KIN 292 1st Edition Lecture 17These are the notes from Professor Starnes’ lecture of Clinical Human Physiology. These come from the slideshows provided by the professor and include extra notes and explanations. Highlighted or bolded information are things that I believe to be information that is important to look over multiple times. The notes in red are my personal additions and quotes of Professor Starnes from the class lecture. Outline of Last Lecture I. 7.1 Overview of the Nervous SystemII. 7.2 Cells of the Nervous SystemIII. 7.3 Establishment of the Resting Membrane PotentialIV. 7.4 Electrical Signaling Through Changes in Membrane PotentialV. 7.5 Maintaining Neural StabilityOutline of Current Lecture I. 8.1 Electrical SynapsesII. 8.2 Chemical SynapsesIII. 8.3 Neural IntegrationIV. 8.4 Presynaptic ModulationV. 8.5 Neurotransmitters (selected): Structure, Synthesis, and DegradationCurrent LectureChemical synapses. Most neurons communicate using this typeFunctional anatomy:- Presynaptic neuron- Postsynaptic neuronThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.- Synaptic cleft ,(30-50 nm wide)- Unidirectional - Usually synapse on dendrites (axodendritic)- Some synapse on soma (axosomatic) or axons (axoaxonic)Active presynaptic neuron- Depolarization by AP opens voltage gated Ca channels- Ca signals vesicles to move toward membrane to fuse and undergo exocytosis of neurotransmitter (NT)- Amount of NT release depends on Ca concentration- Synaptic delay = time from AP at terminal to change on postsynaptic Vm. Approx 0.5 - 5 msec and almost entirely due to steps 2 and 3- 4 fates of NT:Step 4, 6, 7, 8- 7. Reuptake of some NT by reuptake molecules to remanufacture NTPostsynaptic Potential (PSP). Change in membrane potential in response to receptor-neurotransmitter binding- Magnitude of graded potential depends on amount of receptor-neurotransmitter binding- Excitatory postsynaptic potential (EPSP)o Depolarizes toward threshold potentialo Most common neurotransmitter: glutamate- Inhibitory postsynaptic potential (IPSP)o Hyperpolarizeso Decreases likelihood of AP being generatedo Most common neurotransmitter: GABA- Inhibitory Synapses - Neurotransmitter opens K+ or Cl– Channels- Cl– channels can also result in IPSP or membrane stabilization – next slide- Fast response. K+ moves out  IPSP, Increased frequency of APs = more NT released = greater responseThe roles of chloride channels in inhibitory synapses- For neurons actively transporting chlorideout of the cell, Cli is low so when. NT opens a Cl channel Cl goes in – down its concentration gradient IPSP- For neurons without active transport of chloride. Chloride at equilibrium. Thus, when NTopens more channels no net movement occurs- Same as (b) except NT2 binds to an excitatory synapse bringing in positive charge. Cl- moves in to counter or minimize depolarization, thus stabilizing the membranepotential. Considered an inhibitory action.Example of convergence – a neuron gets info from several sources (next)Divergence and convergence. Refers to the amount of communication among neurons. Part of neural integration- Divergence. Axons of neurons typically haveSeveral collaterals that communicate to severalOther neurons- Convergence. A neuron receives information from hundreds/thousands of other neurons via axodendritic and axosomatic synapses- Neural integration - Synapses from many presynaptic neurons must summate to get the axon hillock to threshold potential. Involves temporal and spatial summation to get to threshold for a single AP and to suprathreshold levels to achieve multiple APs (from chap 7)8.4 Presynaptic Modulation- The regulation of communication across a synapseo Axoaxonic synapses function as modulatory synapses Presynaptic facilitation- E+C enhances release from C Presynaptic inhibition- With F+H active, H inhibits release from F8.5 Neurotransmitters: Structure, Synthesis, and Degradation- “The action of any chemical messenger does not depend on the messenger itself, but rather on the signal transduction mechanism activated by the receptor once the messenger binds to it.”- Acetylcholine - synthesis, action, and degradation at cholinergic synapseo Synthesized inAxon terminal by choline acetyltransferaseo Choline obtained through diet and undergoes reuptake after ACh degradation (step 6)o Found in PNS and CNSMost abundant NT in PNS- Acetylcholine Acetyl CoA + choline  acetylcholine + CoA Synthesized in axon terminal Choline acetyl transferase (CAT) = enzyme for synthesiso Breakdown Acetylcholine  acetate + choline Occurs in synaptic cleft Acetylcholinesterase (AChE) = enzyme of degradationo Reuptake of choline for resynthesis of Ach- The subsequent cellular action after Ach binding depends on which type of cholinergic receptor is on the postsynaptic neuron- The action of any chemical messenger does not depend on the messenger itself, but rather on the signal transduction mechanism activated by the receptor once the messenger binds to it.- Nicotinic and muscarinic cholinergic receptorso Nicotinic:Ionotropic channel with 2 ACh binding sites – On skeletal muscle cells and other places Action is EPSPo Muscarinic:Metabotropic– Dominant cholinergic receptor in CNS and lesser role in PNS Action depends on which G protein sensitive channels and enzymes are on postsynaptic neurono Named by drug binding: Nicotine binds to nicotinic receptor, Muscarine binds to muscarinic receptors, but not vice versa- Biogenic Amineso Derived from amino acids Catecholamines: derived from tyrosine- Dopamine- Norepinephrine (also called noradrenalin)- Epinephrine (also called adrenalin) Serotonin: derived from tryptophan Histamine: derived from histidineo Enzymes for degrading biogenic amines Monoamine oxidase (MAO) Catechol-O-methyltransferase (COMT)o Synthesis Cytosol of axon terminal Packaged into synaptic vesicleso Release Dopamine and norepinephrine are common in CNS Norepinephrine is also found in PNS Epinephrine comes from CNS, but is more commonly released as a hormone by the adrenal medulla Epi &norepi receptors (adrenergic receptors) covered in chap 11- Serotonino CNS neurotransmitter Main location - Brainstemo Functions - Regulating sleep; Emotions- Histamine o CNS neurotransmitter  Main location -