Neurotransmmitteers

When substances like Acetylcholine (Ach) and norepinephrine which are small- molecular neurotransmitters are released into the body they bind to receptors on tissue or neurons through our ANS and PNS system. Ach is released by many PNS neurons and some CNS neurons. In the PNS Ach is an excitatory neurotransmitter at some synapses, such as the neuromuscular junction where it binds to ionotropic receptors which open cation channels. Ach can also be an inhibitory neurotransmitter at other synapses, where it binds to metabotropic receptors while opening potassium channels. The enzyme acetylcholinesterase (AchE) inactivates Ach by splitting into acetate and choline fragments. Norepinephrine (NE) is a biogenic amine; most biogenic amines may cause

There are three ways in which a drug can affect a neurotransmission, such its synthesis, storage, and release. An agonist drug that affects synthesis would monoamine oxidase inhibitors because they inhibit the breakdown of serotonin at the serotonin neural

Serotonin, (or 5-hydroxytryptamine) is a neurotransmitter released by neurones in the brain. It is a chemical responsible for good mood and well-being. Therefore one of the possible causes of depression is a chemical imbalance of Serotonin levels in the brain and consequently, ineffective neuronal transmission at the synaptic cleft. (Lovatt, 2010) This has negative implications on mood, sleep and appetite.

The belief is that antidepressants work by increasing levels of a group of chemicals in the brain called neurotransmitters. Certain neurotransmitters, such as serotonin and noradrenaline, can improve mood and emotion, although we do not yet fully understand this process

Gamma-Aminobutyric acid commonly referred to as GABA, and glutamate make up around 80 percent of the neurotransmitters found in brain. GABA dampens the activity in the brain while

Every day, your brain maintains a delicate balance between chemicals that push its cells to fire and opposing chemicals that pull its cells back toward inactivity. Two of the most common neurochemicals that play this tug of war are glutamate and GABA, both of which are classified as neurotransmitters, chemical messengers that communicate between neighboring brain cells. The purpose of glutamate is to elicit action, while the function of the GABA neurotransmitter is to restore calm.

Most people usually think of the brain or heart being the most important part of our body. While they are indeed important, they would be entirely useless if certain substances called neurotransmitters didn’t exist. Neurotransmitters are substances in our body that carry signals from one nerve cell to another. Without these neurotransmitters in our body, we wouldn’t receive crucial signals such as telling our heart to beat. Six of the most common neurotransmitters in our body are dopamine, serotonin, endorphins, norepinephrine, acetylcholine, and gamma-aminobutyric acid (GABA).

The third neurotransmitter family is composed of peptides, compounds that contain at least two and sometimes as many as 100 amino acids. Peptide neurotransmitters are poorly understood: Evidence that they are, in fact, transmitters tends to be incomplete, and restricted to their location within nerve terminals, and the physiologic effects produced when they are applied to neurons. Probably the best understood peptide

Secondly, GABA is an inhibitory neurotransmitter that is very widely distributed in the neurons of the cortex that results in inhibition of the spontaneous firing and acoustically evoked responses of inferior colliculus neurons. It also regulates anxiety. However, some drugs that increase the level of GABA in the brain are used to treat people suffering from Huntington’s disease.

GABA is an inhibitory neurotransmitter critical in regulating anxiety and reducing stress. It does this by preventing overstimulation in the brain, and subduing excitatory neurotransmitters, which can cause anxiety when the brain is overstimulated. Hence, GABA deficiency results in overstimulation in the brain, and consequently, anxiety. Furthermore, those who experience anxiety due to GABA deficiency, often develop anxiety disorder/s (Neurotransmitters, Depression and Anxiety, 2008). Additionally, as GABA induces relaxation, analgesia, and sleep, “dysfunction of the GABA system is implicated in the pathophysiology of several neuropsychiatric disorders, including anxiety” (Neurotransmitters, Depression and Anxiety, 2008). GABA is synthesised by the amino acid glutamate decarboxylase (glutamine); thus, glutamine deficiency will result in GABA deficiency (Graham, n.d.). Whilst glutamine deficiency can be caused by diets lacking protein (Henderson, n.d.), it also results from Epilepsy (Glutamate decarboxylase deficiency, n.d.), which scientists believe have genetics aspects (Fisher and Saul, n.d.). Statistics suggest that in every 100 children born to parents with Epilepsy, between 2 and 5 will inherit Epilepsy (Epilepsy and inheritance, 2012). In cases where the cause of Epilepsy is unidentified, professionals believe that it can be attributed to an inherited low seizure threshold that makes individuals more susceptible to seizures (Epilepsy and inheritance, 2012). Additionally, children with an extensive history of, or mothers with Epilepsy in their genealogy, are more susceptible to the disorder, as shown in Figure

The purpose of the pathway is to both produce and conserve GABA.4 GABA is the major inhibitory neurotransmitter in the central nervous system (CNS) and it has been estimated that at least one-third of all CNS neurons utilize GABA as their primary neurotransmitter.5 The precursor for GABA is usually glucose, however amino acids and pyruvate can also be used. The metabolic synthesis of GABA begins with the amino transfer of (alpha)-ketoglutarate, synthesized by glucose in the Krebs cycle by GABA (alpha)-oxoglutarate transaminase (GABA-T) into L-glutamic acid. Glutamic acid decarboxylase (GAD) catalyzes the decarboxylation of glutamic acid to form GABA.4 GABA release into the synaptic cleft is stimulated by depolarization of presynaptic neurons, which then diffuses across into the post-synaptic neurons and binds to their associated receptors. Reuptake of GABA is the responsibility of both presynaptic nerve terminals and surrounding glial cells.4 GABA taken back up by the nerve terminals is available for reuse however, GABA taken up by glial cells is metabolized to succinic semialdeyde by GABA-T and cannot be re-synthesized because glial cells lack GAD. For GABA to be recovered from glial cells it must be converted to glutamine, which is then transferred back to the neurons where glutamine is converted into glutamate by glutaminase. This allows for re-entry into the GABA shunt

Other drugs, such as amphetamine or cocaine, can cause the nerve cells to release abnormally large amounts of natural neurotransmitters or prevent the normal recycling of these brain chemicals. This disruption produces

The neurotransmitters norepinephrine, serotonin is also thought to play a role in depression (Porth 1371).  There are decreased levels of these neurotransmitters present in the pre and post synaptic cleft.  Dopamine levels have been studied and increased levels of dopamine are found in mania and decreased levels in depression (Porth 1372).

Many psychiatric and psychoactive drugs that are available on the market, pharmaceutically or illegally, closely resemble neurotransmitters and are actually able to mimic it to the extent that it fools the receptors. Basically, these drugs hijack the neurotransmitters. Once these drugs are ingested, it enters into the brain, gets into the synapse and binds itself to the receptor. This then causes the inappropriate release of neurotransmitters and alter the breakdown and recycling of neurotransmitters or can be used to destroy particular neurotransmitters completely (Sapolsky, 2005, p. 14).

Neurotransmitters involved in depression include norepinephrine, dopamine, and serotonin. An imbalance of hormones may also play a role in depression. Many depressed people have higher than normal levels of hydrocortisone, a hormone secreted by the adrenal gland in response to stress. In addition, an underactive or overactive thyroid gland can lead to depression.4