EXS 112 Exam 2: Neuron Basics and Neurotransmitters PDF

EXS 112 Exam 2 Objectives/Summaries Introduction & Organization of the Nervous System L6 L6-#1 Neuron, parts, functions Cell body: the main hub and nucleus, organelles, has general cell functions CNS-Nuclei, PNS-Ganglia Dendrites: receives signals, has a cytoplasm and vesicles Axon...

EXS 112 Exam 2 Objectives/Summaries Introduction & Organization of the Nervous System L6 L6-#1 Neuron, parts, functions Cell body: the main hub and nucleus, organelles, has general cell functions CNS-Nuclei, PNS-Ganglia Dendrites: receives signals, has a cytoplasm and vesicles Axons: generate action impulses to send out (APs) Connects to dendrites Collateral axons: branch to other/multiple cells Axon Hillock: where AP generates Neuron: Base cell w/ body, axon, dendrite Nerve: a bundle of axons- sensory/motor L6-#2 Sensory v Motor v Interneurons Sensory Neuron: Motor Neuron: 1. Receptors to CNS 1. Effectors out of CNS to 2. Unipolar PNS 3. Afferent 2. Somatic v1.Autonomic 1. Skeletal Smooth/Cardiac Muscles Muscles 2. Involuntary 2. Voluntary 3. 4. Located in PNS Sympathetic/Parasympathet ic Interneurons: 4. Ganglions 1. Integrates in CNS 2. Called association neurons L6-#3- Neuroglial Cells 1. Schwann Cells: In PNS, 1 cell/myelin sheath, speeds up impulse and less ion loss per impulse 1. Neurilemma (cytoplasm) 2. Myelin Sheath (Plasma Membrane) 3. Nodes of Ranvier 2. Oligodendrocytes: In CNS, 4. Wraps around multiple axons (white matter) 5. Makes myelin sheath 6. Can cause MS 3. Microglia: CNS, removes foreign objects, maintains healthy cell 7. Overactive= targets healthy cells= Parkinson's/Alzheimer's 4. Astrocytes: 8. Maintains extracellular environment, 9. Influences neuron to non-neuronal interactions (ex: Blood-Neuron), drugs have hard time treating meningitis-neural disease 10. Most abundant L6-#4 Blood Brain Barrier (BBB) 1. Blood capillaries are NOT porous 2. This prevents normal diffusion 3. Astrocytes: Regulates barrier, releases molecules for a controlled diffusion L6-#5 Depolarization, Repolarization, Hyperpolarization 1. Depolarization: Change to a (+) membrane potential, (+) Na enters= excitatory impulses 2. Repolarization: Change to (-) membrane potential, (+) K exits to ECM, inhibitory impulse 3. Hyperpolarization: Dip in (-) charge before resting membrane potential, too much (+) K removal, a bit too (-) for a little bit L6-#6 Na/K Movement to Action Potential How? Voltage-gated Channels a) Stimulus brings membrane to (-55) b) Na gates open, depolarizes (+) rapidly c) Positive feedback loop depolarizes to (+30) (AP!) d) K gates open, Na closes, start repolarization e) K out quickly, repolarization f) Hyperpolarization (K gates close via neg. feedback loop) g) Cell polarity back to resting membrane potential (-70) L6-#7 Explain the All or None Law a) Stimulus strength is based on quantity, a strong stimulus does NOT change the speed of de/repolarization, voltage, or duration b) Voltage/duration are fixed, all or nothing=once process has started=action potential is going/created c) A strong stimulus will just recruit more quantity of axons= more action potentials *All neurons require a refractory period to “recharge”/to get back to resting membrane potential Absolute: No axon response to stimulation Relative: During hyperpolarization, a strong stimulus could generate a new AP L6-#8 Why do Myelin Sheaths make Conduction Quicker? 1. Action potentials generated @ nodes w/ Na/K channels 2. Na/L cannot diffuse through myelin= no ion loss 3. Allows Saltatory Conduction: Action potentials can jump from node to node 1. Jumping is faster than traveling down the whole membrane, 2. Jumping reduces distance, and can go further (longer distances) with a fixed AP duration L6- #9 Axons Axonal Transport: moving proteins/organelles from cell body to axon ends Fast: membrane vesicles Slow: Proteins/Filaments Anterograde Transport: Away from cell body Retrograde Transport: Toward cell body (viruses) L6-#10 Neuron Structures Unipolar- Sensory Neurons, T-shaped Bipolar- Olfactory/Optical, Two Processes Multipolar- Motor Neurons, Several dendrites, Standard Random: Axon Regeneration: sometimes in PNS The cell body must still be alive Schwann cells create regeneration tube Microglia phagocytosis of broken fibers Synapses and Neurotransmitters L7 L7-#1Defining a Synapse Synapse: the connection between a neuron and its target cells In CNS: usually neuron to neuron, pre/post synapse Vs In PNS: usually to a muscle, gland, or effector Synapses are Electrical or Chemical L7-#2 Electrical vs Chemical Synapses Electrical Chemical a) Gap junction cells a) Neurotransmitters a) Ex: muscle cells a) Neurons b) Synaptic cleft: forms from pre/post synapse c) Vesicles release neurotransmitters and cross the ECM L7- #3 Release vs Action of Chemical Synapses Release Action (c/e exchangeable) a) When AP reaches the axon a) Neurotransmitter across cleft and end binds to receptor protein b) Opens voltage-gated Ca b) Receptor stimulates chemical channels regulated gates c) Ca triggers (pre-packed) c) EPSP (excitatory): (+) membrane vesicles with neuros to by entering Na/Ca/depolarization membrane d) Exocytosis into cleft, and d) OR post receives e) IPSP (Inhibitory): (-) membrane by *More AP (a)= more Ca (b)= removing K/Cl or more exocytosis (d)/stimulation re/hyperpolarization of post L7-#4 Channels- once neurotransmitters bind to receptors (in post) Ligand-Gated VS G-Protein Coupled Ligand=neurotransmitter “indirect” ”molecule-gated channel” “GTP gated channel” A, B, C= Secondary Messenger Methodology a) Channel gates open when ligand binds directly to protein channel, a) Neurotransmitter binds to receptor ex: Acetylcholine + receptor b) Receptor activates molecule to go to channel (GTP) c) Molecule (GTP) opens channel ________________________________________________ ________ Ex: dopamine->dopamine receptor, activates GTP, GTP opens channels Types of Receptors: *can be EPSP(+): closes K channel, excites, in skeletal muscles Agonist: Stimulates, ups activity and binding OR VS IPSP(-): opens K channel, inhibits, in heart Antagonist: Inhibits, lowers binding L7-#5 ETC on EPSP and IPSP AP: -Triggers after voltage reaches the threshold -The sum of EPSPs/IPSPs will either add up to an AP or not 2 Types of Sums: Spatial Summation VS Temporal Summation Simultaneous signals from Repeated signal inputs multiple inputs from the same input Ex: Different inputs at the Ex: The same input sends a same time add up to an AP signal at different times close together to add up to an AP L7-#6 Neural Pathways Divergent VS Convergent Neurons with collateral Lots of pre-synaptic axons axon branches (branches Connect to only 1 post- to multiple cells, L6#1) synaptic axon Only 1 pre-synaptic axon L7-#7 Synaptic Plasticity: neurons adapting from the amount of stimulus to strengthen or reduce synaptic activity for that stimulus (basically add more or reduce channels based on stimulus use) Long-Term Potentiation (LTP) VS Long-Term Depression (LTD) Improve synapse Reduce efficiency from efficiency from repeated underused stimulus use of a stimulus Ex: less Ca release Ex: more Ca release Releases Common in hippocampus endocannabinoids to and memory suppress more More channels= more neurotransmitters (+ efficiency feedback loop) Less channels= less efficient L7-#8 Synaptic Inhibition inhibitory neurotransmitters: hyperpolarize post-synapse which means… a) Ca (+) excitatory channels close b) Decreased/no excitatory neurotransmitters released c) Post-synapse has no AP d) Excitatory neurotransmitters have to work hard to depolarize the synapse back *All A-D cause Synaptic Inhibition Clinical Application: Opioids Reduces pain via inhibiting neurotransmitters, which means they inhibit the release of excitatory neurotransmitters, like Substance P, which relays pain to post-synapse L7-#9 Neurotransmitters (1) Glutamate VS GABA 1. CNS 1. Inhibitory neurotransmitter 2. Excitatory neurotransmitter, ups 2. Inhibits/decreases nerve signaling synaptic plasticity (efficiency) 3. Releases Cl- 3. Releases Na+ Clinical Application: Clinical Application: Too little/low: Overexcited neurons= anxiety, autism, schizo Too much: Too much/high: Need a lot of excitatory a) overactive neurons=damaged neuros to compensate= addiction to neurons= Alzheimer’s excitatory b) OR overactive neurons=throw off *GABA can treat anxiety, used as an anti- dopamine= Parkinson’s convulsant/sedative L7-#10 Neurotransmitters (3)- Acetylcholine 1. Located @ NMJ (neuromuscular junctions)- between muscles and neurons 2. PNS 3. Muscle contractions Clinical Application: If Blocked by Antagonists= inhibits muscle contraction Ex: Curare: Blocks Ach receptors, muscle relaxer  L7-#11 Neurotransmitters (4) Monoamines Monoamine Oxidase Inhibitors (MAO) 1. Amino acids as Blocks/prevents neurotransmitters monoamines from 2. Has an amine group degrading in synaptic cleft Catecholamines Serotonin 1. Dopamine Mood Clinical Application: 2. Epinephrine Appetite Treats 3. Norepinephrine *Behavior =(stress/pleasure) depression/panic/anxiety L7-#12 Neurotransmitters (5) Dopamine 1. In midbrain Nigrostriatal System Mesolimbic System 1. Motor movement 1. Emotional rewards Clinical Application: Clinical Application: Degradation of Overactive dop/receptors= dop=overstimulated Parkinson’s=tremors, responses= Schizophrenia motor dysfunction Duality of Dopamine: Treat with MAOs Treating 1 may lead to other disease/symptoms L7-#13 Neurotransmitters (6) Norepinephrine PNS CNS 1. Sympathetic neurons 1. Stimulates brain neurons (autonomic) 2. Stimulates behavior 2. Has background contraction (ex: heart) Clinical Application: Amphetamines: stimulates norepinephrine pathways in the brain Treats depression Side effects: Raises BP, Raises HR, Jitters b/c of stimming sympathetic PNS