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BIOL 460: Test 2
Thyroxine
|
-T4, contains 4 iodine atoms, most abundant.
-Thyroid Gland
-In blood stream its bonded to a carrier protein
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Thyroid H Family Action
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1. Enters blood bonded to TBG
2. Weak bond that breaks free and diffuses across plasma. T4 is converted to t3
3. Enters nucleus via binding protein translocate
4. Thyroid hormone nucleur receptors all ready bonded to HRE, correpresor protons bonded to it when thyroxine is absent repressing transcript
5. T3 Binds to ligand bonding domain of RXR + TR and get Heterodimer=
6. Genomic Action are transcribed mRNA= Hormon
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Goiter
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dietary deficiency of iodine, thyroid cannot function properly, stimulates growth of thyroid gland
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What are the components of an inactive RXR receptor? How is it activated?
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-RXR bound to DNA, w/ corepressor bound to inhibit transcription
-ligand binding activates receptor, causing the release of the corepressor and binding of a coactivator (starts transcription)
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characteristics of 9-cis retinoic acid:
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-hormone class: isoprene derivatives
-derivative of vitamin A
-binds to nuclear retinoic acid X receptors in many tissues
-forms heterodimers with other receptors such as vitamin D and thyroid hormone receptors
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heterodimer
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protein containing 2 nonidentical subunits
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hydrophilic hormones
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freely circulate
CANNOT diffuse through lipid bilayer
generally bind to receptors on surface of the cell (g-protein couple receptors)
signal through second messenger
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adenylate cyclase
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converts ATP to cyclic adenosine monophosphate (cAMP)
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PhospholipaseC
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Generates IP3 and DAG, IP3 then induces release of 2nd messenger; Ca2+ and DAG then activate protein kinase C; involved in immune response and learning/memory
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Genomic effects of steroid hormones
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Steroid binds to nuclear receptor and then translocates to DNA and changes what genes are on and off and activates genes
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Hormone-response Element
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- located upstream from the start of target genes
- gene expression changes when a regulatory protein, such as a steroid hormone-receptor complex, binds to a hormone-response element for that gene
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Steroid Action
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1. When in blood, need a carrier, unbind to diffuse into the target cell
2. Receptors in the cytoplasm, nucleus or cytoplasm then translocate into nucleus
3. the hormone receptors bind both half sites of DNA binding domain on (HRE) and activate genes= Dimerization of homodimer
4. mRNA is created and moves into the cytoplasm
5. translation produces new proteins for cell processes
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hormone action of Lipophilie
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- alter plasma membrane permeability to open and close channels
- stimulate protein synthesis
- activate and deactivate enzymes
- induce secretory activity
- stimulate mitotic activity
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Transitory
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weak bond by thermal energy to carrier protein. Equilibrium Reaction
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transcription factors
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proteins that bind DNA and influence gene expression
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lipophilic
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Receptors are in cytoplasm or nucleus
Cannot be digested
can cross plasma memebrane
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pre-pro-hormones and pro-hormones
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are inactive forms of the hormones (they can't bind to their target tissue receptors to trigger cell response) with additional amino acid sequences added on
-the amino acid sequences need to be cleaved off for hormones to be active
-Secreted by Endocrine gland
-Thyroxine is released into blood stream and iodine is removed=T3
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hormone classification
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peptide: Preprohormone (large, inactive), Prohormone (post translationam mod), peptide hormone receptor complex
steroid: lipphilic and can enter cell. Cytoplasmic/nuclear recetpors are slower acting than membrane receptors (aldosterone and estrogen). Activate DNA for protein synthesis
Tyrosine derivatives (Amine): Catecholamines (E and NE, dopamine) and Thyroid Hormones
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Hydrophilic hormones
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Cannot cross the plasma membrane and so bind to cell surface receptors. This interaction triggers signal transduction pathways that alter activity of a preexisting protein. These include peptides such as insulin and small charged molecules like epinephrine (adrenaline).
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lipophilic hormones
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diffuse freely across cell membranes and bind to intracellular receptors of the nuclear hormone receptor superfamily. This results in a conformational change in tertiary structure that activates the receptor. The receptors form dimers and functions specific transcription factors that bind to cis-acting elements in target genes such as enhancers
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glycoproteins
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class of hormones, proteins bound with carbohydrate groups
ex. follicle stimulating hormone (FSH) and luteinizing hormone (LH)
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Classifying Hormones chemically
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Amine- Adrennall medulla
Polypeptides and Proteins- short A.A. chains
Glycoproteins-Proteins+Carbohydrate=Sex, Cortico
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Neurotransmitter vs Hormone
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NT - act at sites close to release
Hormones - act at site distant from release (travel through circulation)
Many substances function as both hormones and NT - epinephrine, norepinephrine, insuline\
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antidiuretic hormone
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-released by the posterior pituitary gland during exercise; reduces urinary secretion of H2O and prevents dehydration
-Polypeptide
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Insulin & Growth Hormone
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Protein
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Endocrine
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-secrete hormones into blood (NO DUCTS)
-loose connective tissue with epithilium
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Exocrine
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Secreting externally; hormonal secretion from excretory ducts.
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chemo receptors
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respond to decreased blood oxygen, increased blood carbon dioxide, increased blood acidity (PH)
stimulate increased rate and depth of breathing
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Stretch Receptors
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Mechanically gated Ion Channels
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Propranolol
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Beta-adrenergic receptor antagonists
Non selective beta blocker that decreases HR and CO especially during exercise or in the presence of increased sympathetic activity. It is the most lipid-soluble beta blocker. Interferes with glycogenolysis.
-Bronchodialation
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Atenolol
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Selective - B blocker - Adrenergic Antagonist
Causes: Decreased HR, Decrease Cardiac Output, Decreased AV cond., Decreased O2 demand
Used to treat: HTN, angina, arrhythmia, CHF
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Post Ganglionic in Autonomic
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doesn't release acetycholine or norinepherine
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beta blockers
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- (blocks beta receptors, in heart and lung)
- lower BP
-lower heart rate
- increase in cardiac output
( broncho constriction)
-propanolol, atenolol, terbutaline
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(Terbutaline)
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((Adrenergic: Beta-2 agonist (bronchodilator))
Epinephrine Inhalors
Bind to B1 and b2 on heart and cause High Blood Pressure
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variscosities
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numerous bulbous swellings in smooth muscle that release neurotransmitter into a wide synaptic cleft in the general area of the smooth muscle cells. These junctions are called diffuse junctions.
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Alpha 2 Andonergic Receptors
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Negative Feedback-moderation of sympathetic mass activation
1. located in brain and terminal boutons, NE is released into synaptic cleft
2. Open fewer ca+ VG channels bc the IPSP weekens depolirization
3. Drugs: Clonidine, Catapress-agonist
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Synapse En Passant
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A postganglionic ANS innervation system consisting of varicosities releasing neurotransmitters throughout smooth muscle.
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Beta Adrenergic Receptors
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1. Bond to NE from Adrenulla Medulla
2. G-protein Turns on Adenylate Cyclase
3. ATP----cAMP + Pyrophosaphate
4. Protein Kinase- Polypeptide Dimer
5. Absence of cAMP=Inhibitory bonds to catalytic and turns off, if present= Regulatory subunit has a better infinity for cAMP
6. Beta Andonergic on heart= EPSP
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phospodiesterase inhibitors
|
inhibit breakdown of cAMP, increasing Ca influx
causes vasodilation, bronchodilation, positive inotropy
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Protein Phosphotases
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Reverse effect of Protein Kinases
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Protein kinase
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-Enzyme that transfers phosphate groups from ATP to a protein, thus phosphorylating the protein
-Changes conformation
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Beta Receptors
|
-Andenylate Cyclase/cAMP
1. NE binds to beta receptor G-Protein linked
2. Subunit turns on Adenylatecyclase
3. Cyclic AMP acts on Dimer Protein Kinase
4. Catalytic Subunit- absence of cAMP binds to Catalytic
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IP3 (Inositoltriphosphate)
|
1. Diffuses through cytoplasm to E.R.
2. Opens Calcium Ligand Gated Channels
3. Ca diffuses from ER to Cytoplasm
4. Ca bonds to ca/calmodulin complex
5. Ca/calmodulin acts on protein kinases
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Calmodulin
|
Activated by calcium; Induces active conformation change in CA2+/calmodulin dependent protein kinases
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Diacyglycerol (DAG)
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-Phospholice C hydrolyzes a membrane phospholipid
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Alpha 1 Receptors
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-Vasoconstrictiion of blood vessels
1. G-protein activates phospholipid C/ca secondary messenger
2. Phospholipase C/ca hydrolyzes a membrand phospholipd producing (IP3) and (DAg)
3. IP3 diffuses through cytoplasm to E.R. and opens calcium gated ligand channels
4. Ca+ diffuses from ER to cytoplasm and binds to Ca/Calmodulin complex
5. Acts on Protein Kinase=EPSP=Vascoconstriction of skin
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Beta 2
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Bronchiole Tubes- IPSP, causes bronchodialation
Viscera-IPSP, decreases activity in intestines and caint digest food
Fight or Flight
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adrenergic
|
related to the adrenal gland where epinephrine and norepinephrine are made
Most sympathetic neurons are
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Beta 1
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heart
increase HR - chronotropic
contractility - inotropic
EPSP
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Beta 2
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vasodilation bronchial dilation
relax of bladder
GI muscle and activity
release of glucagon
Viscera
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Alpha 1
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EPSP causing blood vessels vasoconstriction
Viscera-why you feel sick to stomach and dry mouth
|
Cholinergic neurons
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acetylcholine (ACh)
They include
-1. All Automic NS sympathetic and parasympathetic preganglionic neurons.
2. a few Sympathetic postganglionic neurons that innervate most sweat glands.
3. mostparasympathetic postganglionic neurons.
|
Cholinergic receptors
|
muscarinic-EPSP & IPSP
nicotinic- Ionotropic, EPSP, Adrenall Medulla
ACh works on both
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Sympathetic Neurons
|
Axons of preganglionic travel in spinal nerves of cell bodies at T1-L2
Supplies visceral effectors of somatic (Glands, smooth)
Mass activation
Adrenall Medulla
Somatic
Fight or Flight
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Parasympathetic neurons
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No mass activation
Rest, Digest
Craniosacral
Axons leave brain to Cranial nerves
Pre ganglionic neurons make axons in 4 cranial nerves
Travel and synapses to post ganglion cell bodies whos axons are at Terminal Ganglion
S2,3,4= Splanchnic Nerve-
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Splanchnic nerve
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Pelvic Nerve that runs in the abdominal cavity
Supply rectum, bladder, and reproductive
S2,3,7
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Terminal Ganglia
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Tissues of the target organ for post ganglions send out neurons to gland
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Vagus Nerve
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Cranial nerve # 10
A wonderer that supplies most of the pararympathetic innovation in the body
Finger thick
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Sacral Segments
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cell bodies in nuclei of brain (S2-S4)
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Adrenal Medulla
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Hormone-epinephrine and norepinephrine
target:many tissues
effect: fight or flight response
Formed from ectoderm
Neural Crest
Is a modified sympathetic collateral ganglion=sympathadrenal system
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9-cis-retinoic acid
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A Dimer with T3 nucleur receptor a derivative of vitamin A
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Steroid H Family Action
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1. Transported through blood via carrier proteins- break free and pass through plasma membr
2. Binds to receptor protein in cyto
3. translocates into nucleus binds to ligand bonding nucleur H receptors, HRE binds to DNA
4. Nuclear receps act as transcription factors- 2 regions Ligand bondin domain & DNA bondin
5. Receptors dimirize form Homodimers which initiate "Genomic Action of Steroid Hormon"
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hormone response element (HRE)
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stretch of DNA in the promoter region of a gene that activates receptor
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Transitory
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Weak thermal bond
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Nucleur H receptors
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Lipophilic receptors that activate genetic transcription
Transcription factor
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Adenylate Cyclase/cAMP
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1. NE or E bind to G protein
2. G-Protein dissociates and activates Adenylate Cyclase which catalyzes ATP-->cAMP+PPi
3. cAMP (2nd mess) diffuse down cytoplasm and activates Protein Kinases by remving regulatory subunit
4. PK- Phosphorolates proteins (chng Conf) and opens Ion channels= EPSP and IPSP
5. Protein Phospatases @ Phosphodiesterases
|
Protein Kinases
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Activated by cAMP which removes regulatory subunit and leaves catalytic making it active.
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PhospholipaceC-ca+
|
1. E/NE binds to Alpha 1 receptors which have a G-protein
2. G-protein dissociat--activates Phospholipace C which hydolz Mem Phoslipase
3. Mem Phos splits into (IP3) and (Dag) IP3 diffus throug cytop into E.R. opens Ca+ Lig G Chan
4. Ca+ diffuses from e.r to cyto bind to calmodulin/ca
5. Calmod/ca activat Prot Kinas- open ion chans and lead to Vascoconstriction
|
Tyrosine Kinase Second Messenger System
|
1. Insulin binds to alpha ligan in extrecc,( Epidermal Growth Factor)
2. Beta subunits stimulated and autophosphorolation each other activating Tyrosine kinase
3. Insulin receps phosphor insulin receptor substrate proteins that activates sign molecules
4. sig molec-- cause transporter carrier prot for uptake of glucose to tissue cells
|
MONAMINE NT FUNCTION
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HAVE TO BE ELIMINATED FROM SYNAPTIC CLEFT
1. Action potent---depoliriz------Ca open----monamine stored in synaptic vess fusion & exocytosis
2. Taken up from from Synap Clef by facilitated diffusion via transporter
3. Deactivated by Monoamine Oxidase in Terminal Bouton
4. Or-------Catechol-o-methyl-transferase
5. Adnylate Cyclase
|
Catechol Group (Tyrosine)
|
Dopamine
Norepinephrine
Epinephrine
|
Serotonin
|
Tryptophan
|
Monoamine oxidase Inhibitor
|
inhibits (MO) causing build up of monamine in synaptic cleft enhancing effects
|
Catechol-o-methyl transferace
|
found in cytomplasm of post-synaptic and deactivates catecholamines
|
Nitric oxide and Viagra
|
1. Produced by L-arginine via nitric oxide synthetase
2. diffuses into smooth muscle cell and activates Guanylate Cyclase which catalyzes GTP---cGMP+PPI
3. cGMP causes ca+ VG channs to close producing relaxation in muscle causing vasodialaiton=erection---------
4. Viagra inhibits phodiesterase
|
Sacral Segments
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cell bodies in nuclei of brain (S2-S4)
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Telencephelon
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Cerebral Hemispheres
Cerebrum
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Diencephalon
|
forms thalamus, hypothalamus, and epithalamus
-becomes surrounded by the telencephalon
-Pituatary Gland
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Mesencephalon
|
Nigrostriatal system
mesolimbic system
TECTUM
and
TEGMENTUM
|
Met
Metencephalon
|
1.Cerebellum- controls skeletal movement
2.Pons- relays info from spinal to brain
|
Myelencephalon
|
Medulla oblongata- brain stem, like spinal chord many centers
|
Substance P
|
Involved in perception of pain
Substance pre-released by neurons with pain
Polypeptide
|
Endogenous opiods
|
Analgesia euphoria causes feel good pain
Found in proteins in CNS that bind with opium and morphine
agonists of exogenous
natural polypeptide
|
long-term potentiation
|
increase in a cell's firing potential after brief, rapid stimulation.
Later: 100 vessicals release
|
Glutamic Acid Bonding to receptor
|
2 types: Na/Ca and Na channels
1. Ca enters, produces NO (retrograde)
2. No diffuses through plasma membrane pre cell
3. enters terminal bouton and turns on STP that increases the release of glutamate
|
Inhibitory Amino Acids
|
Generate IPSP
Glycine
Strychanine
Tetanus
Botox
|
Glycine
|
Activate in spinal chord
innovate skeletal muscle
Contract biceps by releasing EPSP simultaneously Brain sends IPSP for relaxation of tricep
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Strychnine
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1. Poison that binds to glycine receptors causing sparatic paralysis
|
Tetanus
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Destroying snare complexes in glycine receptors
|
Botox
|
Disrupts snare complex and blocks release of ACH lead to Flacid Paralysis- cannot contract muscle
|
Mesolimbic Dopamine system
|
Behavior and Reward pathway in brain
tegmenton of Mesencephalon
Cocaine and Amphetamine
|
Limbic System
|
Masses of grey matter nuclei in Telencephelon Hemispheres
|
Cocaine
|
Dopa transporter blocker
blocks reuptake of domaine
|
Amphetamine
|
Increases amount of dopamine
1. Dop-transporter
2. Diffusion into terminal bouton and enter synaptic vessicles
3. For every dop out theres a dop in
|
Dopamine
|
Nigrastriatal dop system
Motor behavior, pleasure, arrousal
|
Nigrastriatial Dopamine System
|
Initiation of skeletol muscle movements
|
Substantia Nigra
|
Found in Tegmentom
Black Substance
|
Melanin
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The pigment that is responsible for skin color
|
Lipid Neurotransmitters
|
1. Endocannabnoids--Euphoria
2. Anandamids--Delight, Retrograde Neurotransmitter
|
retrograde neurotransmitter
|
released from post synaptic neuron; inhibits further neurotransmitter release for presynaptic neuron
|
arrector pili
|
smooth muscle. it extends from the upper dermis to the side of the hair follicle.
Somatic component
|
Flacid Paralysis
|
-go limp and collapse
-block ACh receptors
|
visceral effector
|
smooth muscle, cardiac uscle, or gland
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Adrenal Medulla
|
Ectoderm
Produce EN & N
Modified Sympathetic Collateral Ganglia
Neural Crst
Innation by Sympathetic
|
Adrenal Cortex
|
Mesoderm
Produce Corticosetoid
No inovation only Pituitary Gland
|
Neural crest
|
forms all ganglia in PNS
|
Axon Convergence
|
3 axons of sympathetic ganglia converge on post ganglia
|
Parasympathetic Axon length and divergence
|
Preganglionic neurons with long axons usually synapse with four to five postganglionic neurons with short axons that pass to single visceral effector
Branching
Mass activation
|
Neurohypophysis
|
Storage hormones produced in hypothalamus
Posterior Lobe
Formed from down growth of the brain
|
Pituitary Gland or Hypophysis
|
Inferior aspect of brain or Diencephalon
Attatched to hypothalamus by infundibulum
|
Adenohypophysis
|
Anterior Lobe
Produces and secretes major homones
No neural connection with hypothalamus
|
Antidiuretic homone (ADH)
Neuroendocrine Reflexes
|
secreted by the posterior lobe of the pituitary gland increases reabsorption of water by the kidney
1. Osmoreceptors detect osmo press then genrate axon potent
2. Exocytosis of (ADH) into Capillary Bed
3. Dumps ADH into blood triggering kidneys to retain water
|
Oxytocin Reflex
|
1. Sensory neurons from child contacting with breast sends to hypothalamus
2. neurons produce oxytocin and released by exocytosis
3. Carried to breasts via blood and acts on smooth muscle
4. Contract of breast to produce milk
|
Hypothalamic-neurohypophysis
|
Axons of neurons whose cell bodies are in supraoptic
|
Portal System
(Adrenohypophysis-Hypathalamus tract)
|
Two Capillary beds in the circuit
1. Cells in Hypothal produce releasing and inhibitory molecules
2. Release at axon from capillary bed
3. Carried via porta vein to bood stream then cappilary bed in adrenohypophysis
4. Cause adrenohypophysis not to relase hormones or cause it to release
|
Thyroid Stimulating Hormone
|
Travels to via portal vein Adenohypophyisis
Produce Throptropin
|
Sympathetic Pathways
|
1. Spinal chord--axon---white ramus communicans----chaing ganglion---diaphram---splanchnic nerve---abnominal---collateral ganglion---synapse with postgangion----axon----effector---visceral
2. associates with chain gang--synapse---post gang--axon---grey ramus---spinal nerve---visceral effects( sweat gland, arrector pili
3. up or down chain gang---grey ramus synapse---axon to vesceral---can branch
|
Rathke's Pouche
|
Epthilial tissue makes up adenohypophysis
|
Raphie nuclei
|
Serotonergic neurons are found here
|
Hypothalamic-hypophyseal portal system
|
System that allows releasing hormones from hypothalamus to immediately reach anterior pituitary; blood from capillary bed in hypothalamus flows through portal vein into
Anterior pituitary where it goes into a second capillary network
|
Releasing and Inhibitory Hormones
|
1. Release from Hypothalamus cappillary bed
2. Travels throught portal vein--to cappillary be inadenohypophysis
3. Causes adenohypophysis to inhibit the release of a homone or it to release
|
Trophic Hormones
|
Secreted by adrenohypophysis
|
Thryoid Stimulating Hormone
|
Hypotholamusrelases it and travels to adrenohypophysis where it can cause negative feedback
|
Adrenall Cortex
|
Hormonally controlled
secrete corticosteroids
1. Zona Glomerulosa--Mineralocorticoids (Aldosterone)
2. Zona fasciculata-Glucocorticoids
3. Zona Reticularis-Sex steroids
|
Aldosterone
|
Reabsorbes H20 and NA while secretting K+-----Increases blood volume and pressure and regulate electrolytes
Hperkalemia---Elevated K+ act on adrenall cortex to secrete aldosterone
1. Renin-----Angiotenson-----Aldosterone
|
Glucocoricoids
|
Metabolism of glucose to conserve
Immune system regulator
|
Cortisol
|
1. Glucogenesis-production of glucose from unuasual sources
2. Restricts entry of glucose in cells
3. Stimulates Lipolysis---breakdown of lipids for energy
4. Suppresses immune system and inflamation
|
Adrenall Gland (Stress Reppresor)
|
General Adaption Syndrome
1. Alarm and Reaction
2. Stage of Resistance
3. Stage of Exhastion---Sickness
Stimulates Pituitary Adrenal Axis---Glucocorticoids
|
Stess on Adrenall Gland
|
1. Hypotrophy-Growth in Adrenall Cortex
2. Atrophy of lymphoid Tissue
3. Bleeding petpic ulcers
|
Negative Feedback of the andenohpophysis
|
Sectretion of ACTH is inhibited by rise in thyroxine
|
Adenohypophysis hormones
|
1. Adrenocorticotropic (ACTH)
2. Thyroid Stimulating Hormone(TSH)
3. Gonadotpropic(FSH and LH)
Stimulate adrenal cortex thyoid and gonads
|
Hypothalamic control of the Adenohypophysis
|
No neural connection. Controlled by hormones made by hypothalamus. Hormones are releasing hormones and inhibiting hormones. They arrive at the adenohypophysis by the hypothalamo-adenohypophyseal portal system. Portal veins supply capillary beds- two instead of the usual one. Releasing and inhibiting hormones travel to the second capillary bed in the adenohypophysis.
Thyroptropin Releasin Homone(TRH)
|