Action Potentials

Action Potentials and Impulse Conduction

Excitable tissues

muscle

nerve

Graded potentials

properties

proportional to magnitude of triggering event

show decremental decay and propagation

can be depolarizing or hyperpolarizing

can be summed

important examples

postsynaptic potentials

receptor potentials

end-plate potentials

pacemaker (ramp) potentials

Action potentials

terminology

polarization

depolarization

hyperpolarization

repolarization

threshold potential

channel gating

types

voltage-gated channels

chemical-messenger gated channels [ligand-gated channels]

gates are all-or-nothing

depolarization results from opening voltage-gated Na⁺ channels

Na⁺ permeability increases to 600 × K⁺ permeability

duration 0.5 msec

closing of inactivation gates

repolarization results from opening voltage-gated K⁺ channels

K⁺ permeability increases to 300 × Na⁺ permeability

Na⁺ channels return to original configuration

K⁺ channels close

Na⁺- K⁺ pump restores ion concentration gradients

propagation

role of the axon hillock

conduction by local current flow

nondecremental

saltatory conduction

myelination

multiple sclerosis

refractory period

role of the Na⁺ activation gates

all-or-nothing law

Synapses

information is transmitted by nerve action potentials through a succession of neurons

along the way, the impulse may be

blocked in its transmission

changed from a single impulse into repetitive impulses

integrated with other impulses into intricate successive neurons

two types of synapses

electrical

direct, open fluid channels (gap junctions)

chemical

neurotransmitter substance

membrane receptor proteins

unidirectional transmission

synaptic morphology

presynaptic neuron

synaptic knob

synaptic vesicles

neurotransmitter substance

postsynaptic neuron

subsynaptic membrane

synaptic cleft

mechanism of transmitter release

voltage-gated calcium channels

influx of calcium ions

synaptotagmin

exocytosis of synaptic vesicles

function of postsynaptic receptor proteins

receptor proteins

binding component

ionophore component

ion channels

cation channels (Na⁺) — excitatory

anion channels (Cl^-) — inhibitory

second-messenger activator

G-proteins

three components — α, β, & γ

functions of α component:

1. opening specific ion channels

2. activation of cAMP or cGMP

3. activation of intracellular enzyme(s)

4. activation of gene transcription

exocytosis of synaptic vesicles

excitatory synapses

mechanisms

opening sodium channels

depressed conduction through chloride or potassium channels, or both

changes in metabolism of the cell

excitatory postsynaptic potential (EPSP)

disorder of excitatory synapse: Parkinsonism

dopamine deficiency

treatment with L-dopa

inhibitory synapses

mechanisms

opening chloride channels

increased conduction through potassium channels

activation of receptor enzymes

inhibitory postsynaptic potential (IPSP)

action of strychnine

competes with glycine at postsynaptic receptor

no IPSPs generated

results in unchecked excitatory input

action of tetanus toxin

prevents release of gamma-aminobutyric acid (GABA)

results in unchecked excitatory input

presynaptic inhibition

presynaptic inhibition in the crayfish

Permission for use pending from Dr. Zen Faulkes at Marmorkrebs.org

modulation of synaptic transmission

desensitization

homosynaptic plasticity

heterosynaptic plasticity

pharmacological intervention

synaptic delay

Small-Molecule, Rapidly Acting Transmitters

Class I

acetylcholine

Class II: Amines

norepinephrine

epinephrine

dopamine

serotonin

histamine

Class III: Amino acids

gamma-aminobutyric acid (GABA)

glycine

glutamate

aspartate

Class IV

nitric oxide (NO)

Neuropeptide, Slowly Acting Transmitters
or Growth Factors

Hypothalamic-releasing hormones

thyrotropin-releasing hormone

gonadotropin-releasing hormone

somatostatin

Pituitary peptides

adrenocorticotropic hormone

β-endorphin

α-melanocyte-stimulating hormone

prolactin

luteinizing hormone

thyrotropin

growth hormone

vasopressin

oxytocin

Peptides that act on gut and brain

leucine enkephalin

methionine enkephalin

substance P

gastrin

cholecystokinin

vasoactive intestinal polypeptide (VIP)

nerve growth factor (NGF)

brain-derived neurotropic factor

neurotensin

insulin

glucagon

From other tissues

angiotensin II

bradykinin

carnosine

sleep peptides

calcitonin

neurotransmitter removal from the synaptic cleft

cholinesterase (AChase)

monoamine oxidase (MAO)¹

catalyzes degradation of serotonin, epinephrine, & norepinephrine

MAOIs

catechol-O-methyltransferase (COMT)

catalyzes degradation of catecholamines (dopamine, epinephrine, & norepinephrine)

also important in the metabolism of catechol drugs used in the treatment of hypertension, asthma, & Parkinsonism

COMTIs

the grand postsynaptic potential (GPSP)

temporal summation

spatial summation

Go to beginning

Questions for thought
1.		What is an ion gradient? How is an ion gradient established across a membrane? How does an ion gradient across a membrane result in an electrical potential?
2.		What is the role of the Na⁺,K⁺–ATPase in establishing the electrical potential? Describe how the Na⁺,K⁺–ATPase works.
3.		Describe an action potential. What initiates it? How does it move along the membrane?
4.		Explain the all-or-nothing principle. What is the result of a subliminal (subthreshold) stimulus? What is the result of a stimulus with a magnitude that exceeds threshold?
5.		Diagram and label a synapse. What is the role of synapses?
6.		What are neurotransmitters? Why are they necessary? After their release, how are they removed from the synaptic cleft? What would happen if they were not removed from the synaptic cleft?
7.		What is the difference between a voltage-gated ion channel and a ligand-gated ion channel? What different roles does each play? How does a G-protein–coupled receptor work?

Go to beginning