Lec 3 - Conduction of action potential, Communication of Nervous System, and Integration of Neural Information Transfer

Local current flow (Fig 8.13)?

When an axon section depolarizes, positive charges move into adjacent sections of cytoplasm; on the extracellular surface, current flows toward the depolarized region.

Conduction of action potentials Step 1

A graded potential above threshold reaches the trigger zone.

Conduction of action potentials Step 2

Voltage-gated Na+ channels open and Na+ enters the axon.

Conduction of action potentials Step 3

Positive charge flows into adjacent sections of the axon by local current flow.

Conduction of action potentials Step 4

Local current flow from the active region causes new sections of membrane to depolarize.

Conduction of action potentials Step 5

The refractory period prevents backward conduction; loss of K+ from the cytoplasm repolarizes the membrane.

What does continuous entry of Na+ along the axon create?

An electrical signal whose strength remains constant over distance.

Which 3 regions are labeled along the conducting axon (Conduction of action potentials)?

Refractory region, active region, inactive region.

Which neurons conduct action potentials faster by size?

Larger neurons.

Which neurons conduct faster by myelination?

Myelinated neurons.

Why is conduction faster in myelinated neurons?

Resistance of the axon membrane to ion leakage out of the cell.

Define saltatory conduction.

Conduction that jumps between nodes of Ranvier; action potentials appear to jump from one node to the next.

Which part of a myelinated axon has voltage-gated Na+ channels?

Only the nodes of Ranvier.

What do demyelinating diseases do (Saltatory conduction)?

Reduce or block conduction when current leaks out of previously insulated regions between nodes.

What does current leak lead to in demyelination?

Reduced conduction and possible action potential failure (degenerated myelin sheath).

How do many chemicals alter conduction of action potentials?

By binding to the channel.

Which ECF ions affect electrical activity?

Ca2+ and K+.

Effect of hyperkalemia on a neuron?

Brings the neuron closer to threshold.

Effect of hypokalemia on a neuron?

Moves the neuron further from threshold.

Which ion is primarily responsible for resting membrane potential (Potassium and cell excitability)?

Potassium (K+).

Normal plasma [K+]?

3.5-5 mM.

Normokalemia: subthreshold vs suprathreshold stimulus?

Subthreshold graded potential does not fire an action potential; a suprathreshold stimulus fires one.

Hyperkalemia effect on cells (Potassium and cell excitability)?

Depolarizes cells; brings membrane closer to threshold so a normally subthreshold stimulus can trigger an action potential.

Hypokalemia effect on cells (Potassium and cell excitability)?

Hyperpolarizes cells; makes the neuron less likely to fire in response to a stimulus that would normally be above threshold.

Where do neurons communicate?

At synapses.

Electrical synapses: how do they pass signals?

Through gap junctions.

Electrical synapse signal direction?

Can be bi-directional.

What does an electrical synapse do for a network?

Synchronizes the activity of a network of cells.

Chemical synapses?

Use neurotransmitters that cross synaptic clefts.

Neurocrines include which 3 types?

Neurotransmitters, neuromodulators, neurohormones.

Ionotropic receptors?

Receptors that directly control ion channels.

Metabotropic receptors?

G protein-coupled receptors for neurotransmitters.

Which neurotransmitter does not bind a specific receptor?

NO (nitric oxide).

Acetylcholine (ACh) receptor family?

Cholinergic.

Nicotinic receptor (nAChR): type?

Ionotropic channel receptor (ICR) for Na+, K+.

Nicotinic receptor location?

Skeletal muscles, autonomic neurons, CNS.

Nicotinic agonist and antagonists?

Agonist: nicotine. Antagonists: curare, bungarotoxin.

Muscarinic receptor (M): type?

GPCR.

Muscarinic receptor location?

Smooth and cardiac muscle, endocrine and exocrine glands, CNS.

Muscarinic agonist and antagonist?

Agonist: muscarine. Antagonist: atropine.

Where and from what is ACh synthesized?

In axon terminals, from choline (from membrane phospholipids) and acetyl CoA (from the citric acid cycle).

Nicotinic receptors: where and what kind of channel?

On skeletal muscles and in the autonomic division of the PNS and CNS; monovalent cation channels (Na+ and K+).

Muscarinic receptors: where and what type?

In the CNS and on target cells for the autonomic parasympathetic division of the PNS; G protein-coupled receptors.

Where are amine neurotransmitters active?

In the CNS.

What are amines derived from?

A single amino acid.

Serotonin is derived from?

Tryptophan.

Histamine is derived from?

Histidine.

Dopamine, norepinephrine and epinephrine are derived from?

Tyrosine.

Which neurotransmitter do adrenergic/noradrenergic neurons secrete?

Norepinephrine.

Adrenergic receptors?

Bind norepinephrine and epinephrine; G protein-coupled receptors; alpha and beta classes.

Glutamate: effect and location?

Excitatory; CNS.

Name the two glutamate receptors listed.

AMPA receptor and NMDA receptor.

AMPA stands for?

Alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid.

NMDA stands for?

N-methyl-D-aspartate.

GABA: effect and location?

Gamma-aminobutyric acid; inhibitory; brain.

How does GABA inhibit target cells?

Hyperpolarizes them by opening Cl- gates.

Synaptic communication and neurotransmitter release Step 1

An action potential depolarizes the axon terminal.

Synaptic communication and neurotransmitter release Step 2

Depolarization opens voltage-gated Ca2+ channels, and Ca2+ enters the cell.

Synaptic communication and neurotransmitter release Step 3

Calcium entry triggers exocytosis of synaptic vesicle contents.

Synaptic communication and neurotransmitter release Step 4

Neurotransmitter diffuses across the synaptic cleft and binds receptors on the postsynaptic cell.

Synaptic communication and neurotransmitter release Step 5

Neurotransmitter binding initiates a response in the postsynaptic cell.

Classical model: what does Ca2+ bind?

Regulatory proteins, which initiate exocytosis.

Kiss-and-run pathway?

Vesicles fuse with presynaptic membrane to form a fusion pore; neurotransmitters pass through a channel.

What does cell-to-cell communication coordinate (Fig 8.19)?

Function, and maintains homeostasis (uses chemical and electrical signaling).

Ways neurotransmitter activity is terminated?

Diffusion away from the cleft; enzymatic breakdown; uptake into cells.

Enzyme that breaks down ACh?

Acetylcholinesterase (AChE).

Where are neurotransmitters taken up?

Presynaptic axon terminal and glial cells.

Synaptic communication and neurotransmitter termination Summary

Neurotransmitters return to axon terminals for reuse or go into glial cells; enzymes inactivate them; they diffuse out of the synaptic cleft.

Synthesis and Recycling of ACh Step 1

ACh is made from choline and acetyl CoA.

Synthesis and Recycling of ACh Step 2

In the synaptic cleft, ACh is rapidly broken down by acetylcholinesterase.

Synthesis and Recycling of ACh Step 3

Choline is transported back into the axon terminal by cotransport with Na+.

Synthesis and Recycling of ACh Step 4

Recycled choline is used to make more ACh.

Breakdown products of ACh?

Choline and acetate.

What indicates stimulus strength (Fig 8.21)?

Frequency of action potential firing.

Weak vs strong stimulus (Fig 8.21)?

Weak stimulus releases little neurotransmitter; strong stimulus causes more action potentials and releases more neurotransmitter.

Which 2 coding types are labeled in Fig 8.21?

Population coding and frequency coding.

Divergence vs convergence?

Divergence: one presynaptic neuron branches to affect many postsynaptic neurons; convergence: many presynaptic neurons influence a smaller number of postsynaptic neurons.

Define synaptic plasticity.

A change of activity at the synapses.

Where does synaptic plasticity primarily occur?

In the CNS.

Duration of synaptic plasticity?

Short-term or long-term.

Effect of synaptic plasticity?

May enhance or reduce synaptic activity.

Slow synaptic potentials involve?

G-protein coupled receptors and second messengers.

Fast synaptic potentials involve?

Opening of ion channels.

EPSP?

Excitatory postsynaptic potential; depolarizing.

IPSP?

Inhibitory postsynaptic potential; hyperpolarizing.

Fast postsynaptic responses are mediated by?

Ion channels; neurotransmitters create rapid, short-acting fast synaptic potentials.

Slow postsynaptic responses are mediated by?

G protein-coupled receptors; neuromodulators create slow synaptic potentials and long-term effects.

Postsynaptic cell channels open leads to?

More Na+ in = EPSP (depolarization); more K+ out or Cl- in = IPSP (hyperpolarization).

Postsynaptic cell channels close leads to?

Less Na+ in or less K+ out = EPSP (depolarization).

Activated second messenger pathway result?

Modifies existing proteins or regulates synthesis of new proteins, giving a coordinated intracellular response.

Spatial summation?

Two or more neurons simultaneously fire and have an additive effect.

Postsynaptic inhibition?

Release of neurotransmitter is inhibitory instead of excitatory.

Temporal summation?

Graded potentials overlap in time and have an additive effect.

Temporal summation is…

Two graded potentials from one presynaptic neuron close together in time; if far apart, no summation (subthreshold); if close, they may sum and initiate an action potential.

Threshold and resting values? (Integration of synaptic Signaling)

Threshold -55 mV; resting potential -70 mV.

Spatial summation? (Integration of synaptic Signaling)

Currents from nearly simultaneous graded potentials combine; multiple presynaptic neurons give input on dendrites and cell body; several subthreshold signals sum to produce an action potential.

Spatial Summation steps?

1. Three excitatory neurons fire (each below threshold)

2. potentials arrive at the trigger zone together and sum to a suprathreshold signal

3. an action potential is generated.

What are the synapses in dendritic spine?

Spine head and neck; excitatory synapses (red) and inhibitory synapses (blue).

What is synaptic inhibition?

1. An IPSP sums with two EPSPs to prevent an action potential

2. Summed potentials are below threshold, so no action potential at the trigger zone.

How can synaptic activity be modified?

Short term and long term; a modulatory neuron terminates on the presynaptic cell and modulates neurotransmitter release.