Synaptic Activity Is Vital For The Passage Of Information Throughout The Nervous System

To send a message, a neuron will send a ripple of electrical energy down its axon. This ripple is called "action potential." The way it works is by changing the chemical makeup of the axon's negatively charged interior. Positively charged sodium ions move into the cell and negatively charged potassium ions move out, then the ions move to their original positions. This produces a wave of positively charged

The cerebral cortex directs functions like speech, behavior, reactions, movement, thinking, and learning. In fact, some research suggests that bipolar disorder originates with problems with the thalamus, which links sensory input to good and bad feelings. The hippocampus also affects depression. It, like the amygdala, is part of the limbic system. It is vital in processing long-term memory. This section of the brain registers recurring fear. In people with clinical depression, the hippocampus is much smaller. Research suggests, even, that ongoing exposure to stress impairs the growth of nerve cells in this part of the brain. One of the most important jobs of the brain is to process senses, through neurons. Neurotransmitters are specific substances that help relay information to the brain. Scientists have identified many neurotransmitters that affect depression. A lack or excess of the neurotransmitters acetylcholine, serotonin, norepinephrine, dopamine, glutamate, lithium carbonate and gamma-aminobutyric acid are thought to contribute to depression. Acetylcholine is involved in learning and enhances memory. Serotonin helps regulate sleep, appetite, and mood, and inhibits pain. Research shows the idea that many depressed people have reduced levels of serotonin. Low levels of a byproduct of serotonin have been linked to a high risk for suicide. Norepinephrine is a neurotransmitter which constricts blood vessels and raises blood pressure. An excess in

The period of time between when a stimulus occurs and when the body elicits a response is called the latent period or reaction time. These times can vary for different stimuli and from person to person. The BIOPAC student manual states that the most important factor that contributes to reaction times is the mechanism behind synaptic transmission. This involves a presynaptic neuron communicating with a postsynaptic neuron via neurotransmitter release. When neurotransmitters are released, they can cause the postsynaptic neuron to have an increase or decrease in excitability, which then factors into the response of the brain. The changes in the release of neurotransmitters can be acute or chronic, and synaptic transmission itself can be inhibited or facilitated by certain factors.

Once a presynaptic neuron is passive, an electrical current is spread along the length of the axon (Schiff, 2012). This is known as action potential (Pinel, 2011). Action potential happens once an abundant amount of depolarisation reaches the limit through the entry of sodium, by means of voltage gated sodium channels

Neurons communicate with each other through an electrochemical process in three steps (Stufflebeam, 2008). An electrical impulse will travel down the axon to axon terminals. This causes the vesicles to open and neurotransmitter molecules are released into the synaptic gap. Neurotransmitter molecules then cross the synaptic gap and enters the receptor sites located on the dendrites of the receiving neuron. The information is carried along axons and dendrites because of changes in electrical properties which we call action potential. An action potential is initiated when a messenger attaches itself to a receptor. This occurrence causes an electrical signal to be triggered and is generated through the neuron. Once the signal reaches the end of an axon, which is at the end of a neuron, a neurotransmitter molecule will return to the synaptic gap where they are received by the sending neuron and the process is repeated or are destroyed by enzymes (Griggs, 2014, p. 41-45).

As well as these there are also the axon of the cell which is covered in myelin sheaths which carried information away from the cell body and hands the action potentials, these are small short bursts of change in the electrical charge of the axon membrane through openings of ion channels, off to the following neurons dendrites through terminal buttons at the end of the axons. Whenever an action potential is passed through these terminal buttons it releases a chemicals that pass on the action potential on to the next neuron through the terminal button and dendrite connection. The chemicals that are

The action potential is connected to the end of the axon, which is a tube that extends from the soma and branches out. The action potential starts where it ends at the end of the axon and travels down to the terminal button, which contains synaptic vesicles. The synaptic vesicles store neurotransmitters once they are synthesized. Once that is done, the neurotransmitters releases from the presynaptic neuron, this is the neuron that transmits the message, and sends a message to the postsynaptic neuron. After the action potential gets to the terminal button, voltage dependent calcium goes to the presynaptic membrane and opens while calcium comes into the cell. The calcium hen connects to the synaptic vesicles and causes the vesicles to break and

Action potentials act as ‘messengers’ to brain in the form of electrical signals. They are generated by depolarization which is a voltage change in the membrane of a neuron cell. An action potential is produced in each nerve cell and travels along the axon of the nerve cell. The action potential causes a release of a neurotransmitters to

Serotonin syndrome is a drug-induced syndrome that results in mental, autonomic and neuromuscular changes. A range of toxic symptoms including clonus, hyperreflexia, tremor, agitation, confusion and shivering are results of the increased serotonin concentrations in the central nervous system (Hall and Buckley, 2003). Serotonin (5-hydroxytryptamine, 5-HT) is a neurotransmitter produced from the decarboxylation and hydroxylation of tryptophan. Serotonin is stored within the vesicles and released into the synaptic cleft when stimulated (Volpi-Abadie et al., 2013). As serotonin influences on mood, sleep, vomiting and pain perception, the serotonin levels are tightly regulated by the reuptake mechanisms, degradation by monoamine oxidase type A and feedback loop (Thanacoody,

Depression is a product of diminished levels of serotonin in the brain, in which there are selective serotonin reuptake inhibitors (SSRIs) available for patients to can take. The purpose of anti-depressants is to assist with the transportation of serotonin to the brain. The function of SSRIs at the synaptic cleft is to increase serotonin levels. Anti-depressants or SSRIs work to increase serotonin levels at the synapse by blocking serotonin reuptake. Selective serotonin reuptake inhibitors have become the drug of choice for patients with depression. SSRIs produce less side effects then other anti-depressants due to their controlled action to reuptake serotonin. Prozac (a very commonly used SSRI), for example, has developed so widely that it is not only used to treat depression. Even though SSRIs are successful way of handling depression, they do still harvest harmful side

The linkage of serotonin to depression has been known for the past five years. From numerous studies, the most concrete evidence of this connection is the decreased concentration of serotonin metabolites like 5-HIAA (5-hydroxyindole acetic acid) in the cerebrospinal fluid and brain tissues of depressed people. If depression, as suggested, is a result of decreased levels of serotonin in the brain, pharmaceutical agents that can reverse this effect should be helpful in treating depressed patients. Therefore, the primary targets of various antidepressant medications are serotonin transports of the brain. Since serotonin is activated when released by neurons into the synapse, antidepressants function at the synapse to enhance serotonin activity. Normally, serotonin's actions in the synapse are terminated by its being taken back into the neuron then releases it at which point "it is either recycled for reuse as a transmitter or broken down into its metabolic by products and transported out of the brain." As a result, antidepressants work to increase serotonin levels at the synapse by blocking serotonin reuptake (2).

It plays a significant role in many neurological functions, including brain plasticity (4), learning and memory (5), and induction of pain (6). Poor or excess release of glutamate can cause serious neurodevelopmental and neurodegenerative disorders such as autism (7-9), epilepsy (7, 10-13), schizophrenia (14), Alzheimer’s disease (14-17) and Parkinson’s disease (18, 19). Physiologically, glutamate is released from pre-synaptic vesicles into neuronal synapses in response to action potential. The concentration of glutamate within the vesicles is reported to be ~100 mmol/L (20). The action potential firing mechanism primarily involves the movement of cations (Ca2+, Na+ and K+) across the neuronal membrane. Two voltage-gated ion-channels located in the axon permit active transport of K+ and Na+, into and out of the cells (20). This ion exchange creates a potential difference of -70 mV (resting potential) through the neuronal membrane. Sudden depolarisation or action potential occurs when potential drops, allowing Na+ to flood into the cells. Action potential is terminated to restore the resting potential of the membrane. Ca2+ channels open to allow the transport of Ca2+ (2). This ultimately causes glutamate to be released from its vesicle into the area between presynaptic membrane and postsynaptic membrane of the subsequent neuron. Through this electrochemical signal

Nerve cells generate electrical signals to transmit information. Neurons are not necessarily intrinsically great electrical conductors, however, they have evolved specialized mechanisms for propagating signals based on the flow of ions across their membranes.

three groups.Monoamine oxidase inhibitor (MAOI) medicines block the monoamine oxidase enzyme (MAO) from destroying monoamine neurotransmitters, which allows them to accumulate, alleviating depression. Serotonin selective reuptake inhibitor (SSRI) medications block the serotonin reuptake pump, allowing the serotonin neurotransmitter to remain and accumulate in the receptor for longer. Speaking of serotonin specifically, depression has been related to a deficiency of the 5-hydroxytryptamine (serotonin) neurotransmitter as evidenced by the concentrations of the

Synaptic transmissions, otherwise referred to as neurotransmissions, are important to look at when investigating how physiological changes have an effect psychologically as changes have an affect on behaviour. Neurons are nerve cells that send electrochemical messages to the brain in the response from a stimuli and neurotransmitters transfer information from the neurons by diffusing across synapses. Synaptic transmission is the process by which neurons transfer the information; the neurotransmitters are released by neurons and bind to the receptors of postsynaptic neurons.