Communication between neurons (chemical)

Action potential

Saltatory conduction Passive current is much faster within myelin (speed of conduction can range from 1 to 100 meters/sec 2. Na/K pumps only in the nodes (saves energy)

Action potential – super-threshold depolarization in nearby regions Saltatory conduction Action potential – super-threshold depolarization in nearby regions Opens Na+ channels

Action potentials in a non-mylinated neuron Relatively slow Consumes more energy (need more channels along the membrane)

Action potentials characteristics (regardless of myelin): All or none (always same shape and size) Does not diminish with distance (or splits along the axon) until it reaches the terminal buttons that form synapses with the target neuron

The Action Potential is All or None So how can we differentiate btw strong and weak stimulations? The rate law The strength of the signal = frequency of Action potentials NOT magnitude of potential

Decreases with distance Passive conductance (graded potentials) Decreases with distance Rate of decrease depends on properties of axon (like diameter)

Graded Potential vs. Action potential All or none: fixed magnitude Larger for stronger triggers Strength Active Does not decay. Saltatory conduction Unidirectional (from soma to axon) Passive Decays with distance from source Multi directional conduction

The synapse Presynaptic neuron vs. Postsynaptic neuron The junction between the terminal button of one neuron and the membrane of another neuron (~20 nm) Presynaptic neuron vs. Postsynaptic neuron

Types of synaptic connections Axo-dendritic Axo-somatic Axo-axonic

Terminal button (structure)

The action potential has reached the terminal button. Now what? Voltage dependent calcium (Ca2+) channels Action potential -> depolarization. Opens Ca2+ ion channels Without Ca2+ - there will be no release of neurotransmitter

Each action potential  release of a fixed # of vesicles Exocytosis - Followed by recycling

Exocytosis

Stages in the process of neurotransmitter release: Docking vesicles containing neurotransmitters An action-potential arrives, and causes voltage-gated Calcium-channels to open (Ca2+ enters the cell) Ca2+ causes fusion of the vesicles with the cell membrane Neurotransmitter in vesicle is expelled (exocytosis) Vesicle membrane either fuses with cell membrane or closes back inside the cell

Now that we have neurotransmitters in the synapse….. Neurotransmitters bind to postsynaptic receptors Open/close neurotransmitter-dependent channels: 1) Direct 2) Indirect

Post-synaptic receptors

How does it affect the cell? Post-synaptic Potential Excitatory postsynaptic potential - depolarization Inhibitory postsynaptic potential - hyperpolarization

Excitatory Post-Synaptic Potential (EPSP)

Inhibitory Post-Synaptic Potential (IPSP)

What determines whether the post-synaptic potential is Excitatory or Inhibitory is NOT the neurotransmitter !!! The same neurotransmitter can have an IPSP or EPSP effect on the target neuron. The ultimate effect depends on the target RECEPTOR and the channels it open !!!

Post-synaptic integration

Neural integration Axon hillock Summation by time Summation by space

A single cell can receive synaptic input from up to ~100,000 !!! Purkinje cell in cerebellum 150,000!! contacts

Neurotransmitter binds to postsynaptic receptors and can Influence neurotransmitter-dependent channels: 1) Direct 2) Indirect

neurotransmitter-dependent channels 1. Ionotropic Receptor 2. Metabotropic Receptors

neurotransmitter-dependent channels 1. Ionotropic receptor 2. Metabotropic Receptors

Inotropic Metabotropic Fast effect Only opens transmitter dependent channels Slow effect may open/close transmitter dependent channels

Sensory neuron Motor neuron Action potential Receptor potential Synaptic potential Action potential

Enzymatic deactivation Diffusion Removal of neurotransmitter from the synapse Reuptake Enzymatic deactivation Diffusion

Regulation of neurotransmitter release Autoreceptors (pre-synaptic) Usually inhibitory effect Presynaptic facilitation/inhibition Axoaxonic synapse

Important notes: IPSP does NOT necessarily mean inhibition of behavior Auto-receptors are pre-synaptic receptors that respond to the neurotransmitter the same cell released. They do not open ion channels on the post-synaptic cell Axo-dendritic and Axo-somatic synapses cause either IPSP or EPSP. Axo-Axonic synapses can regulate the amount of neurotransmitter that will be released. Inihibition => reduction in the amount of neurotransmitter eventually released Facilitation=> increase in the amount of neurotransmitter released.