Neurons transfer molecules {neurotransmitter}|.
purposes
Neurotransmitters can transfer signals, mediate rapid electrical communication, foster neuron survival and pathway formation, elicit synaptic changes, and trigger biochemical changes that modify subsequent signals.
types
Transmitter types are amino acidergic, catecholamine, cholinergic, monoaminergic, peptides, and purines. Cholinergic includes acetylcholine. Neurotransmitters include aspartic acid, dopamine, epinephrine, gamma-aminobutyric acid (GABA), glutamic acid, glycine, histamine, norepinephrine, octopamine, and serotonin.
change
Neurotransmitter used by neuron can change over time. Transmitter changes can last days to weeks, while environmental stimuli last seconds to minutes. Neuron can release transmitter at low stimulation, peptide at high stimulation, and both at intermediate stimulation.
vesicles
Cholinergic, monoaminergic, and amino-acidergic neurons synthesize neurotransmitters mostly in nerve terminals. Synaptic vesicles in unmyelinated axon and cell-body regions release neurotransmitters. Released packets have 1000 molecules. Storage vesicles or granules have only one neurotransmitter type. They release independently.
Peptidergic cells synthesize large proteins in cell body and then split them into active peptides.
Individual neurons all have multiple transmitters.
vesicles: dendrites
Mitral cells, substantia nigra dopaminergic neurons, and olfactory bulb GABAergic axonless granule cells have synaptic vesicles in dendrites.
Acetylcholine {acetylcholine, memory} (ACh) can be a fast neurotransmitter or slow modulator.
modulator
ACh regulates neurite nerve process outgrowth and aids neuronal population survival.
location
ACh is in autonomic parasympathetic ganglia, basal forebrain, caudate nucleus, medulla motor nuclei, neuromuscular synapse, Meynart basal nucleus, putamen, pons, superior olive, spinal cord, cranial-nerve motor nuclei, cerebral-cortex bipolar cells, and submandibular-salivary-gland postsynaptic parasympathetic neurons.
excitation
Acute bipolar-cell or parasympathetic-neuron stimulation releases only acetylcholine. Chronic excitation releases both VIP and acetylcholine, in ratio depending on stimulus duration.
VIP
Acetylcholine inhibits VIP release by interacting with neuron receptors. VIP inhibits acetylcholine release by binding to neuron VIP receptors.
drug
Acetylcholine can treat senile dementia or aid memory.
enzyme
Acetylcholinesterase enzyme hydrolyzes acetylcholine. Added cholinesterase decreases memory.
Enzymes {acetylcholinesterase} can hydrolyze acetylcholine. Added cholinesterase decreases memory.
Amino-acid neurotransmitters {amino acidergic neurotransmitters} include glutamate and aspartate.
Amino acids {aspartate} {aspartic acid} can be excitatory transmitters.
Norepinephrine (NE), dopamine (DA), and epinephrine (E) are 3,4-dihydroxy phenylethylamine derivatives {catecholamine}| (CA) {biogenic amine}.
locations
Catecholamines come from tyrosine in peripheral sympathetic neurons, adrenal medulla, chromaffin tissue, and brainstem nuclei.
Adrenal medulla makes and stores catecholamines in response to stress.
metabolism
Catecholamines phosphorylate postsynaptic receptor proteins, like adenylate cyclase, in vascular smooth muscle, heart, liver, adipocytes, and many brain neurons.
Uptake into presynaptic nerve terminal inactivates catecholamines. Desipramine and cocaine inhibit uptake.
Stimulation by serotonin facilitates presynaptic catecholamine release, which increases intraneuronal cAMP, which inactivates potassium-ion channel, which allows more calcium ion in.
Phenylethylamine derivatives release catecholamines. Bretylium and guanethidine have a highly basic center, linked by one-carbon or two-carbon chain to ring, and block catecholamine release.
vesicles
Catecholamines are in membrane-bound vesicles. Reserpine interferes with catecholamine storage in vesicles. Catecholamine release from vesicles uses exocytosis. Release requires calcium ion.
functions
Catecholamines can cause tachycardia, peripheral vasoconstriction, mydriasis, and peristalsis inhibition.
Choline transmitters {cholinergic neurotransmitters} include acetylcholine [Hille, 2001] [Hobson, 1999] [Steriade and McCarley, 1990] [Perry and Young, 2002] [Perry et al., 1999] [Perry et al., 2002] [Woolf, 2002].
Biogenic amines {dopamine}| (DA) are in hypothalamic arcuate nucleus, midbrain nigrostriatal, and ventral midbrain. Dopamine affects reward processing. It initiates and maintains anticipation behavior, novelty, attention, and action selection. Dopamine interacts with amine and choline modulators.
Dopaminergic neurons use adrenaline or epinephrine, noradrenaline or norepinephrine, dopamine, or serotonin. Dopaminergic neurons can make highly branched networks with small-diameter ascending and descending fibers, low frequency potentials, and slow conduction velocities.
Molecules {effector molecule} can work rapidly and break down or reabsorb rapidly.
Fast-acting inhibitory neurotransmitters {gamma-aminobutyric acid} (GABA) can come from glutamate and can be in basal ganglia, cerebellum, cerebral cortex, hippocampus, hypothalamus, retina, striatonigral, thalamus, and ventral pallidum. 20% of inhibitory neurons, mostly interneurons, use GABA. Valium enhances GABA activity.
Fast-acting excitatory amino-acid neurotransmitters {glutamate} {glutamic acid} can be in spinal cord, brainstem, cerebellum, hippocampus, and cerebral cortex. 60% of excitatory neurons, mostly projection neurons, use glutamate. Glutamate affects dopamine.
Amino-acid inhibitory transmitters {glycine} can be in retina and spinal cord.
Amines {histamine, transmitter} can be in pituitary and medial hypothalamus.
Monoamine transmitters {monoaminergic neurotransmitter}| include norepinephrine, epinephrine, dopamine, and serotonin.
Molecules {nitric oxide}| released by postsynaptic terminals can bind to presynaptic terminals. Enzymes {nitric oxide synthase} (NOS) make nitric oxide from arginine. L-nitro-arginine methyl ester (L-NAME) inhibits nitric-oxide synthesis.
Neurotransmitters {peptide neurotransmitter} can have several amino acids.
Spermidine and spermine competitively inhibit amine receptors {polyamine receptor}.
Purine neurotransmitters {purine neurotransmitter}| include AMP and GMP.
Vasoactive monoamines {serotonin}| {5-hydroxytryptamine} (5-HT) can inhibit or excite metabolic activity, depending on receptor. Serotonin comes from tryptophan.
location
Serotonin is in area postrema, medulla oblongata, pineal gland, gut parasympathetic system, and pons raphé nucleus. Brain has 300,000 serotonergic neurons.
functions
Serotonergic-neuron activity is proportional to arousal, wakefulness, and muscular activity. Serotonin excites cortex pyramidal neurons. It inhibits neurons that receive excitations. It regulates neurite nerve process outgrowth and aids neuronal population survival. It causes or inhibits intestinal contraction. It constricts or relaxes blood vessels. Serotonin enhances substance P release from axons to excite spinal cord. Substance P releases serotonin from terminals inhibited by serotonin.
receptors
Neurons make serotonin and release it into synaptic clefts. Mammals have more than 13 different serotonin receptors. Animals have over 30 different serotonin receptors, which connect to G proteins.
uptake
Serotonin reuptake transport molecules remove serotonin from synaptic clefts. Selective serotonin reuptake inhibitors inhibit serotonin uptake back into cells.
damage
If serotonin level decreases, activity increases. Inhibiting serotonin receptor does not modulate behavior.
derivatives
5-HIAA comes from serotonin and causes higher male social status, more female grooming, and quieter activity.
evolution
Serotonergic neurons and serotonin receptors evolved 500,000,000 years ago. Gene duplication allowed different kinds. Anthropoid apes evolved 40,000,000 years ago and have different promoter sequence for serotonin-reuptake-transport gene than humans do.
Molecules {transporter molecule} can put and get transmitters in synaptic cleft. If synapse has no vesicles, it puts transmitters in cleft.
The evidence is against the hypothesis that synapses release neurotransmitter directly {vesigate} from cytoplasm through membrane pores {operator pore} opened by calcium ions.
4-Zoology-Organ-Nerve-Neural Chemical
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Date Modified: 2022.0225