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.
4-Zoology-Organ-Nerve-Neural Chemical
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Date Modified: 2022.0225