Copyright © 2009 Allyn & Bacon How Neurons Send and Receive Signals Chapter 4 Neural Conduction and Synaptic Transmission
Copyright © 2009 Allyn & Bacon The Neuron’s Resting Membrane Potential Membrane – difference in electrical charge between inside and outside of cell Inside of the neuron is negative with respect to the outside Resting membrane potential is about – 70mV Membrane is polarized (carries a charge)
Copyright © 2009 Allyn & Bacon Ionic Basis of the Resting Potential Factors contributing to even distribution of ions (charged particles) Random motion – particles tend to move down their concentration gradient Electrostatic pressure – like repels like, opposites attract Factors contributing to uneven distribution of ions Selective permeability to certain ions Sodium-potassium pumps
Copyright © 2009 Allyn & Bacon Ions Contributing to Resting Potential Sodium (Na + ) Chloride (Cl - ) Potassium (K + ) Negatively charged proteins (A - ) Found primarily within the neuron
Copyright © 2009 Allyn & Bacon The Neuron at Rest Ions move in and out through ion-specific channels K + and Cl - pass readily Little movement of Na + A - don’t move at all, trapped inside
Copyright © 2009 Allyn & Bacon The Neuron at Rest (continued) Na + is driven in by both electrostatic forces and its concentration gradient K + is driven in by electrostatic forces and out by its concentration gradient Cl - is at equilibrium Sodium-potassium pump – active force that exchanges 3 Na + inside for 2 K + outside
Copyright © 2009 Allyn & Bacon The passive and active factors that influence the distribution of Na+, K+, and Cl – ions across the neural membrane The Neuron at Rest (continued)
Copyright © 2009 Allyn & Bacon Generation and Conduction of Postsynaptic Potentials (PSPs) Neurotransmitters bind at postsynaptic receptors These chemical messengers bind and cause electrical changes Depolarizations (making the membrane potential less negative) Hyperpolarizations (making the membrane potential more negative)
Copyright © 2009 Allyn & Bacon Postsynaptic depolarizations = an Excitatory PSP (EPSP) Postsynaptic hyper- polarizations = an Inhibitory PSP (IPSP) EPSPs make it more likely a neuron will fire; IPSPs make it less likely PSPs are graded potentials – their size varies
Copyright © 2009 Allyn & Bacon EPSPs and IPSPs Travel passively from their site of origination Decremental – they get smaller as they travel
Copyright © 2009 Allyn & Bacon Integration of PSPs and Generation of Action Potentials (APs) One EPSP typically will not suffice to cause a neuron to “fire” and release neurotransmitter – summation is needed In order to generate an AP (or “fire”), the threshold of activation must be reached near the axon hillock Integration of IPSPs and EPSPs must result in a potential of about -65mV in order to generate an AP
Copyright © 2009 Allyn & Bacon Integration Adding or combining a number of individual signals into one overall signal Temporal summation – integration of events happening at different times Spatial summation – integration of events happening at different places
Copyright © 2009 Allyn & Bacon Spatial summationTemporal summation
Copyright © 2009 Allyn & Bacon The Action Potential All-or-none – when threshold is reached the neuron “fires” and the action potential either occurs or it does not When threshold is reached, voltage- activated ion channels are opened
Copyright © 2009 Allyn & Bacon The Action Potential (continued) The opening and closing of voltage-activated sodium and potassium channels during the three phases of the action potential
Copyright © 2009 Allyn & Bacon Refractory Periods Absolute – impossible to initiate another action potential Relative – harder to initiate another action potential Prevent the backwards movement of APs and limit the rate of firing
Copyright © 2009 Allyn & Bacon Conduction in Myelinated Axons: Saltatory Conduction Passive conduction (instant and decremental) along each myelin segment to next node of Ranvier New action potential generated at each node Instant conduction along myelin segments results in faster conduction than in unmyelinated axons
Copyright © 2009 Allyn & Bacon Synaptic Transmission of Chemi- cal Signals: Structure of Synapses Most common Axodendritic – axons on dendrites Axosomatic – axons on cell bodies Dendrodendritic – capable of transmission in either direction Axoaxonic – may be involved in presynaptic inhibition
Copyright © 2009 Allyn & Bacon Synthesis, Packaging, and Transport of Neurotransmitter Molecules Neurotransmitter molecules Small Synthesized in the terminal button and packaged in synaptic vesicles Large Assembled in the cell body, packaged in vesicles, and then transported to the axon terminal
Copyright © 2009 Allyn & Bacon Release of Neurotransmitter (NT) Molecules Exocytosis – the process of NT release The arrival of an AP at the terminal opens voltage-activated Ca 2+ channels The entry of Ca 2+ causes vesicles to fuse with the terminal membrane and release their contents
Copyright © 2009 Allyn & Bacon Activation of Receptors by NT Molecules Released NT molecules produce signals in postsynaptic neurons by binding to receptors Receptors are specific for a given NT Ligand – a molecule that binds to another A NT is a ligand of its receptor
Copyright © 2009 Allyn & Bacon Receptors There are multiple receptor types for a given NT Ionotropic receptors – associated with ligand-activated ion channels Metabotropic receptors – associated with signal proteins and G proteins
Copyright © 2009 Allyn & Bacon Ionotropic Receptors NT binds and an associated ion channel opens or closes, causing a PSP If Na + channels are opened, for example, an EPSP occurs If K + channels are opened, for example, an IPSP occurs
Copyright © 2009 Allyn & Bacon Metabotropic Receptors Effects are slower, longer-lasting, more diffuse, and more varied (1) NT 1 st messenger binds. (2) G protein subunit breaks away. (3) Ion channel opened/closed OR a 2 nd messenger is synthesized. (3) 2 nd messengers may have a wide variety of effects.
Copyright © 2009 Allyn & Bacon Ionotropic and Metabotropic Receptors
Copyright © 2009 Allyn & Bacon Reuptake, Enzymatic Degradation, and Recycling As long as NT is in the synapse, it is active – activity must somehow be turned off Reuptake – scoop up and recycle NT Enzymatic degradation – a NT is broken down by enzymes
Copyright © 2009 Allyn & Bacon Amino Acid Neurotransmitters Glutamate – Most prevalent excitatory neurotransmitter in the CNS GABA Most prevalent inhibitory NT in the CNS
Copyright © 2009 Allyn & Bacon Pharmacology of Synaptic Transmission Many drugs act to alter neurotransmitter activity Agonists – increase or facilitate activity Antagonists – decrease or inhibit activity A drug may act to alter neurotransmitter activity at any point in its “life cycle”
Copyright © 2009 Allyn & Bacon
Agonists – Two examples Cocaine – catecholamine agonist Blocks reuptake – preventing the activity of the neurotransmitter from being “turned off” Benzodiazepines – GABA agonists Binds to the GABA molecule and increases the binding of GABA
Copyright © 2009 Allyn & Bacon Antagonists – Two examples (continued) Atropine – Ach antagonist Binds and blocks muscarinic receptors Many of these metabotropic receptors are in the brain High doses disrupt memory Curare – Ach antagonist Bind and blocks nicotinic receptors, the ionotropic receptors at the neuromuscular junction Causes paralysis
Copyright © 2009 Allyn & Bacon