Rod and Cone Cells

Rod and Cone Cells

E.2 Structure of the Eye

E.4 Neurotransmitters and synapses

 a) Explain how pre-synaptic neurons can affect post-synaptic transmission of impulses (7)

Typically a presynaptic neurone excites a post synaptic neurone – the impulse is transmitted across the synapse. This is called an excitatory synapse. When the action potential reaches the are of the terminal buttons of the pre-synaptic neuron, it causes calcium ions to diffuse into the terminal buttons. Vesicles containing neurotransmitters fuse with the plasma membrane and release them into the synaptic cleft. The neurotransmitters bind with a receptor protein on the postsynaptic neurone membrane, this binding results in an ion channel opening and sodium ions diffusing through this channel. This initiates the action potential to begin moving down the post-synaptic neurone because it has been depolarized (made more positive).

However, some synapses are inhibitory synapses; the release of neurotransmitters into the cleft inhibits an action potential being generated in the post-synaptic neurone. At an inhibitory synapse the release of neurotransmitters into the synaptic cleft triggers the opening of ion channels, which allows Cl- ions to enter the neurone and K+ to leave. This makes the interior of the post-synpatic neurone more negative (hyperpolarised) and therefore less likely to initiate an action potential.

b) Explain the process of synaptic transmission (7)

At the far end of axons are swollen membranous areas called terminal buttons. Within these terminal buttons are many vesicles filled with neurotransmitters.

When an action potential reaches the area of the terminal buttons, it causes calcium ions to diffuse into the terminal buttons. Vesicles containing neurotransmitters fuse with the plasma membrane and releases the neurotransmitters into the synaptic cleft. Neurotransmitters diffuse across the synaptic cleft from the presynaptic neurone to the postsynaptic neurone.

Neurotransmitters bind with a receptor protein on the postsynaptic neurone membrane. This binding results in an ion channel opening and sodium ions diffusing in through this channel. This initiates the action potential to begin moving down the postsynaptic neurone because it’s been depolarized.

The neurotransmitter is degraded and broken into two or more fragments by specific enzymes. They’re then released from the receptor protein. The ion channel closes to sodium ions. The neurotransmitter fragments diffuse back across the synaptic gap to be reassembled into the terminal buttons of the presynaptic neurone.

 

Excitatory drugs

Nicotine
• Nicotine in tobacco products is a stimulant which mimics acetylcholine (Ach). Thus, it 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 the enzyme cannot break down the nicotine molecules which bind to the same receptos. This excites the postsynaptic neurone and it begins to fire, releasing a molecule called dopamine. Dopamine gives the feeling of pleasure, a molecule of the ‘reward pathway’ of our breains.

Cocaine

• Dopamine transporters are responsible for removing dopamine molecules from the synaptic cleft after they have done their job
• Cocaine blocks these transporters, leaving dopamine trapped in the synaptic cleft. As a result, dopamine binds again and again to the receptors overstimulating the cell
• Cocaine concentrates in the reward pathway. It's also active in the part of the brain controlling voluntary movements. This is why cocaine abusers are unable to stay still.

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 noraderenaline
• It moves directly into the cesicles of the presynaptic neurone and causes their release into the synaptic cleft. Normally, these neurotransmitters would be broken down by enzymes in the synapse, but amphetamines interefere with the breakdown.
• Thus in the synapse high concentrations of dopamine cause euphoria, and high concentrations of noradrenaline may be responsible for alterness and high energy effect of amphetamines.

Inhibitory Drugs

Benzodiazepine
• Reduces anxiety can also be used against epileptic seizueres.
• Its effect is to modulate the activity of GABA which is the main inhibitory neurotransmitter. When GABA binds to the postsynaptic membrame, it causes Chloride ions to enter the neurone.
• This hyperpolarizes the neurone, and resists firing.
• Benzodiazepine increases the binding of GABA to the receptor and causes the post synaptic neurone to become more hyperpolarized.

Alcohol

• Inhibitory neurotransmitters, called GABA, are active throughout the brain. These neurotransmitters act to control neural activity along many brain pathways. When GABA binds to its receptors, the cell is less likely to fire.
• However, in another area of the brain, another neurotransmitter called glutamate acts as the brain’s general-purpose excitatory neurotransmitter.
• When alcohol enters the brain it delivers a double sedative punch. First, it interacts with GABA receptors to make them even more inhibitory.
• Second, it binds to glutamate receptors, preventing the glutamate from exciting the cell.
• Alcohol particularly affects areas of the brain involved in memory formation, decision-making and impulse control.

Tetrahydrocannabinol (THC)
• Main psychoactive chemical in marijuana.
• Before marijuana enters the system, inhibitory neurotransmitters are active in the synapse. These neurotransmitters inhibit dopamine from being released
• When activated by the body’s own native cannabinoid (called anandamide), cannabinoid receptors turn off the release of inhibitory transmitters. Without inhibition, dopamine can be released.
• THC, the active chemical in marijuana, mimics anandamide and binds to cannabinoid receptors. Inhibition is turned off and dopamine is allowed to squirt into the synapse.
• Anandamide is known to be involved in removing unnecessary short term memories. It is also involved for slowing down movement, making us feel relaxed and calm.
• Unlike THC, anandamide breaks down very quickly in the body. That explains why anandamide doesn’t produce a perpetual natural ‘high’.

THC (Tetrahydrocannabinol) / Marijuana

Marijuana is usually smoked as a cigarette or in a pipe. When someone smokes marijuana, THC rapidly passes from the lungs into the bloodstream, which carries the chemical to the brain and other organs in the body.

THC acts on specific sites in the brain called cannabinoid receptor. They start off a series of cellular reactions that lead to the “high” that users experience when they use the drug. Some brain areas have many cannabinoid receptors while others have few or none. The highest density of cannabinoid receptors are found in parts of the brain that influence pleasure, memory, thinking, concentrating, sensory and time perception and coordinated movement. Marijuana intoxication can caused distorted perceptions impaired coordination, difficulty with thinking and problem solving and problems with learning and memory.

Cocaine

Cocaine is a powerfully addictive central nervous system stimulant. This drug usually makes the user feel euphoric and energetic, but also increases body temperature, blood pressure and heart rate. Users risk heart attacks, respiratory failure, strokes, seizures, abdominal pain and nausea.

Cocaine also causes dopamine release. Cocaine blocks removal of dopamine from the synapse so that it builds up. This leads to over stimulation of the postsynaptic neurone. The synaptic effect of cocaine results from its ability to sustain the level of dopamine in the synapse. Since dopamine is the neurotransmitter in the ‘reward pathway’, the longer it stays in the synapse the better you feel.