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Organisation of the Body

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Characteristics of hormone receptors   High affinity for hormone Hormone specific Binding is saturatable  
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Kds   Binding constant 10^-12 to 10^-9 Very little hormone needed for activation  
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EC50   Conc of hormone that gives 50% response  
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Receptor classes   Ligand gated ion channels G protein coupled receptors Enzyme linked Intracellular receptors  
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Ligand gated ion channels   Open in response to NTs Leads to a change in membrane potential due to ion movement Instantaneous response  
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nACRs   5 protein 2 homodimers and 1 extra protein Blocked by cobra toxins Open in response to ACh binding - non-selective cation channel  
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Katp channel   Glucose enters beta cells and is metabolised to produce ATP This binds to K channels and blocks them Leads to depolarisation and Ca influx Insulin release triggered ATP acts as a hormone  
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G protein coupled receptors   Hormone binds to receptor leading to G protein mobilisation They interact with enzymes through a second messenger system Timescale - seconds/minutes  
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What activates GPCRs   Protein hormones - glucagon Amines - adrenaline Lipids - prostaglandins  
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Family of GPCRs   Around 820 in the human body All have similar structures - hard to design drugs specific to one, so unwanted effects are common  
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Structure of GPCRs   7 transmembrane regions Extracellular N-terminus Often post translationally glycosylated and phosphorylated to regulate activity  
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M2 muscarinic receptors   Found in the heart - slow heart rate QNB - antagonist  
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G proteins   Get their name from their ability to bind GTP and GDP They exist in an active GTP bound and an inactive GDP bound form Active G proteins bind and activate signalling enzymes causing a specific response Heterotrimeric - alpha, beta and gamma subunits  
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Types of GPCRs   Gq - activates PLC Gi - inhibits adenylate cyclase Gs - stimulates adenylate cyclase G12/13 - Rho family Gb - activates inwardly rectifying potassium channels  
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The G protein cycle   Inactive - loosly associated with proteins Ligand binds and recruits G proteins GTP exchange causes dissociation of the protein Subunits have different effects GTP hydrolysis causes reassociation  
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Downstream effectors of GPCRs   Adenylate cyclase Phospholipase C Ion channels  
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Adenylate cyclase   Stimulated by Gs and inhibited by Gi Converts ATP into cAMP This activates PKA by releasing its catalytic subunits cAMP degraded by phosphodiesterase  
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Effects of Cholera   A GPCR agonist Binds to Gs - increased cAMP and PKA Activates CTFR Overactive CTFR causes Cl loss into lumen of gut followed by Na and water Leads to internal dehydration Enkephalin - stimulates Gi to reduce effects  
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cAMP in steroid synthesis   ACTH stimulates Gs - cAMP produced Immediately upregulated cholesterol synthesis by cholesterol ester hydrolase Over a few hours allows uptake of cholesterol by mitochondria  
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PLC   Activated by Gq receptors Cleaves PIP2 into DAG and IP3 DAG activates PKC - phosphorylates proteins IP3 activates store operated calcium ion channels leading to Ca efflux from SR - activation of intracellular proteins  
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Role of Gq/Gs switch in beta cells   Normal B cells us a Gs pathway to secrete insulin involving GIP and GLP-1 Following chronic hyperglycemia and chronic sulfonylurea treatment they switch to Gq  
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Ion channels in GPCR   Channels phosphorylated - less active e.g. G protein gated inwardly rectifying potassium channels in the heart  
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Smooth muscle contraction   Uses multiple mechanisms Ligand gated ion channels Voltage gated ion channels Gq proteins - IP3 activates Ryr channels  
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Amplification   Reaction cascades cause massive signal amplification Proteins made can last a long time, so short activation affects function for longer periods  
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Enzyme linked channels   Receptor is also the effector enzyme e.g. tyrosine cyclase enzyme activity Receptors dimerise on ligand binding Autophosphorylation at tyrosine and serine residues  
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Insulin receptor   Tyrosine kinase receptor Leads to insertion of Glut4 into cell membranes Under fasting conditions no insulin = no glucose uptake as no Glut4 channels in membrane  
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Intracellular receptors   Control of DNA transcription e.g. steroid hormones and Vit D (for Ca uptake) Takes hours for proteins to be produced  
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Steroid receptor structure   DNA strand contains specific hormone response elements Contains regions for transcriptional regulation, DNA binding and hormone binding  
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What binds to intracellular receptors   Androgens Estrogen Progesterone Glucocorticoids Mineralocorticoids Thyroid hormone Vit D  
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Turning off the signal   Removal or degradation of the hormone Desensitisation of the receptor Internalisation of the receptor  
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Desensitisation of GPCRs   Phosphorylation of certain residues at the C terminus by GRK Arrestin binds to the receptor and prevents G protein interaction  
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Resensitisation   Phosphatases remove the phosphate from the C terminus Causes arrestin to dissociate  
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Role of phosphodiesterase's in glucose control   Serves as a connection between glucagon and insulin pathways Insulin drives activation of phosphodiesterase to downregulate the role of glucagon Breaks down cAMP  
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Receptor internalisation   Receptors taken into the cell by endocytosis Basically receptor mediated endocytosis Dopamine D1 receptors are permanently downregulated due to overuse in addiction - via internalisation and DNA metylation  
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What causes disease at receptors   Failure of ligand binding Failure of signal transduction Constitutively active signal receptor systems Antibodies to receptor  
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Inactivating receptor mutations   Receptor does not function despite hormone present  
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Activating receptor mutations   Receptor continually active without hormone bound  
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Dwarfism   Due to growth hormone releasing hormone inactivating receptor mutations No signalling - reduced growth hormone release No long bone or muscle growth Treated by administering growth hormone  
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Activating receptor mutations   Precocious puberty - puberty starting at 5-9 years Constant activation of LH receptors without the presence of the hormone Ovary - estrogen Testes - testosterone  
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Physiological response to receptor activation   Vesicle fusion Gene transcription Protein production  
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Types of cell signalling   Depolarisation induced - Ca entry dependant Depolarisation independent - Ca entry dependant  
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