1. Dendrites - after receiving stimulus from presynaptic cells
2. Non-spiking neurons
1. very small
2. high membrane resistance
3. vertebrate retina, insect nervous system
3. Cable properties of axon/dendrite - signal will decay over distance
1. resistance of cytoplasm -some resistance does exist
2. resistance of membrane -high but finite
4. Length/Space Constant - distance a singnal will travel along an axon before 63% of its potential is gone

S_R_m / R_i + R_o S- length/space constant

R_m-membrane resistance

R_i -resistance inside cell

R_o-resistance extracellular space
 
 
 
 

1. Most common spread of signal
2. Uses electrotonic spread to depolarize membrane - 5x as much as is needed to provide a safety margin, reason cold block will stop an AP
3. Spreads only in one direction - due to Na⁺ channel inactivation

1. Measured using from muscle experiment - stim two places on nerve and record time difference between each stimulus
2. Factors
1. resistance of interior - increase axon size
2. membrane resistance - increase with myelination, decreases capacitance as well

1. Internodes -
1. Myelination - Glia wrap their membranes around areas of nerve
2. Increased resistance - due to myelination
3. Lack voltage-gated Na⁺ channels
2. Nodes of Ranvier AP gets recharged here
1. No myelination
2. high concentration of V-gated Na⁺ channels
3. Diseases ex - MS - myelin sheath is destroyed so nerves no longer can send AP’s effeciently

1. Current passes directly (cell to cell)
2. Passive spread - signal weakens over distance
3. Very rapid
4. Generally passes well in both directions
5. Crayfish nervous system, vertebrate retina, cardiac muscle

1. Found between nerves and at neuromuscular junction
2. Steps
1. AP reaches axon terminal
2. V-gated Ca²⁺ and Na⁺ channels open
3. Ca²⁺ allows neurotransmitter release
4. Neurotransmitter binds to receptors on post-synaptic membrane
3. Can involve multiple transmitters - Fast and slow transmission can occur at the same synapse at the same time
4. Fast
1. synthesis and packaging at nerve terminal
2. affects ionic current on post synaptic side
3. short term - hundreds of ms
5. Slow
1. synthesis and packaging in cell body
2. affects intracellular messengers via G-proteins
3. long lasting (sec-hours)
6. Can be excitatory or inhibitory

1. Structure
1. Active Zones - areas where there is an increased concentration of synaptic vessicles
2. junctional folds - folds in the opposing postsynaptic membrane (muscle) just across from the active zones, holds released neurotransmitter
3. synaptic cleft - space between pre- and postsynaptic membrane - transmitter (ACh) is released into this space.
1. enzymes (eg Acetylcholinesterase) - breakdown neurotransmitter
2. uptake - by presynaptic neuron or glia
2. Potentials (end plate potentials)
1. effect of neurotransmitter binding receptor on postsynaptic side (depolarization)
2. Channels open - current flows through channels, type of current and direction depends on selectivity of channel
3. blocked at receptor level curare (blow dart poison) binds to ACh receptor
3. Reversal Potential (E_rev) potential at which current will reverse direction of flow
1. same as equilibrium potential (E_x) -find using Nernst or Goldman
2. V_m will never go past E_rev in cell - when V_m = E_rev, then no more ions flow, so V_m can no longer change
4. Postsynaptic excitation and inhibition
1. Excitation (epsp) - increases chances of an AP
2. Inhibition (ipsp) - decreases chances of an AP
3. Determined by receptor - the neurotransmitter itself does not determine whether the postsynaptic membrane is excited or inhibited, but the ions which flow through the receptor/channel
5. Presynaptic inhibition Draw picture
1. inhibition at the presynaptic terminal
2. presynaptic membrane is hyperpolarized - input from another neuron, prevents NT release
3. postsynaptic membrane is not affected

1. NT binds to receptor linked to G-protein affects second messengers
1. G-protein open an ion channel
2. Other cell processes are affected mRNA, protein synthesis
3. Longer lasting effects
4. involved in synaptic plasticity and LTP - changes in proteins, receptor levels, make a synapse stronger or weaker

1. Basic unit/package of NT release -10,000 molecules of ACh/synaptic vessicle
2. MEPP (miniature endplate potential) - the amount of potential change caused by one synaptic vessicle
3. Probability of release - increased by depolarization, greater depolarization (more frequent AP)= greater # of vessicles released
4. Ca²⁺ required for release

1. No AP required for release
2. Amount of NT released directly related to intensity of stimulus

1. Application must cause same response as stimulating the presynaptic side
2. Substance must be released by presynaptic membrane when stimulated
3. Effects must be blocked by same agents which block natural transmission

1. Released into extracellular fluid
2. Affect many postsynaptic neurons