Write an essay including diagram/s to describe the structure and mechanism of action of one named integral plasma membrane receptor of your choice (80%). Include a discussion of how the protein interacts with the plasma membrane’s lipid bilayer (20%).
Receptors are protein molecules that receive chemical signals in the form of ligands and induce responses at cellular level. They are localized at the cell surface, in the cytoplasm or the nucleus, a result of protein trafficking depending on their amino acid sequences. Receptors are ligand-specific due to the unique structures of their binding sites which complement those of ‘their’ ligands which results in a very high affinity (and subsequently low Kd or dissociation constant) of receptors
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Using benzodiazepines as an example, the binding of this drug to the benzodiazepine site increases the affinity of the receptor to GABA by triggering a conformational change in the GABA binding site. Binding of two molecules of GABA (one at each site) is sufficient to induce chloride ion channel opening through the rotation of the five kinks that block the passage of chloride ion in addition to other conformational changes not yet known. A wide enough route is provided for the energetically favorable influx of chloride ion (∆G < 0) into the postsynaptic neuron due to the higher concentration of chloride ion in the synaptic cleft (extracellular) as well as the electrostatic attraction between the positively charged arginine or lysine at the entrance and the chloride ion, resulting in hyperpolarization or inhibitory postsynaptic potential (IPSP). This decrease in postsynaptic membrane potential (more negative) causes the generation of action potential less likely as the threshold is harder to be reached. This results in a sense of ‘calmness’ or …show more content…
Instead, they are constantly cycled repeatedly between the plasma membrane and cytoplasmic compartments. This process is known as receptor internalization, and is vital in controlling the availability of the GABAA receptors on postsynaptic membrane. Normally this occurrence happens after drug withdrawal. This down regulation mechanism is dependent on the rate of endocytosis of the receptors and the level of GABAergic compounds in the synapses. Recycling happens when the receptors internalized are reinstated into the plasma membrane, post-, peri- or extra-synaptically. Those failed to be reinstated will be sent to lysosome for degradation and replaced with newly assembled complexes via secretory
So you could find a multitude of acetylcholine in each synaptic vessel. The vesicles' contents are then released into the synaptic cleft, and about half of the acetylcholine molecules are hydrolyzed by acetylcholinesterase, an enzyme that causes rapid hydrolysis of acetylcholine. But soon, there are so many acetylcholine molecules that this enzyme cannot break them all down, and the remaining half reach the nicotinic acetylcholine receptors on the postsynaptic side of the
Receptor tyrosine kinase is a cell membrane receptor system that can trigger multiple cellular responses simultaneously. It requires two receptor tyrosine kinase proteins, which are initially individual polypeptides that each have a signal-binding site, an α helix spanning the cell membrane, and a tail of multiple tyrosines. When signal molecules bind to both proteins they attach through a process called dimerization, forming a dimer. This process activates, or phosphorylates, the ends of the tyrosines, also known as tyrosine-kinase regions. Once the dimer is activated, multiple inactive relay proteins are able to bind to the tyrosine-kinase regions. Each of these proteins trigger a cellul...
The presynaptic terminal stores high concentrations of neurotransmitter molecules in vesicles, which are tiny nearly spherical packets. These molecules are then released by depolarization. Depolarization opens voltage-dependent calcium gates in the presynaptic terminal. After calcium enters the terminal, it causes exocytosis, which is the burst of release of neurotransmitters from the presynaptic neuron. After its release from the presynaptic cell, the neurotransmitter diffuses across the synaptic cleft to the postsynaptic membrane, where it attaches to the receptor.
The Role of Dopamine Receptors in Schizophrenia. Retrieved March 3, 2005, From Stanford University, Chemistry department web site, http://www.chem.csustan.edu/chem44x0/SJBR/Mann.htm Naheed, M., & Green, B. (2000). Focus on Clozapine. Retrieved February 7, 2005. From http://www.priory.com/focus14.htm Waddinton, J.L., & Buckley, P.F. (1996).
Action potentials in neurons are facilitated by neurotransmitters released from the terminal button of the presynaptic neuron into the synaptic gap where the neurotransmitter binds with receptor sites on the postsynaptic neuron. Dopamine (DA) is released into the synaptic gap exciting the neighboring neuron, and is then reabsorbed into the neuron of origin through dopamine transporter...
receptor substrate 1 or IRS-1. When IRS-1 is activated by phosphorylation, a lot of things
Neurotransmitters are 'chemical messengers that carry signals between neurons in the body' (Cherry K, 2014). They are released after an action potential has reached the pre-synaptic terminal. The neurotransmitter then crosses the synaptic gap to reach the receptor site of the post-synaptic neuron. Reuptake of the neurotransmitter is when it attaches to the receptor site and is reabsorbed by the neuron so it can be used again to pass along another action potential. They can be categorised as one of six types: acetylcholine, amino acids, neuropeptides such as endorphins, monoamines such as serotonin and dopamine, purines and lipids and gases (Cherry K, 2014).
glutamate receptors using antibodies, that tag on to the receptor itself. The proteins that make up the
The entire process starts off when an agonist involved is bound to receptors specific to it, expressed on the endothelial cell surface, activating enzymes like phospholipase C (PLC) directly through vascular endothelial growth factor receptors (VEGFR) or by thrombin or histamine through G protein coupled receptors (GPCR).
γ-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the CNS. GABAA is a ligand gated ion channel composed of five subunits. Through positive allosteric modulation ethanol binds to the δ subunit of the receptor and enhances the inhibitory effect of GABA. Once ethanol has bound to the GABAA receptor, chloride ions enter the post-synaptic neuron. This cascade of ions hyperpolarises the neuron, thus increasing inhibitory effects and makes the neuron less excitable. Ethanol alters the enzyme kinetics enabling the ion...
Transmission of action potentials from one neuron to the next involves the release of neurotransmitters from a presynaptic neuron to postsynaptic neurons across a synaptic g...
First, the Electrical synapse relies on having two cells spanning across two membranes and the synaptic cleft between them (Shepard and Hanson, 2014, para. 2). Overall, the purpose of the Electrical synapse for the nervous system is for the synapse to carry out impulses and reflexes. On the contrary, the neuronal structure of the Synapse’s Chemical synapse involves the role of neurotransmitters in the nervous system. Located between the nerve cells, the gland cells, and the muscle cells, the Chemical synapse allows neurons for the CNS to develop interconnected neutral circuits. According to Davis (2007), “Interconnected logical computations that underlie perception and thought” (p.17). Generally, regarding the Chemical synapse’s role in the nervous system, this classification of the Synapse has a valuable role on how drugs affect the nervous system actions on synapses. As a result, the activity of the neurotransmitters becomes the key contributor for the Chemical synapse to effectively process drugs in the nervous system and throughout the human autonomy. Defines as a chemical released across the Synapse of a neuron, neurotransmitters manipulates the body to believe the drugs are neurotransmitters as well (Davis, 2007, p. 19). Significantly, the role of drugs in the human body help prevents the obliteration of neurotransmitters in the nervous system (Davis, 2007, p. 19).
The primary inhibitory neurotransmitter in the brain is the gamma-aminobutyric acid (GABA), which exerts its effects mainly through the GABAAreceptor. Alcohol exposure results in activation of the GABAAreceptor, which in turn leads to reduced postsynaptic nerve excitability and thus contribute to alcohol’s sedative effects. In response to chronic alcohol exposure, the CNS adapts to the alcohol-induced GABAA activation by reducing GABA-mediated neurotransmission. Thus after chronic alcohol exposure and during withdrawal, GABA activity at the synapse...
The refractory period, which is before the resting potential is rebalanced by the pump, prevents the action potentials from traveling both ways down an axon at one time due to the neurons inability to respond to stimuli as a result of the imbalance of Na+ and K+ ions. This entire process repeats in a sort of chain reaction down the axon of the neuron until the impulse reaches the synapse, which is the gap between two neurons. When the neuron is depolarized, voltage-gated Ca2+ channels are activated and opened, releasing Ca2+ into the cytoplasm of the presynaptic neuron. This flow of Ca2+ ions causes synaptic vesicles to fuse with the cell membrane and release the chemical messengers (neurotransmitters) which diffuse across the synapse to the postsynaptic neuron from an area of high concentration to low concentration. The protein receptors, located on the dendrites of the postsynaptic neuron then receive the neurotransmitters which act like the stimulus that then converts the signal back to an electrical signal so the action potential can continue to
Canonically, GPCRs are thought to interact, or couple, almost exclusively with a particular type G protein. For example, tachykinin receptor 2 is now appreciated to signal through both Gs to activate adenylyl cyclase and Gq to mobilize calcium in response to neurokinin A, and that this coupling can preferentially be altered by a negative allosteric modulator towards Gq. Drugs that bias signal transduction through G protein coupling, like through G protein or arrestin, may bias likewise allow for the activation of desired pathways while leaving others