communication between neurons and sites of drug actions

Question 1

describe the structures and functions of presynaptic cells that are involved in synaptic communication:

Answer 1

• Dendritic spines= small protrusions that stud the dendrites of several types of large neurons in the brain.
• Presynaptic membrane= at the end of the terminal buttons ad face the postsynaptic membrane and through which the neurotransmitter is released.
• Postsynaptic membrane= cell membrane opposite the terminal button in a synapse, the membrane of the cell that receives the message.
• Synaptic vesicles= small, hollow, bubble-like/ beadlike structure found in terminal buttons, contains molecules of a neurotransmitter.

Question 2

describe neurotransmitter relseases:

Answer 2

A number of small synaptic vessels located just inside the presynaptic membrane and then break open, causing the contents to move into the synaptic cleft. Once the vesicle releases neurotransmitter into the synapse, the molecules of the neurotransmitter move from an area of high concentration (inside) to low concentration (outside), due to diffusion.

Question 3

contrast ionotropic and metatropic receptors?

Answer 3

• Ionotropic receptors= direct method of how neurotransmitters open ion channels. A simple method that is equipped with its own binding site. When a molecule of the appropriate neurotransmitter attaches to it, the ion channel opens.
• Metabotropic receptors= indirect method of how neurotransmitters open ion channels. More of a complicated methos: ligand binding to some receptors doesn’t open ion channels directly- starts a chain of chemical events. They involve steps that require the cell expend metabolic energy. Located closely to G Protein. Activated when the two molecules of the neurotransmitter bind and will then activate an enzyme that stimulates the production of a chemical called a second messenger.

Question 4

compare the functions of EPSP and IPSPs in postsynaptic cells:

Answer 4

• EPSP= (excitatory postsynaptic potential) sodium potassium transporters keep sodium outside the cell, waiting for the forces of diffusion and electrostatic pressure to push it in. when sodium-channels get opened, the result is depolarised.
• IPSP= (Inhibitory postsynaptic potential) open the chloride channels instead of potassium channels. This is due to potassium being positively charged as its efflux will hyperpolarise the membrane.

Question 5

explain how postsynaptic potentials are terminated:

Answer 5

• Through reuptake and enzyme deactivation.
• Reuptake= the way in which neurotransmitters are terminated by postsynaptic potentials. Rapid removal from the synapse. After the neurotransmitter us released into the synapse, the presynaptic membrane used transported molecules to return the molecules of the neurotransmitter from the synapse to the cytoplasm of the presynaptic cell. Uses energy.
• Enzymatic deactivation= accomplished by an enzyme that destroys molecules of the neurotransmitter. AChE (acetylcholinesterase) deactivates ACh (acetylcholine) by breaking it into chlorine and acetate. The postsynaptic potential is terminated once the molecules of ACh are broken apart- neither substance is able to activate postsynaptic receptors.

Question 6

summarise the process of neural integration of EPSPs and IPSPs:

Answer 6

• The rate a neuron fires is controlled by the relative excitatory and inhibitory input to its dendrites and soma. If the activity of excitatory synapses goes up, the rate of firing will increase. If the activity of inhibitory synapse goes up, the rate of firing will decrease.
• The release of a neurotransmitter produces depolarising in the dendrites of the neuron. They are transmitted down the dendrites across the soma, to the axon hillock located at the base of the axon. If the depolarisation is still strong enough when it reaches this point, the axon will fire.

Question 7

differentiate between the locations and functions of auto-receptors and postsynaptic receptors:

Answer 7

• Auto-receptors (location)= located on the membrane at any part of the cell.
• (functions)= when stimulated by a molecule of the neurotransmitter, they regulate internal processes, including the synthesis and release of the neurotransmitter- most cases is inhibitory.
• Postsynaptic receptors (location)= terminal button in an axoaxonic synapse
• (functions)= increases the amount of neurotransmitter released by the postsynaptic terminal buttons.

Question 8

identify the fucntion of axoaxonic synapses:

Answer 8

• Don’t contribute directly to neural integration
• Alter the amount of neurotransmitter released by the terminal buttons
• Produce presynaptic modulation: inhibition or facilitation.

Question 9

summarise how drug molecules can increase or decrease neurotransmitter synthesis:

Answer 9

In some cases, the rate of synthesis and the release of a neurotransmitter is increased if a precursor is administrated- agonist. If a drug inactivates one of the enzymes that control the synthesis of neurotransmitters, it will prevent it from being produced- antagonist.

Question 10

describe examples of nonsynaptic communicaton:

Answer 10

• Neuromodulators= a naturally secreted substance that acts like a neurotransmitter except its not restricted to the synapse but diffuses through the extracellular fluid.
• Peptide= a chain of amino acids joined together by peptide bonds. Most neuromodulators, and some hormones, consist of peptide molecules.
• Hormone= a chemical substance that is released by endocrine gland that has effects on target cells in other organs.
• Endocrine gland= a gland that releases chemical messengers into the extracellular fluid around capillaries and into the bloodstream.
• Target cell= the type of cell that is directly affected by a hormone or other chemical signal.

Question 11

distinguish between the effects of agonists and antagonists on storage and release of neurotransmitters:

Answer 11

Agonist= bind with the proteins and directly trigger the release of the neurotransmitter.
Antagonist= prevent the release of neurotransmitters from the terminal button buy deactivating the proteins that cause the synaptic vessel to fuse with the presynaptic membrane and expel their contents into the synapse.

Question 12

contrast the effects of agonist and antagonists at the receptor:

Answer 12

• Direct agonist= drug attaches to the binding site where the neurotransmitter normally attaches allowing the receptors to function normally and the ions can pass through the channels to produce postsynaptic potentials.
• Direct antagonist= drugs that bind with the receptors but don’t open the ion channel/ trigger other intracellular events- prevent neurotransmitter from binding to the receptor to open ion channels or produce other intracellular events.
• Indirect agonist= if a drug attaches to one of the alternative sites and facilitates the opening of the ion channel.
• Indirect antagonist= if a drug attaches to one of the alternative sites and prevents the ion channels from opening.

Question 13

describe the effects of agonists on neurotransmitter reputake and deactivation:

Answer 13

1. Molecules of the drug attach to the transporter molecules that are responsible for reuptake and block it.
2. Molecules of the drug bind with the enzyme that normally deactivates the neurotransmitter and prevents enzymes from working
   * They prolong the neurotransmitter un the synaptic cleft.