PSYCH 2210 1st Edition Lecture 6Outline of Last Lecture I. Action Potential II. Local vs. Action PotentialsIII. Steps in Action Potential IV. Steps following arrival of action potential Outline of Current Lecture I. Conclusion of Last LectureII. Post-synaptic potentialsIII. Excitatory postsynaptic potential (EPSP)IV. Inhibitory postsynaptic potential (IPSP)V. Explain disordersVI. Explain how drugs workVII. Otto Loewi: Identification of AcetylcholineVIII. Drugs and the brain a. examplesCurrent LectureI. Conclusion of Last Lecturea. Termination of Signal: synaptic transmission is rapidly stoppedi. Re-uptakeii. Enzymatic Breakdownb. Pre-Synaptic modulation: transmitter may activate presynaptic receptors, decreasing transmitter release. II. Post-synaptic potentialsa. Neurotransmitters bind with specific post-synaptic receptorsi. Receptors are linked to specific ion channelsii. Channels open when neurotransmitter binds to receptoriii. Ions move across membrane of dendrites, producing local potentialsThese 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.1. EPSP2. IPSPIII. Excitatory Postsynaptic Potential (EPSP)a. Produces a small local depolarizationb. Makes inside more positivec. Results from Na+ or Ca++ entering the cell. IV. Inhibitory Postsynaptic Potential (IPSP)a. Produces a small hyperpolarizationb. Makes cell more negative insidec. *If IPSP’s are missing, motor neurons are activated d. Results from: i. Chlorine ions (Cl-) entering the cellii. Potassium ions (K+) leaving the cell V. Explain Disordersa. (REM Behavior Disorder, Bipolar Disorder)b. Voltage gated ion channels: maintain neuron excitabilityc. Genomic studies: have identified variations in ANK3 (Ankyrin-G) on chromosome 10q21 (gene that is required for the clustering of voltage-gated sodium channels at axon initial segments)d. Lithium carbonate: the gold standard for treatment of bipolar disorder, was shown to down-regulate both ANK3 and subunits of the calcium channels.VI. Explain how drugs worka. Binding lets in more CL- ions produces IPSP’s, hyperpolarize amygdala neurons (valium) VII. Otto Loewi: Identification of Acetylcholinea. Acetylcholine (Ach): first transmitter to be discoveredi. Applied a stimulus to slow the heartii. Collected the surrounding fluidiii. Applied fluid to a second heartiv. It also slowed, showing the presence of a chemical signalVIII. Drugs and the Brain a. Drugs produce their effects by altering ongoing electrical or chemical processes (help fire more or less often, more or less released)b. Drugs alter Neurotransmitter effectsi. Agonists: enhance the actions of neurotransmitters (amplify effects)ii. Antagonists: inhibit the actions of neurotransmitters (decrease effects)c. Drugs can alter pre-synaptic processi. Presynaptic process: 1. Conduction down Axon2. Transmitter production 3. Transmitter release4. Transmitter clearance: enzymes; transportersd. Novocaine (dentists)i. Blocks Na+ channels on pain axonse. TTXi. Blocks ALL Na+ channels in body f. Drugs which affect release of neurotransmittersi. Botox: blocks release of acetylcholine and prevents muscles from contacting.ii. Meth: releases dopamineg. Drugs which affect transmitter clearancei. Cocaine: blocks re-uptake of dopamine at transporters and prolongs effect of dopamine at receptor (agonist for dopamine)ii. Aricept: blocks enzyme (acetylcholinesterase) that break down acetylcholine (agonist for acetylcholine)h. End result??i. Aricept is a member of ACHE inhibitor drugsii. Aricept leads to increased levels of Acetylcholine iii. It is an ACH AGONISTiv. Sarin: ACHE inhibitor (blocks acetylcholinesterase, but has killed many people because it is a much higher dose)v. What happens when ACH is uncontrolled? vi.i. What happens when ACH is uncontrolled? i. Initial symptoms following exposure to sarin are a runny nose, tightness in the chest and constriction of the pupils. ii. *Block ACH receptors= Atropine: ACH receptor