NeuroTransmitters are chemicals (Small Molecules or Hormones), stored in small Synaptic Vessicles clustered at the tip of the Axon (terminal buttons).
They are released into the Synapse when a Nerve Impulse arrives for transmission to the next Neuron.
NeuroTransmitters cross the Synapse enabling impulse transmission to an adjacent Neuron, or the Stimulation of an Effector Cell (Muscle or Gland). Once in the Synapse, they are active for only a short time - between 0.5 and 1 millisecond.
Enzymes in the Synapse inactivate NeuroTransmitters, which are either taken back into the Axon (ReUptake) and transported back to the Neuron for re-useage or destroyed.
When a NeuroTransmitter is received by a Receptor (PostSynaptic), it either Excites (Depolarizes) or Inhibits (Hyperpolarizes) the PostSynaptic Neuron.
When a Neuron is Depolarized, the membrane becomes more Permeable to Na+ (Sodium) and is closer to firing (Action Potential). When a Neuron is Hyperpolarized the membrane becomes Impermeable to Na+ and will not fire.
The NeuroTransmitters cross the Synapse, binding to receptor molecules on the next Neuron, prompting transmission of the messages along that Neuron's membrane.
NeuroTransmitters are either destroyed by specific Enzymes in the Synapse, diffuse out, or are reabsorbed by the Neuron. More than 100 organic molecules are thought to act as NeuroTransmitters.
Some are Excitory, such as Acetylcholine, NorEpinephrine (precurser to Adrenaline), Serotonin, and Dopamine; others are associated with Relaxation, such as Dopamine and Serotonin.
CatecholAmines are a group of Biogenic Amines that are NeuroTransmitters, and include Dopamine, NorEpinephrine and Epinephrine (Adrenaline). Imbalance of CatecholAmines can result in Autonomic Dysfunction.
Dopamine - ß - Hydroxalase Deficiency is characterized by Sympathetic NorAdrenergic denervation and AdrenoMedullary failure, but intact Vagal and Sympathetic Cholinergic function.
It is a rare, congenital, nonhereditary form of severe Orthostatic Hypotension, caused by complete absence of Dopamine-ß - Hydroxylase, the enzyme involved in the conversion of Dopamine to NorEpinephrine.
MonoAmine Oxidase (MAO) is an enzyme that degrades (breaks down) Dopamine. There are two types of MAO [(alpha) and ß(beta)]. In Parkinson's Disease, it is beneficial to block the activity of MAO ß.
The Basal Ganglia (the Caudate Nucleus, the Striatum & the Putamen) control Movement, Balance, and Walking.
The Substantia Nigra is a small area containing a cluster of black-pigmented Neurons, which produce Dopamine that is then transmitted to the Striatum; the Neurons of the Striatum require Dopamine to function. View: Image
Dopamine release seems related to sensations of Pleasure. Endorphins are natural Opioids that Produce Elation and Reduction of Pain, as do artificial chemicals such as Opium and Heroin.
Some Neurological Diseases are due to imbalances of NeuroTransmitters, Parkinson's Disease is from a Dopamine deficiency and Huntington's Disease from the malfunctioning of an Inhibitory NeuroTransmitter.
NorEpinephrine is a NeuroTransmitter found mainly in areas of the Brain that are involved in governing Autonomic Nervous System activity, especially Blood Pressure and Heart Rate.
Aromatic L - Amino Acid Decarboxylase Deficiency: an enzyme of the Lyase Class that Catalyzes the Decarboxylation of Aromatic Amino Acids, notably converting Dopa to Dopamine, Tryptophan to Tryptamine, and HydroxyTryptophan to Serotonin.
The enzyme is then bound to a Pyridoxal Phosphate Cofactor and occurs particularly in the Liver, Kidney, Brain, and Vas Deferens.
Clinical Presentation: symptoms may include Temperature Instability, Ptosis of the Eyelids, HyperSalivation, Distal Chorea, Swallowing Difficulties, Drowsiness, Irritability, Truncal Hypotonia, Oculogyric Crises, Pinpoint Pupils.