Biological Psychology

Week 3 & 4:
Synapse
Kalat, J.W. (2015). Biological Psycholgy.(12th ed.) Boston:
Cengage Learning. Ch 2.
Itır Kaşıkçı
Istanbul Commerce University
Oct’18
Synapses
• A specialized gap between • 1906, Sherrington: Physiological
neurons where they demonstration of the
communicate (by transmitting communication between one
chemicals). neuron and the next differs from
communication along a single
axon (and naming synapse).
• 1800s, Cajal: Anatomical
demonstration of a synapse.
• Sherrington studied reflexes.
• Automatic muscular responses to
stimuli.
The Reflex Arc
• The Reflex Arc:
The circuit from
sensory neuron
to muscle
response.

• The flexion and

extension
reflexes are
controlled by
the spinal cord.
• Cannibal
female
spiders.
• Flexor muscles draw an extremity toward the trunk of the body.
• Extensor muscles move an extremity away from the body.
Properties of Reflexes
1) Reflexes are slower than conduction along an axon.

Synapse!

2) Several weak stimuli presented at nearby places or times produce a

stronger reflex than one stimulus alone does.
3) When one set of muscles becomes excited, a different set becomes
relaxed.
 Properties of Synapses
• Several weak stimuli presented at How to explain this property of reflexes?
nearby places or times produce a
stronger reflex than one stimulus alone
does.

• Temporal Summation: Repeated

stimuli within a brief time have a
cumulative effect.

• Spatial Summation: Synaptic inputs

from separate locations combine their
effects on a neuron.

• Temporal summation and spatial

summation ordinarily occur together.
• Integrating these inputs provides
complexity.

• Graded Potential
Graded Potential

• Graded potentials may be either;

• Excitatory (depolarization).
• Inhibitory (hyperpolarization).
• Unlike action potentials, which are always depolarizations!

• Graded depolarization of the postsynaptic membrane is called

excitatory postsynaptic potential (EPSP).
• An EPSP causes the Na+ channels to open.
• An action potential at the postsynaptic neuron starts if the treshold is reached.
• If not, the depolarization decays over time.
Temporal & Spatial Summation
• John Eccles (1964), attached microelectrodes to stimulate axons of
presynaptic neurons while he recorded from the postsynaptic neuron.
Properties of Reflexes - continued
• When one set of muscles becomes excited, a different set becomes relaxed.
• How to explain this?
Muscle contraction
• A pinch on the foot
sends a message
along a sensory
neuron to an
interneuron (an
intermediate neuron)
that excites the
motor neurons:
• connected to the
flexor muscles of
that leg.
• the extensor
muscles of the
other legs.

• Also inhibits:
• the extensor
muscles in that leg
• flexor muscles of
the other legs.
Inhibitory Synapses
• If an input from an axon hyperpolarizes the postsynaptic
cell, this temporary hyperpolarization of a membrane is
called an inhibitory postsynaptic potential (IPSP).
• Remember: Temporary depolarization of a membrane is called an
excitatory postsynaptic potential (EPSP).

• An IPSP occurs when synaptic input selectively opens the

gates for K+ to leave the cell or for Cl- to enter the cell.
• Remember: EPSPs are causing the Na+ channels to open.

• IPSP makes it harder for that cell to produce action

potential.
• Remember: EPSPs are making it easier for that cell to produce an
action potential.
Relationship among EPSP, IPSP,
and Action Potentials
The Neuron as Decision Maker
• The EPSPs and IPSPs reaching a
neuron at a given moment
compete with one another,
• The net result is a complicated,
not exactly algebraic summation
of their effects.
• We could regard the summation of
EPSPs and IPSPs as a “decision”
because it determines whether or
not the postsynaptic cell fires an
action potential.
• Not complex decisions!

• Spontaneous firing rate: A

periodic production of action
potentials even without synaptic
input. If that’s the case:
• EPSPs increase the frequency
of action potentials above the
spontaneous rate,
• IPSPs decrease it.
Mathematical Models
Chemical Events at the Synapse
• The discovery of Chemical Transmission at Synapses
• T. R. Elliott, British scientist (1905)
• Applied the hormone adrenaline directly to the surface of the heart, the
stomach, or the pupils.
• Observed the same effects neuronal stimulation caused.

• Otto Loewi, a German physiologist (1920)

• Stimulated the vagus nerve & decreased a frog’s heart rate.
• Took the fluid of the heart, injected it to a second frog’s heart.
• Found that the second heart also decreased its rate of beating.
• He did the same, the other way around (increasing). That worked too.

• In 1950s, researchers established that chemical transmission

predominates throughout the nervous system.
• Encouraged research developing drugs for psychiatric uses.
Synaptic
Transmission
The Sequence of Chemical events at a Synapse

1. The neuron synthesizes chemicals that serve as neurotransmitters.

• Synthesizes the smaller neurotransmitters in the axon terminals.
• Synthesizes neuropeptides in the cell body.
2. Action potentials travel down the axon. At the presynaptic terminal,
an action potential enables calcium to enter the cell. Calcium
releases neurotransmitters from the terminals and into the synaptic
cleft, the space between the presynaptic and postsynaptic neurons.
3. The released molecules diffuse across the cleft, attach to receptors,
and alter the activity of the postsynaptic neuron.
4. The neurotransmitter molecules separate from their receptors.
5. The neurotransmitter molecules may be taken back into the
presynaptic neuron for recycling or they may diffuse away.
6. Some postsynaptic cells send reverse messages to control the further
release of neurotransmitter by presynaptic cells.
Release and Diffusion of NTs
• Depolarization at the end of an axon, caused by action
potential, opens voltage-dependent Ca++ channels in the
presynaptic terminal.
• Ca++ enters the terminal and causes exocytosis—bursts of
release of NTs from the presynaptic neuron.

• Many neurons release a combination of two or more NTs.

• Some neurons release two NTs at the same time,
• Some release one at first and another one slowly later.
• Some release different NTs from different branches of its axon.
• An experience can cause a neuron to stop releasing one NT
and release another one instead.
Neurotransmitters (NTs)
• The chemicals released by a neuron and affect another neuron.
Synthesis & Storage of NTs
• Neurons synthesize
nearly all NTs from
amino acids.

• Small ones are

synthesized in the
axon terminals.
• Neuropeptides in
the cell body.

• The presynaptic terminal stores high

concentrations of NT molecules in vesicles.
• A neuron can accumulate excess levels of a NTs
• Neurons that release serotonin, dopamine, or
norepinephrine contain an enzyme, MAO
(monoamine oxidase), that breaks down these NTs
into inactive chemicals.
• The first antidepressant drugs that psychiatrists
discovered were MAO inhibitors.
Neuropeptides (or Neuromodulators)
• Many of them
exert their
effects by
altering gene
activity.

• Their effects
are long-
lasting, in the
range of 20
minutes or
more.

• They are
important for
hunger, thirst,
and other long-
term changes
in behavior and
experience.
Activating Receptors
of the Postsynaptic Cell
• Until this point we focused on
what happens in the
presynaptic neuron. Now we
look at the postsynaptic one.

• The NTs diffuses across the

synaptic cleft to the
postsynaptic membrane,
where it attaches to a
receptor.
• When NT attaches to the
receptor, the receptor may
either create an ionotropic or a
metabotropic effect.
Ionotropic effect
• Opens transmitter-gated or ligand-gated channels on the post-synaptic
cell membrane.
• Ligand: A chemical that binds to another chemical
• When the neurotransmitter binds to an ionotropic receptor, it twists the
receptor enough to open its central channel, which is shaped to let a particular
type of ion pass through.
• Brief on/ off effects.
• Begin quickly, decay quickly.
• Well suited to conveying visual & auditory info.

• Some ionotropic NTs:

• Glutamate: Main excitator NT.
• GABA (gamma-aminobutyric acid): Main inhibitor NT.
• Opens Cl- gates.
• Glycine: Inhibitory, found mostly in the spinal cord.
• Acetylcholine: Excitatory in most cases.
• Ionotropic synapse has effects localized to one point on the membrane.
 Ionotropic
Acetylcholine
Receptor
• (a) A cross-section of
the receptor at rest,
as viewed from the
synaptic cleft. The
membrane surrounds
it.

• (b) A similar view

after acetylcholine
has attached to the
side of the receptor,
opening the central
channel wide enough
for Na+ to pass
through.
Metabotropic effect
• A sequence of metabolic reactions that are relatively slower and
longer lasting.
• NTs: Dopamine, norepinephrine and serotonin . . . and sometimes
glutamate and GABA
• Emerge 30 ms or more after the release of the NT.
• They last up to a few seconds, but sometimes longer.
• Well suited for enduring effects such as taste, smell and pain.
• Important for many aspects of arousal, attention, emotion.

• NTs→Receptor→release of G protein→increased concentration

of a second messenger→Several effects.

• A metabotropic synapse can influence activity in all of the cell.

• Open or close ion channels in the membrane.
• Activate a portion of a chromosome.
Metabotropic effect
Variation in Receptors
• The brain has a great variety of receptors differing in their
structure
• At least 26 types of GABA receptors
• At least 7 families of serotonin receptors
• The serotonin receptor type 3 mediates nausea & drug ondansetron blocks it.
• Receptors differ in their:
• Chemical properties,
• Responses to drugs,
• Roles in behavior.
• A given receptor can have different effects
• for different people,
• even in different parts of one person’s brain,
• Certain proteins tether the presynaptic neuron to the
postsynaptic neuron and guide NTs to their receptors.
• Abnormalities of these scaffolding proteins have been linked to
increased anxiety, sleep disorders, and other behavioral problems.
Drugs Act by Binding to Receptors
• Hallucinogenic drugs:
• Drugs that distort perception.
• Eq: Lysergic acid diethylamide (LSD)
• They chemically resemble serotonin.
• They attach to serotonin type 2A (5-HT2A) receptors.
• Provide stimulation at inappropriate times or for longer-than usual durations.
• Nicotine:
• Stimulates a family of acetylcholine receptors (nicotinic receptors.)
• Increases dopamine release.
• Dopamin is associated with reward, so nicotine stimulation is rewarding also.
• Typical antipsychotic drugs block dopamine receptors, often producing side
effects of decreased pleasure and motivation.
• Opiate drugs: Derived from, the opium poppy.
• Eq: Morphine, heroin, and methadone.
• Brain produces certain neuropeptides now known as endorphins—a
contraction of endogenous morphines (Pain killers in the brain).
• Opiate drugs exert their effects by binding to the same receptors as
endorphins.
Inactivation & Reuptake of NTs
• Various NTs are inactivated in different ways.
• The neuropeptides, however, are not inactivated. They
simply diffuse away.
• Because these large molecules are resynthesized slowly,
a neuron can temporarily exhaust its supply.

• Acetylcholine:
• It is broken down by the enzyme acetylcholinesterase
• Into: acetate & choline.
• Choline diffuses back to the presynaptic neuron.
• Meets acetate there and formes Ach again.
Serotonin and Catecholamines
• Reuptake: The presynaptic most of the released NTs
intact and reuses them.
• Reuptake occurs through special membrane proteins called
transporters.
• Stimulant drugs, including amphetamine and cocaine, inhibit
the transporters for dopamine, thus decreasing reuptake and
prolonging dopamine’s effects.
• Amp: Blocks D&S&NE reuptake, Methamp: Stronger than amp.
• Methylphenidate (Ritalin) vs cocaine

• Breakdown: COMT (catechol-o-methyltransferase).

• NTs are broken down and washed away.
• Low dopamin following drug use.
Negative Feedback from
the Postsynaptic Cell
• Autoreceptors:
• Are found at presynaptic terminals.
• Respond to the released transmitter by inhibiting further
synthesis and release.

• Postsynaptic neurons release chemicals that travel

back to the presynaptic terminal to inhibit further
release of NTs.
• Eq: Nitric oxide, anandamide, 2-AG.
Your
Brain
on
Drugs
Your
Brain
on
Drugs
 Electrical Synapses
• A few special purpose synapses.
• Electrical transmission is fast.
• Faster than even the fastest chemical
transmission.
• Evolved in cases where exact synchrony
between two cells is important.
• Cells that control your rhythmic breathing .

• Gap junction: The place where the

membrane of one neuron comes into direct
contact with the membrane of another at an
electrical synapse.
• Large pores of the membrane of one neuron
line up precisely with similar pores in the
membrane of the other cell.
• Large enough for Na+ and K+ to pass
• Pores remain open constantly.
• Whenever one of the neurons is depolarized,
Na+ from that cell can pass quickly into the
other neuron and depolarize it, too.
Hormones
• Hormone: A chemical secreted by
cells in one part of the body and
conveyed by the blood to
influence other cells.
• Many chemicals serve both as
hormones and as NTs.
• NT: telephone vs Hormone: radio
station.
• Neuropeptides are intermediate.
They diffuse only within the brain.
• Useful for coordinating
longlasting changes in multiple
parts of the body.
• Migrating birds.

• Endocrine glands: Hormone-

producing glands.
• Hormones secreted by the brain
control the secretion of other
hormones
 Protein hormones & Peptide hormones
• Composed of chains of amino acids.
Hormones (Peptides are shorter.)
• Attach to receptors & activate a second
messenger.
The Pituitary Gland
Anterior pituitary
• Composed of glandular tissue
• Synthesizes GH, ACTH, TSH, FSH, LH,
prolactin.
• Hypothalamus secretes releasing
hormones, they flow through the blood
to the AP.
• There they stimulate or inhibit the
release of other hormones.

Posterior pituitary
• Composed of neural tissue,
• Considered an extension of the
hypothalamus.
• Hypothalamus synthesize oxytocin and
vasopressin (antidiuretic hormones),
they migrate down axons to PP.
• PP releases them into the blood.
The Role of Hypothalamus
• Produces vasopressin & oxytocin.
• Produces releasing & inhibiting
hormones and control the release of
hormones synthesized at anterior
pituitary.

• Maintains constant circulating levels of

certain hormones through a negative
feedback system.
• Eq: When the level of thyroid hormone is
low, it releases TSH-releasing hormone
• TSH-releasing hormone stimulates the
AP to release TSH,
• TSH causes the thyroid gland to secrete
more thyroid hormones.
• Thyroid hormones, in turn, act on the
hypothalamus to decrease its secretion
of the TSH-releasing hormone.
An Overall Look to Ch 2
• acetylcholine • G protein • opiate drugs
• acetylcholinesterase • hallucinogenic drugs • oxytocin
• amino acids • hormone • peptide hormones
• amphetamine • ionotropic effects • pituitary gland
• anterior pituitary • ligand-gated channels • posterior pituitary
• autoreceptors • MAO • protein hormones
• cannabinoids • metabotropic effects • releasing hormones
• catecholamines • methylphenidate • reuptake
• cocaine • neuromodulators • second messenger
• COMT • neuropeptides • transmitter-gated
channels
• endocrine glands • neurotransmitters
• transporters
• exocytosis • nicotine
• vasopressin
• gap junction • nitric oxide
• vesicles
Ch 1 & Ch2 Combined
Who can tell & draw:
• The structure of a neuron?
• Dendrites, cell body, axon, axon terminals?
• The mechanism of nerve impulse?
• Action potential?
• The synapse and how it works?
• Release of NTs from presynaptic cell?
• Effects on postsynaptic cell?
• How it causes (or hardens) a nerve impulse?