NEUROTRANSMITTERS AND SYNAPSESOption E.4
Assessment Statements
E.4.1 State that some presynaptic neurons excite postsynaptic transmission and others inhibit postsynaptic transmission.
E.4.2 Explain how decision-making in the CNS can result from the interaction between the activities of excitatory and inhibitory presynaptic neurons at synapses.
E.4.3 Explain how psychoactive drugs affect the brain and personality by either increasing or decreasing postsynaptic transmission.
E.4.4 List three examples of excitatory and three examples of inhibitory psychoactive drugs.
E.4.5 Explain the effects of THC and cocaine in terms of their action at synapses in the brain.
E.4.6 Discuss the causes of addiction, including genetic predisposition, social factors and dopamine secretion.
Synaptic transmission
Neurons communicate with each other chemically across a space called a synapse
One side of the synapse is the presynaptic membrane of the sending neuron and on the other side of the synapse is the postsynaptic membrane of the receiving neuron
Molecule which moves across the space (synaptic cleft) between the two membranes is called a neurotransmitter
Specific neurotransmitter is received by a specific receptor
Excitation and Inhibition
Some neurotransmitters are excitatory and stimulate the next neuron to forward the message
Do this by increasing the permeability of the postsynaptic membrane to positive ions, making it easier for positive ions to move in
Some neurotransmitters are inhibitory and cause the positive ions to move out of the postsynaptic cell
Positive ions move back in to the synaptic cleft chemically depressing the postsynaptic cell and makes it much harder to excite
Decision making in the CNS Impulse which moves down
the presynaptic neuron is called the action potential
As action potential reaches axon bulb, calcium ions rush into the end of the neuron
Vesicles containing neurotransmitters fuse with the presynaptic membrane
Neurotransmitter released into the synaptic cleft
Neurotransmitter binds to specific receptors on the postsynaptic membrane
Receptors let ions enter or leave when the neurotransmitter binds to them
Excitatory neurotransmitters
One example: acetylcholine Generates action potential Increases permeability of the postsynaptic membrane to
positive ions Causes positive sodium ions to diffuse into the
postsynaptic neuron Localized depolarization occurs Inside of neuron develops a net positive charge compared
to the outside Depolarization continues as sodium ions diffuse to the
next area of the neuron Impulse is carried along the nerve If threshold is not met, the neuron does not carry the
impulse to the next neuron
Inhibitory neurotransmitters
Example: GABA Inhibit action potentials Causes hyperpolarization of the neuron Inside of the neuron becomes more negative
making it difficult for an action potential to be generated
GABA binds to specific receptor Causes negatively charged chloride ions to move
across the postsynaptic membrane into the postsynaptic cell OR it can cause positively charged K+ ions to move out of the postsynaptic neuron
Movement of Cl- into the neuron or K+ out causes hyperpolarization
Putting it together
A neuron is always on the receiving end of many excitatory and inhibitory stimuli
Neuron sums up the signals If the sum of the signals is inhibitory
then the axon does not fire If the sum of the signals is excitatory,
the axon fires Summation of the messages is the
way that decisions are made by the CNS
Cholinergic synapses
Acetylcholine is released by all motor neurons and activates skeletal muscle
If it remained in the synapse, the postsynaptic membrane would go on firing indefinitely
Acetylcholinesterase breaks it down Acetylcholine is involved in the
parasympathetic nervous system Causes relaxation rather than flight
Nicotine stimulates transmission in cholinergic synapses which is why it has a calming effect on the body and personality
People addicted to nicotine become very agitated if they cannot have a cigarette
Adrenergic synapses
Noradrenaline depolarizes the postsynaptic neuron
Noradrenaline is involved in the sympathetic sysem
It causes a “fight or flight” reaction Cocaine and amphetamines both
cause increased alertness, energy and euphoria
Cholinergic Adrenergic
Neurotransmitter Acetylcholine (Ach) Noradrenaline
System Parasympathetic Sympathetic
Effect on mood Calming Increased energy, alertness, and euphoria
Drugs increasing transmission at synapse
Nicotine Cocaine and amphetamines
Effect of drugs on the brain
Can alter your mood or your emotional state
Excitatory drugs (nicotine, coaaine, amphetamine) increase nerve transmission
Inhibitory drugs (benzodiazepines, alcohol, and THC) decrease the likelihood of nerve transmission
Drugs can change synaptic transmission in the following ways:
Block a receptor for a neurotransmitter (structure similar to the transmitter)
Block release of neurotransmitter from the presynaptic membrane
Enhance neurotransmission by mimicking a neurotransmitter
Block removal of neurotransmitter from the synapse and prolong the effect of the neurotransmitter
Excitatory drugs and how they actNicotine mimics acetylcholine (Ach)
Acts on the cholinergic synapses of the body and the brain to cause a calming effect
After Ach is received by the receptors, it is broken down by acetylcholinesterase but it cannot break down nicotine
This excites the postsynaptic neuron and it begins to fire, releasing a molecule called dopamine
Dopamine gives you a feeling of pleasure
Cocaine stimulates transmission at adrenergic synapses and causes alertness and euphoria
Causes dopamine release
Cocaine blocks removal of dopamine from the synapse so that it builds up
Leads to overstimulation of the postsynaptic neuron
Leads to euphoria
Both of these drugs causes addiction
Amphetamine stimulates transmission at adrenergic synapses and gives increased energy and alertness
Amphetamine acts by passing directly into the nerve cells which carry dopamine and noradrenaline
It moves directly into the vesicles of the presynaptic neuron and causes their release into the synaptic cleft
Normally these would be broken down, but amphetamines interfere with breakdown
High concentrations of dopamine cause euphoria and high concentrations of noradrenaline may be responsible for the alertness and high energy effect
Inhibitory drugs and how they act
Benzodiaizepine reduces anxiety Can be used against epileptic
seizures Modulates the activity of GABA which
is the main inhibitory neurotransmitter
When GABA binds to the postsynaptic membrane, it causes Cl-to enter the neuron
Causes hyperpolarization and resists firing
B increases the binding of GABA to the receptor and therefore greater hyperpolarization
Alcohol acts similarly to B in that it increases the binding of GABA to the postsynaptic membrane
Decreases activity of glutamate, an excitatory neurotransmitter
Alcohol helps to increase the release of dopamine by a process which is not well understood
Appears to stop the activity of the enzyme which breaks down dopamine in the synaptic cleft
Tetrahydrocannabinol (THC) is the main pschoactive chemical in marijuana
THC mimics the neurotransmitter, anandamide
THC binds to the same receptor and cause the postsynaptic neuron to be hyperpolarized
Anandamide may play a role in memory functions, such as eliminating information from our memory that is not needed
Marijuana disrupts short-term memory in humans
THC effects
Feelings of relaxation, lightheadedness, haziness
Decrease in learning, coordination, problem-solving, and short-term memory
Stays in synapse longer than anandamide
High concentrations of receptors found in hippocampus (short-term memory); cerebellum (coordination)
Cocaine effects
Euphoria, talkativeness, increase in mental alertness
Temporary decrease in the need for food and sleep
Large amts. Cause erratic and violent behavior
Sustains level of dopamine in the synapse
Causes of addiction
Body develops a tolerance and needs more of the drug to produce the same result
Chemical dependency is caused by drug “rewiring the brain” and becoming an essential biochemical in the body
Role of abused drugs is to stimulate the reward pathway located in the brain
Withdrawal symptoms Anxiety, depression,
craving Seizures, severe
shaking
Continued addiction Lung damage Risk of contracting
HIV, hepatitis B and C
Kidney disease
Genetic predisposition Studies in male twins find that when
one twin suffers an addiction to alcohol or drugs, the rate of addiction in the second twin is 50% greater among identical twins than among fraternal twins
Other experiments indicate that a genetically determined deficiency of dopamine receptors predisposes certain people to addiction
Persons who become addicted to drugs that increase dopamine levels do so to compensate for that deficiency
Social factors of addiction
Family addiction, family parenting skills, mental health problems of family or child
Often related to peer group; users teach new users what effects to expect and what altered state is desirable
Alcohol at social gatherings fosters the paradigm that it must be available to have a party
Alcohol very rare in Saudi Arabia since it is prohibited
Dopamine secretion
Neurotransmitter which activates the reward pathway and gives us a sense of pleasure or satisfaction
During cocaine use, dopamine builds up in the synapse
Over-stimulation decreases the number of receptors and the remaining receptors become less sensitive to dopamine (desensitization or tolerance)
With tolerance, exposure to the drug causes less response that it previously caused
More and more of the drug is needed to have even the normal sense of well-being
Type of neuroadaptive change
Knockout mice
Genetically manipulated mice addicted to cocaine
Studies show that glutamate may oversee the learning and memories which lead to cocaine-seeking
Mouse party