90% of the cells in the brain and spinal cord are not neurons but are referred to as glia (glue). Glia are defined simply as not being neurons. They include astrocytes (star shaped cells) which supply nutrients to the neurons and help regulate their function. Other non-nerve cells are Schwann cells which wrap around the axons of neurons (a process called myelination) and increase the conduction speed of their impulses. This allows the neurons to communicate with each other in a smaller time-frame. There are also micro-glia which function as a kind of brain immune system. They fight off bacteria and viruses within the brain and also remove dead cells.
Neurons - neurons can be as wide as 1 inch, or thinner than a human hair.
The dendrites of neurons receive information from neighbouring nerve cells and pass it along to the cell body (soma).
At the axon hillock it is decided whether or not the information is passed along the axon to the axon terminal.
Neurons can be considered to either be switched 'on' or 'off'. When the neuron is off it is maintaining a resting potential. Neurons communicate through electrical signals brought about by the movement of chemicals called ions. Ions are charged atoms and can be either positively or negatively charged. Positive ions outside of the neuron keep it off or 'quiet'. Ions are kept out of the cells by pumps which pump the positive ions out of the cell. This causes the net charge within the cell to be negative.
Whenever a neighbouring neuron sends chemical messengers across the synapse and onto the dendritic receptors of the cell we are considering, a channel opens up. This channel allows the positive ions to move into the cell which causes a change in charge. This change in charge determines whether or not the nerve cell will fire. The nerve cell must receive enough neurotransmitters at its dendritic receptors in order to create an adequate amount of positive ions to accumulate at the axon hillock. The axon hillock also contains channels and when enough positive ions build up at his area these channels will open up and allow even more positive ions to enter the nerve cell. This influx of more positive ions causes even more channels at the axon hillock to open up and therefore results in more positive ions entering. This causes an influx of positive ions into the rest of the axon including the axon terminal. Once this happens, the terminal releases chemical messengers / neurotransmitters into the synaptic cleft and these are received by the next cell, restarting this whole process within the new cell. There is a threshold value of positive ions that are necessary in order for the axon hillock to propagate the impulse along the axon and into the terminal. If this threshold is not reached, the nerve cell remains off and does not fire. This is known as the action potential of the cell.
-The neuron that transmits a signal is referred to as the pre-synaptic neuron
-The neuron that receives a signal is referred to as the pre-synaptic neuron
-The gap between both neurons is called the synapse
When a neuron receives a signal there are 2 main types of effect that can be produced.
1) Temporal Effect:
b) The signal causes an influx of negative ions which discourage the post-synaptic neuron to transmit information (inhibitory response)
2) Genomic effect: when a neurotransmitter attaches to a receptor on the post-synaptic neuron, it may influence the activation of a transcription factor. This may bring up cellular changes, e.g. causing the cell to produce more receptor channels upon it's dentrites. Neurons which have more receptors are more responsive to equal amounts of neurotransmitters compared to those with fewer receptors. This results in strengthening of the synaptic connections between this post-synaptic neuron and any neurons which release a neurotransmitter that binds to the receptor channels that have increased production. Conversely, if a genomic effect brings about a reduction of receptor channels for a specific neurotransmitter then the post-synaptic and pre-synaptic cell connection will decrease in strength.
It is possible for neurons to respond to many different neurotransmitters whether inhibitory or excitatory. A single neurotransmitter is also able to affect multiple neuron types which may be located in different areas of the brain and have different functions.
Examples of neurotransmitters:
-Epinephrine (adrenaline) - does not create any emotions, it amplifies the intensity of any emotion which is subsequently generated, based on an experiment where people were injected with adrenaline without realising. When they were exposed either to a person showing frustration or joy they experienced the emotion they were exposed to with a high intensity.
While neurons in the brain respond to many different neurotransmitters, those associated with neuromuscular junctions typically use only one type.
Neuropharmacology - this can be regarded as the external manipulation of synaptic events. When treating psychological ailments the general idea is to either increase or decrease the strength of synaptic connections within the brain. Ways of increasing synaptic connectivity includes increasing the amount of neurotransmitter substances which are released by the pre-synaptic neuron and also causing these chemical messengers to linger in the synapse. These can be accomplished by reuptake and degradation prevention.
Reuptake - when a neurotransmitter has already bonded with the receptor site of the dendrite on the post-synaptic neuron, it is usually taken back into the pre-synaptic neuron. If this did not occur then the neurotransmitter would continuously signal to the post-synaptic neuron to keep opening its ion channels and hence repeatedly excite it. Protein pumps on the nerve cells will pump the used up neurotransmitters back into the pre-synaptic neuron.
Degradation - enzymes present within the synaptic cleft will catabolise the neurotransmitters to form breakdown products, these breakdown products are then either taken back into the nerve cell or else removed by various fluids. Breakdown products can be detected in the cerebrospinal fluid, blood and also in urine. This has some use in the diagnosis of diseases but is typically inconclusive.
Neurotransmitters can be forced to remain in the synapse if reuptake and degradation are inhibited.
Neurotransmitter-receptor activity can be increased by improving the efficiency with which the neurotransmitter binds to the receptor sites of the post-synaptic neuron. This amplifies the neurotransmitter signal and strengthens the synaptic response. In order to weaken the synaptic response all that is needed is to block any of the processes required for the transmission of chemical messengers e.g. blocking neurotransmitter receptors, neurotransmitter release and decreasing receptor activity.
Neuropathology - It is difficult to measure amounts of neurotransmitter substances within the brain, especially in a living patient. Such measurements are usually made through break-down products as mentioned earlier. In Parkinson's disease there is a decrease in dopamine in areas of the brain related to motor movements. If, however, you were to attempt to treat this localised dopamine shortage by giving the patient more dopamine which travelled to the whole brain, then other problems would arise. Some patients have developed psychotic symptoms as a result of this treatment.