Nerve chemicals {neural chemical} {nerve chemical} are hormones, ions, modulators, receptors, regulators, transmitters, and structures.
transverse motion
Only biological cells use transverse ion motion to make depolarization wave. If axon has nodes of Ranvier, depolarization jumps from node to node and transverse ion motion is same strength in all directions around axon circumference. If axon has no nodes of Ranvier, transverse ion motion is all around axon circumference but is most at least-resistance point. Ions repel each other, so differences are small. Depolarization waves travel down lines on axon surfaces, following least-resistant path, and can spiral down axon.
Calcium ions move from mitochondria and endoplasmic reticulum through channels {calcium ion channel} onto receptors. Calcium ions phosphorylate synapsin proteins and cause vesicle fusion with membrane, to trigger neurotransmitter release. Calcium ions clear from receptors by active transport back into mitochondria and endoplasmic reticulum.
Dendrite voltage-gated Ca++ channels can provide non-linear coupling between inputs.
Transmitter-gated calcium-ion channels are like other channels {P/Q-type calcium channel}.
Serotonin and cyclic AMP regulate calcium-ion entry into cells, including neurons.
Cells have chloride-ion channels {chloride ion channel}.
Cells have seven potassium-ion channel types {potassium ion channel}.
cAMP mediated receptors {S channel} close potassium-ion-channel type. cAMP mediated receptors reduce a potassium-ion-channel size, to allow longer action potentials and allow more calcium ion to flow into presynaptic area and increase transmitter release.
Cells have sodium-ion channels {sodium ion channel}.
Brain neurons secrete chemicals {neurohormone} that affect other neurons more slowly than neurotransmitters. Neurohormones can cause signal pattern from neuron group [McEwen, 1976].
Circulating vasoconstrictor molecules {angiotensin} can bind to presynaptic noradrenergic nerve terminals. Kidney renin enzyme changes angiotensinogen to angiotensin.
Bone proteins {bone morphogenetic proteins} regulate whether neural precursors become neurons or glia.
Brain releases peptides {bradykinin} in response to injury to stimulate neurons.
Hormones {brain-derived neurotrophic factor} (BDNF) can increase NMDA-receptor phosphate binding and can develop immature sympathetic and sense neurons and glia.
Most endocrine-hormone or neurotransmitter gastrointestinal-system peptides {gut-brain peptide} {brain-gut peptide} {brain-gut axis} are also brain hormones or neurotransmitters. Most gastrointestinal system peptide receptors are also in brain. Brain and gut peptides include bombesin, cholecystokinin (CCK), gastrin, motilin, neurotensin, pancreatic polypeptide, secretin, substance P, and vasoactive intestinal peptide (VIP).
Medullary-motor-nuclei transmitters {calcitonin-gene-related peptide} (CGRP) can regulate phenotypic expression.
brain peptide {carnosine}.
Glycoproteins {neurotrophin} {cell adhesion molecule} (CAM) {axon guidance molecule} can guide growing nerve processes to appropriate target neurons. Hormones develop immature neurons and glia. For example, neurotrophin-3 increases oligodendrocyte number. 1,1-CAM protein helps begin myelination.
Peptides {cholecystokinin} (CCK) can cause satiation by binding to solitary tract nucleus (NTS) receptors, enhances dopamine actions, and is in gut, cerebral cortex, medulla oblongata, solitary tract nucleus, and ventral midbrain.
Hormones {ciliary neurotrophic factor} (CNTF) can decrease immature neuron and glia death and supports eye ciliary-ganglion parasympathetic neuron survival. Perhaps, CNTF is survival or trophic factor, mitogen, or transmitter-regulating factor for other neurons.
Brain hormones {circulating hormone}, such as angiotensin, calcitonin, glucagon, and insulin, can release into blood.
Three genetically different endorphin peptide families are proopiomelanocortin (POMC), proenkephalins, and prodynorphin {dynorphin}. Dynorphin peptides act like opioids. Gut, posterior pituitary, hypothalamus, basal ganglia, and brainstem make prodynorphin. Leucine-enkephalin leads to dynorphin. Dynorphin in nucleus accumbens neurons inhibits VTA neurons and so reduces dopamine.
Hormones {galanin} can be in basal forebrain and hypothalamus.
Brain and gut peptide hormones {gastrin}| can control stomach secretion.
Hormones {glial growth factor-2} (GGF-2) can increase glia number.
Hormones {glial-derived neurotrophic factor} (GDNF) {glial cell line-derived neurotrophic factor} can make new axon branches in motor neurons.
Hormones {gonadotropin-releasing hormone} can release gonadotropin in hypothalamus.
Hormones {growth-hormone-releasing hormone} can release growth hormone in hypothalamus.
Hypophysis makes oxytocin, neurophysins, and vasopressin {hypophyseal hormone} {neurohypophyseal hormone}.
Hormones {hypothalamic releasing hormones} can release hormones, such as growth-hormone-releasing, gonadotropin-releasing, and luteinizing-hormone-releasing hormones, from hypothalamus.
Hormones {insulin-like growth factor} (IGF-1) can help develop immature neurons and glia.
Peptides {kyotorphin} can act as opioids.
Hormones {lipotropin} can be from pituitary.
Norepinephrine, epinephrine, dopamine, and serotonin {monoamine}| are slow-acting neuromodulators, come from brainstem, and affect arousal and sleep.
Peptides {motilin} can be in gut and cerebellum.
Hormones {nerve growth factor} (NGF) can go into sympathetic-neuron and sense-neuron axon terminals and transport to cell body, where it increases transmitter levels. Olfactory bulb, cerebellum, and striatum make nerve growth factor and nerve growth factor receptor.
enzyme
In hippocampal neurons, NGF increases choline acetyltransferase (CAT), which synthesizes acetylcholine and can reverse poor spatial memory.
disease
NTRK1 gene makes neurotrophin tyrosine kinase receptor type 1. NTRK1 gene mutation causes rare autosomal recessive disease (CIPA) with pain insensitivity, no sweating, self-mutilation, fever, and mental retardation.
Molecules {netrin} attract and repel axons to guide axon directions.
Peptides {neuropeptide} can have high concentrations in nervous-system regions and low concentrations in other cells and organs. Neuropeptides include brain-gut peptides, circulating hormones, hypothalamic releasing hormones, neurohypophyseal hormones, opioid peptides, pituitary hormones, bradykinin, carnosine, epidermal growth factor (EGF), neuropeptide Y, proctolin, and substance K. Brain hormones, such as opioids, act slowly [McEwen, 1976].
Peptides {neuropeptide Y} (NPY) can be in cerebral cortex and medulla oblongata. Arcuate-nucleus appetite region sends neuropeptide Y to second appetite region.
Hypophysis makes nerve hormones {neurophysin}.
Steroids {neurosteroid} can induce sleep, be analgesic at high concentration, and come from cholesterol or progesterone.
Peptides {neurotensin} can be in gut, hypothalamic arcuate nucleus, medulla oblongata, retina, solitary tract nucleus, and ventral midbrain.
Hormones {notch growth factor} can regulate whether neural precursors become neurons or glia.
Macrophages make protein {oncomodulin} that regenerates nerve.
Peptides {pancreatic polypeptide} can be in brain and gut.
Peptides {peptide hormone}, such as endorphins and enkephalins, can produce slower effects than neurotransmitters and come from 20% of inhibitory cells. Enzymatic hydrolysis inactivates such peptides, so they do not reabsorb into synaptic terminals or glial cells [McEwen, 1976].
Pituitary hormones {pituitary hormone} are alpha melanocyte-stimulating hormone (alpha MSH), corticotropin (ACTH), growth hormone (GH), lipotropin, luteinizing hormone, prolactin, somatotropin, and thyrotropin.
Hormones {presenilin} can decrease neural stem-cell division.
Peptides {proctolin} can be in brain.
Peptides {secretin} can be in brain and gut.
Molecules {semaphorin} can attract and repel axons to guide axon directions.
Thalamus, cortex, and hippocampus hormones {somatostatin} (SS) can mimic hypothalamus sympathetic-neuron substance-P regulation. Somatostatin treats diabetes.
Hormones {somatotropin} can be in pituitary.
Hormones {sonic hedgehog growth factor} {sonic hedgehog gene} can regulate immature-neuron cell division. Sonic hedgehog gene activates pathway that affects central-nervous-system development.
Peptides {substance K} can be in brain.
Proteins {survival motor neuron proteins} can preserve motor neurons.
Chemicals {neuroregulator} {neuromodulator} can amplify or negate neurotransmitters by altering transmitter-receptor interactions, changing ion flux, or activating neuroreceptor enzymes.
Molecules {ampakine} increase glutamine binding to AMPA receptor and increase glutamate release from AMPA receptor, affecting memory and cognition.
Molecules {diacylglycerol} (DAG) can phosphorylate ion channels.
Molecules {inositol triphosphate} (IP3) can phosphorylate ion channels.
Proteins {alpha-integrin} can bind to cell membranes, maintain long-term potentiation (LTP), and aid memory.
Enzymes {protein kinase Mz} can be necessary and sufficient for long-term potentiation.
Chemicals {retrograde messenger} can diffuse back from postsynaptic to presynaptic membrane. For example, upon protein-kinase activation, nitric oxide synthase makes nitric oxide from l-arginine. Nitric oxide diffuses back from postsynaptic to presynaptic membrane and causes increase in vesicle release, if membrane is still active.
Proteins {beta-adrenergic catecholamine receptor} {beta-receptor} {adrenergic catecholamine} can bind catecholamines. Binding couples to G protein and adenylate cyclase metabolism. Beta-receptor protein strongly binds ISO, binds epinephrine, and weakly binds norepinephrine. Binding can cause vasodilation, uterine contraction inhibition, cardiac stimulation, and bronchodilation. If guanosine triphosphate (GTP) is present, beta-receptors have only low-affinity catecholamine binding.
Proteins {agrin} can cluster other proteins between neurons and muscle cells and at immune synapses.
Sympathetic noradrenergic nerve terminal proteins {alpha-receptor}, such as alpha-2 receptor, bind to norepinephrine strongest, epinephrine middle, and isoproterenol (ISO) lowest. Binding can cause vasoconstriction, uterine contraction, and mydriasis. Alpha-receptor agonist and alpha-receptor antagonist affect alpha-receptors.
Proteins {AMPA receptor} {aspartate receptor} can bind aspartate, glutamate, and glutamine. Binding is fast, opens sodium ion channels, and causes excitation.
Proteins {angiotensin II receptor} can bind angiotensin in presynaptic noradrenergic nerve terminals.
Neuron receptors {autoreceptor} can be on presynaptic membranes, for negative feedback.
Nociceptors {cannabinoid receptor} (CB1) can have cannabis receptors. Anandamide, 2-arachidonoyl glycerol (2-AG), and marijuana delta-9-tetrahydrocannabinol (THC) bind in hypothalamus, basal ganglia, amygdala, brainstem, hippocampus, cerebellum, and neocortex. Hypothalamus affects appetite, sex, and hormones. Basal ganglia affect motor acts and planning. Amygdala affects emotion, anxiety, and fear. Brainstem affects pain and reflexes. Hippocampus affects memory and learning. Cerebellum affects motor acts. Neocortex affects sense qualities and cognition.
2-AG flows from receptor cell back to transmitting cell to decrease GABA {depolarization-induced suppression of inhibition} (DSI) [Earleywine, 2002] [Grinspoon and Bakalar, 1993].
immune
CB2 receptor is only in immune system.
Proteins {CD45 protein} can be for synapse and immune-synapse adhesion.
Proteins {D1 receptor} {D1 dopamine receptor} {dopamine D1 receptor} can bind dopamine. Binding is slow, uses cAMP, opens potassium ion channels, closes calcium ion channels, and inhibits.
Proteins {D2 receptor} {D2 dopamine receptor} {dopamine D2 receptor} can bind dopamine. Binding is slow, uses cAMP, opens potassium ion channels, closes calcium ion channels, and inhibits.
Dopamine receptors {DRD4 dopamine receptor} can be in brain. Perhaps, DRD4-gene allele {attention-deficit hyperactivity disorder, dopamine} arose 40,000 years ago and allowed bolder and more-curious personalities.
Receptor complexes {GABA receptor} {gamma-aminobutyric acid receptor} can bind GABA.
types
Type A {GABA-A receptor} is fast, opens chloride-ion channels, and inhibits. Type B {GABA-B receptor} is slow, opens potassium-ion channels, closes calcium-ion channels, uses IP3 and DAG, inhibits, and uses second-messenger system, probably cyclic AMP.
parts
Endogenous benzodiazepine-receptor protein is part of GABA-receptor complex and increases extent or period of GABA-operated chloride-ion channel opening.
drugs
Benzodiazepines and anxiety-reducing neuromodulators {anxiolytic drug, GABA} increase GABA affinity for GABA neuroreceptors and enhance GABA-mediated synaptic potentials. Perhaps, anesthetics bind to GABA-A. Perhaps, neurosteroids from progesterone and cholesterol bind to GABA-A.
Proteins {glycine receptor} can bind glycine. Binding is fast, opens chloride-ion channels, and inhibits. Dorsal-horn neurons have glycine receptors for inhibition. ACEA competitively blocks glycine receptor. Strychnine affects glycine receptor. Prostaglandins block glycine receptors and so excite dorsal horn neurons.
Outer-membrane receptors {G-protein-coupled receptor} (GPCR) can have seven alpha helices in cell membrane and has active protein part inside cell membrane next to G protein. For example, olfactory sense neurons have membrane receptors that activate G protein. For slow 0.1-second to 10-second effects, receptor activates G protein, which binds GTP to make second messengers such as cyclic AMP, diacylglycerol (DAG), or inositol triphosphate (IP3), which phosphorylate ion channels.
Ion channels {ionotropic receptor} {transmitter-gated ion channel} can bind neurotransmitters, such as glutamine, and then open quickly. Response to ion flows is 10 to 30 times faster than metabolotropic response.
Proteins {kainate receptor} can bind glutamate. Binding is fast, opens sodium ion channels, and excites.
Proteins {M receptor} can bind acetylcholine. Binding is slow, opens calcium ion channels, excites or inhibits, and uses IP3, cAMP, or DAG.
Neurotransmitters, such as glutamate, can bind to receptors {metabotropic receptor}, which affect G protein, which activates adenyl cyclase, which changes ATP to cAMP, which binds to cAMP-dependent protein-kinase regulatory subunit, which affects catalytic subunit, which phosphorylates protein, which opens or closes ion channels, which increases calcium ion. Such receptors amplify signals 100-fold and cause cell-effect patterns.
factors
Calcium ion and other second messengers affect cAMP activity. Metabolism uses IP3 and DAG.
speed
Response to neurotransmitter-neuroreceptor activation is 10 to 30 times slower than ionotropic response.
Proteins {mGluR5 receptor} can bind glutamate and affect cocaine dependence.
Acetylcholine receptors {muscarinic ACh} can use second messenger.
Proteins {N receptor} can bind acetylcholine. Binding is fast, opens sodium ion channels, and excites.
Cell membranes between two neurons or immune cells can form tubes {nanotube, cell} that can transfer calcium, proteins, or viruses.
Protein receptors {neuropilin} can be at synapses and immune synapses.
Nicotine is similar to acetylcholine. Immune cells and neural cells have acetylcholine receptors. Nicotine inhibits cytokine release by macrophages. Proteins {nicotinic receptor} {alpha-7 nicotinic receptor} {alpha-7 acetylcholine receptor} can bind nicotine and stimulate NMDA receptors [Granon et al., 2003].
If postsynaptic membrane depolarizes and glutamate releases from presynaptic neurons, postsynaptic neuron proteins {NMDA receptor, neuron} {N-methyl-D-aspartate receptor} can bind glutamate [Miller et al., 1989] [Tang et al., 1999] [Watkins and Collingridge, 1989] [Wittenberg and Tsien, 2002]. Binding is fast.
effects
Binding opens sodium ion channels, opens potassium ion channels, opens calcium ion channels, and excites or inhibits. Binding increases cell response non-linearly. Binding rapidly controls connectivity between cells, allowing transient cell assemblies.
In neocortex pyramidal cells, binding causes slow, long lasting ESP that rises to peak in 10 milliseconds to 75 milliseconds and can stay altered for days or years.
process
NMDA receptors have magnesium ion inside. Glutamate binding removes magnesium ion and allows calcium-ion flow. Calcium ion aids protein-kinase phosphorylation. Protein kinases then phosphorylate AMPA receptors for early LTP. Protein kinase A (PKA), MAP kinase (MAPK), and calcium/calmodulin protein kinase (CaMK) phosphorylate CREB. In cell nucleus, CREB activation turns on genes that make late LTP proteins. Active synapses have chemical sites {molecular tag} that bind late LTP proteins.
factors
Brain-derived neurotrophic factor (BDNF) increases NMDA-receptor phosphate binding.
antagonists
Ap5, CGS 19755, CPP, and D-CPP-ene affect NMDA receptor. NMDA antagonists can block visually induced activity in visual-cortex superficial layers, but not deep layers.
Proteins {presynaptic neuroreceptor} can enhance or reduce neurotransmitter release, by responding to previously released neurotransmitter {autoregulation} or to other neurotransmitters or neuromodulators {heteroregulation}. Presynaptic neuroreceptors regulate noradrenaline release from heart, spleen, vas deferens, and brain. Central and peripheral adrenergic-nerve-axon synapses can have both negative and positive feedback.
Proteins {talin} can be for synapse and immune-synapse adhesion.
Proteins {calmodulin protein kinase} {calcium protein kinase} (CaMK) {calcium-calmodulin protein} can phosphorylate, enter cell nucleus, and activate CREB gene.
Proteins {calmodulin-binding protein} can bind to calmodulin and perhaps bind to actin.
At high concentrations, cAMP-dependent protein-kinase catalytic subunits {cAMP-dependent protein kinase} phosphorylate transcription factors, such as cAMP-response element binding protein-1 (CREB-1), C/EBP transcription factor, and tissue plasminogen activator (tPA), which express genes in cell nucleus to initiate change or growth. Repeated action potentials, from stress or high activity, make cAMP-dependent protein kinase concentration high.
Calcium ion entry can activate proteins {cAMP-response element} {cyclic-AMP response element} (CRE) (CRE-1) {cAMP-response element binding protein-1} (CREB-1) {CREB protein} that bind to regulatory regions and activate cyclic-AMP and cyclic-AMP-receptor genes. CREB also activates immediate early genes, such as ubiquitin hydrolase and C/EBP transcription factor, to initiate synaptic growth. CREB regulates endorphin production.
Enzymes {caspase 9} can cause neuron death and so prune networks.
Proteins {C/EBP transcription factor} {C-EBP transcription factor} can activate synaptic protein genes.
Molecules {CREB enhancer} can increase CREB protein by inhibiting phosphodiesterase.
Molecules {CREB suppressor} can decrease CREB protein.
Enzymes {mitogen-activated protein kinase} {MAP kinase} (MAPK) can phosphorylate CREB-2 repressor to prevent CREB-1 binding to CRE-1. MAPK8 regulates cell movement.
Amines {octopamine} can be neuromodulators for behavior.
Enzyme series {phospholipid cascade}| can regulate intracellular phospholipid by regulating gene transcription. Calcium ion, phosphorylation, and phospholipid pathways regulate each other.
Enzyme series {phosphotidylinositol cascade} can regulate intracellular phospholipid by regulating gene transcription.
Enzymes {protein kinase A} (PKA) can phosphorylate and activate mitogen-activated protein kinases.
Proteins {spectrin} {fodrin} can bind to actin and calmodulin.
Proteins {synapsin} can phosphorylate by causing calcium-ion influx.
Proteins {tissue plasminogen activator} (tPA) can activate genes for neuron terminals and spines.
Amines {tyramine} can be neuromodulators for behavior.
Enzymes {tyrosine hydroxylase} (TH) can be rate-limiting enzyme in catecholamine biosynthesis. Increased neuronal firing increases catecholamine-pathway enzyme synthesis in perikarya. Axons transport enzymes to axon terminals. Catecholamine pathway requires pteridine, iron, and oxygen and converts tyrosine to L-DOPA. Dopamine and norepinephrine inhibit tyrosine hydroxylase by feedback inhibition. Stressful stimuli increase TH. Acetylcholine phosphorylates TH using cyclic AMP.
Enzymes {ubiquitin hydrolase} can be in ubiquitin proteasomes, break down PKA regulatory subunit in sense neurons, and so enhance catalysis, typically when cAMP is decreasing.
Proteins {fibronectin} can be in extra-cellular matrix.
Proteins {laminin} can be in extra-cellular matrix.
Proteins {telencephalin} can be cell-adhesion molecules.
Proteins {tubulin} can be in microtubules.
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.
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Date Modified: 2022.0225