
highly selective serotonin reuptake inhibitor (SSRI):
a chemical that blocks reuptake of serotonin from
the synapse, in this way boosting its concentration
and prolonging its effects. In condition 2 (the
control) participants were given a placebo (a
harmless substance with no active effect). The
design was counter-balanced, and this was a
double-blind study an inhibitory neurotransmitter
that is involved in sustaining stable mood and
regulating sleep cycles, for instance. This example
has been selected intentionally to demonstrate that
researchers attempt to establish links between
seemingly distant variables. Effects of
neurotransmission on something such as mood or
fatigue are believable because these are rooted in
biological processes, but prosocial behaviour seems
to be a person's own choice or free will. How can a
person's free will be affected by a biological factor?
After taking the drug, participants were given a
series of moral dilemmas that involved choosing
between a utilitarian outcome (saving five lives) and
aversive harmful actions (such as killing an innocent
person). Aversive harmful actions in the scenarios
were of two types: personal (for example, pushing a
man off a bridge to stop a train and prevent it from
hitting five people) and impersonal (for example,
pressing a lever to divert a train off a track where it
will hit five people to a track where it will hit one).
Results showed a specific pattern of activation in
the brains of participants in response to the
photographs of their loved ones: activation was
observed in dopamine-rich neural systems, primarily
the ventral tegmental area (VTA) and caudate
nucleus. Both these regions are rich in dopamine
and form the key part of the so-called dopaminergic
pathway-a system that generates and transmits
dopamine and increases dopamine-related activity
in the brain. It is a reward system because
dopaminergic activity is associated with motivation
and feelings of pleasure. In this way, dopamine
activity in the brain plays a role in romantic love.
‫نتایج الگوی خاصی از فعال‌سازی را در مغز شرکت‌کنندگان در پاسخ به‬
‫ فعال‌سازی در سیستم‌های عصبی غنی از‬:‫عکس‌های عزیزانشان نشان داد‬
‫ عمدتًا ناحیه تگمنتال شکمی‬،‫( دوپامین‬VTA) ‫ هر دو این‬.‫و هسته دمی مشاهده شد‬
‫ناحیه غنی از دوپامین هستند و بخش کلیدی مسیر به اصطالح دوپامینرژیک را‬
‫ سیستمی که دوپامین را تولید و انتقال می‌دهد و فعالیت مرتبط با‬- ‫تشکیل می‌دهند‬
‫ این یک سیستم پاداش است زیرا فعالیت‬.‫دوپامین را در مغز افزایش می‌دهد‬
‫ به این ترتیب فعالیت دوپامین‬.‫دوپامینرژیک با انگیزه و احساس لذت مرتبط است‬
‫در مغز در عشق رمانتیک نقش دارد‬

The role of dopamine in Parkinson's disease

Freed et al (2001) studied the role of dopamine in
Parkinson's disease. Parkinson's disease is a
degenerative disorder that mainly affects the motor
functions of the nervous system. The early
symptoms of the disease are shaking, rigidity, and
difficulty with movement and walking. Later in the
development of the disease, thinking and
behavioural problems also occur. Currently there is
no cure for Parkinson's disease and the exact causes
are unknown. In the study by Freed et al, the
sample consisted of 40 patients who were 34-75
years old and had severe Parkinson's disease, with
the mean duration of 14 years.
The sample was randomly divided into two groups:
the experimental group received a transplant of
nerve cells and the control group underwent sham
surgery. In the transplant group, nerve tissue
containing dopamine-producing neurons was taken
from embryos aborted 7-8 weeks after conception
and transplanted into the patients' putamen-a
structure of the limbic system involved in
movement regulation. All surgeries were performed
with the patient awake. Local anesthesia was
administered to the skin of the forehead and four
holes were drilled through the frontal bone, after
which the tissue was transplanted through long
needles. In the sham surgery group, holes were
drilled in the skull but the dura (a thick membrane
that surrounds the brain) was not penetrated.
Otherwise, the procedure was identical.

The protocol of the study and the consent form

describing the risks and potential benefits were
approved by the ethics committee. A separate
written informed consent form was used for the
women who donated fetal tissue from abortions.
A number of measures were taken both before and
after the surgery. They included clinical observations
and interviews, and brain scans- positron emission
tomography (PET). All patients were followed up
longitudinally for one year.
Results of the study indicated the following. ⚫
Irrespective of the age group, PET scans revealed
increased growth of dopamine- producing cells in
the putamen.

⚫ A reduction of symptoms by 28% was found in the

patients in the transplant group, but only the
younger ones (aged 60 or younger). No
improvement was registered in the older sub- group
of patients (aged over 60).

The overall conclusion was that transplantation of

dopamine-producing neurons in the putamen of
patients with severe Parkinson's disease results in
some clinical benefit in younger but not older
patients. Less response to treatment in the older
patients despite successful growth of dopamine
neurons may be attributed to lower neuroplasticity
of the brain.
The role of serotonin in depression

Serotonin has been shown to be involved in the

symptoms of major depressive disorder. If you study
abnormal psychology (see Unit 5) as an option you
will learn a lot more about this topic. The serotonin
hypothesis states that low levels of serotonin in the
brain play a causal role in developing depression.
Studies have mainly involved clinical trials with two
groups of patients. The experimental group would
be given a drug that affects levels of serotonin in the
brain and the control group would be given a
placebo (a harmless substance that the patient
believes to be a drug), after which the symptoms of
depression would be compared. If a drug that is
known to affect serotonin (for example, an SSRI)
leads to a reduction of symptoms in the
experimental group, it is concluded that the level of
serotonin is the cause of depression.
However, this logic has a number of limitations.
First, drugs affect neurotransmitters within minutes,
but the behavioural effects do not manifest
immediately. Sometimes it takes weeks. This
suggests that the influence may be indirect or there