anatomy unit 14: synapse, neurotransmitters, and neural circuits

synapse

point where an axon terminal meets the next cell (another neuron, gland cell, muscle cell)

neuron to neuron synapse

an action potential arrives at the end of the axon of the presynaptic neuron; it releases neurotransmitter; and the postsynaptic neuron responds to it

electrical synapses

how it works: direct physical contact between cells-links the cytoplasm of adjacent cells. is liked by gap junctions (connexons) that lets ions pass

where: parts of the brain, the eye, ciliary ganglia, cardiac muscle cells; also between some neurons, neuroglia, and single unit smooth muscle

advantage: must faster - no delay for release, diffusion, and binding of neurotransmitter

disadvantage: cannot integrate information

chemical synapse

how it works: a signal crosses a gap by chemical neurotransmitters. the two cells do not touch

where: most between neurons; neuromuscular junction

advantage: can integrate information (allows decision making)

disadvantage: slower because of synaptic delay

synaptic cleft

gap between neurons

discovered by Ramón y Cajal through histological observations

otto loewi

in 1921 demonstrated that neurons can communicate by releasing chemicals

flooded exposed hearts of two frogs with saline

stimulated vagus nerve of first frog and its heart flowed

removed saline from first frog and found it slowed heart of second from

acetylcholine

the first known neurotransmitter

first known as Vagusstoff (vagus substance)

synaptic celft

gap between presynaptic neuron and postsynaptic neuron; typically only 20 nm wide

axon terminal of presynaptic neuron

contains synaptic vesicles containing neurotransmitter

many vesicles are docked on releases of sites on plasma membrane in the axon terminal ready to release neurotransmitter

postsynaptic neuron’s membrane

contains a postsynaptic density of neurotransmitter receptors and ion channels

ligand-gated ion channels

open wide when the neurotransmitters bind to them

synaptic delay

happens because cells don’t touch

.2-.5 msec occurs between the arrival of the action potential at the terminal and its effect on the postsynaptic membrane

happens because the neurotransmitter must be released, diffuse across the cleft, bind to a receptor, and cause the receptor to open an ion channel

monosynaptic reflexes

involves only one synapse

faster

polysynaptic reflexes

involves multiple synapses

slower

synaptic fatigue

occurs when neurotransmitters cannot recycle fast enough to meet demands of intense stimuli

excitatory neurotransmitter

depolarizing

inhibitory neurotransmitter

hyperpolarizing

acetylcholine

formed from acetic acid and choline

neurotransmitters affect the cell directly by binding onto a plasma membrane receptor

amino acids

include glycine, glutamate, aspartate, and y-aminobutyric acid

neurotransmitters affect the cell directly by binding onto a plasma membrane receptor

monoamines (biogenic amines)

synthesized from amino acids

Ex: serotonin and the catecholamines epinephrine, norepinephrine, and dopamine

how they act: indirectly: second-messenger system (G protein)

catecholamines

Monoamines

are derived from the amino acid tyrosine

gases

nitric oxide and carbon monoxide; synthesized as needed rather than stored in vesicles.

These gasses affect cells by diffusing into a cell and affecting intracellular enzymes

Neuropeptides

chains of 2-40 amino acids; Stored in large secretory granules (dense-core vesicles)

• Some also function as hormones or neuromodulators

Ex: cholecystokinin (CCK) and endorphins; indirect effect

serotonin

a CNS neurotransmitter that affect attention and emotional states. decreased production may be responsible for some cases of severe chronic depression, treated with selective serotonin reuptake inhibitors such as prozac and paxil

Norepinephrine

released at adrenegic synapses; excitatory and depolarizing; widely distributed in the brain and parts of the ANS

involved in alertness and automatic activity

Dopamine

a CNS neurotransmitter that may be excitatory or inhibitory and is used for movement control.

Parkinson’s disease and cocaine use

damage to dopamine-producing neurons happens with this

cocaine

blocks dopamine removal from the synapse, increasing the postsynaptic effect (the high) and causing down-regulation of dopamine receptors

endorphines

relieve pain perception by inhibiting the release of the neuropeptide substance P at synapses that relay pain sensations

excitatory cholinergic synapse

acetylcholine is the neurotransmitter

1. an action potential depolarizes the axon terminal and opens voltage gated Ca 2+ channels

2. Ca 2+ enters and triggers exocytosis of the vesicles holding ACh

3. ACh diffuses across the cleft and binds to ligand-gated Na+ channels on the postsynaptic cell, which open; Na+ diffuses in

4. Na+ entry depolarizes the cell, producing an (excitatory) postsynaptic potential

5. if strong enough, the depolarization spreads to the trigger zone and reaches threshold, triggering an action potential

cholinergic synapse

specialized junction between a neuron and another cell (such as another neuron or a muscle fiber) that uses acetylcholine (ACh) as its primary neurotransmitter

an inhibitory GABA-ergic synapse

an amino acid neurotransmitter

an action potential triggers the release, and the receptors are linked the chlordie channels

gaba opens the Clc channels. there is more Cl outside than inside, so Cl enters and hyperpolarizes the postsynaptic membrane

the postsynaptic neuron is inhibited - less likely to create action potential

excitatory adrenergic synapse

Norepinephrine is the neurotransmitter

Monoamines and neuropeptides bind to G-protein coupled receptors on postsynaptic membrane

• Activate second-messenger systems such as cyclic AMP (cAMP)

• Slower to respond than cholinergic and GABA-ergic synapses

• Has advantage of enzyme amplification

cessation of the signal

it is important not only to stimulate postsynaptic cell but also to turn off the stimulus

to end the cell the presynaptic cell stops releasing neurotransmitter

the neurotransmitter already in synapse is cleared in various ways

neurotransmitter degradation

enzyme in synaptic cleft breaks down neurotransmitter

example acetylcholinesterase breaks ACh down into acetate and choline

Reuptake

neurotransmitter or its breakdown products reabsorbed into axon terminal

example: choline from ACh recycled to make new ACh

monoamine oxidase

helps break down certain monoamines. MAO inhibitors (MAOIs) are a class of antidepressants that interfere with this enzyme

diffusion

neurotransmitters or its breakdown products simply diffuse away from synapse into the nearby ECF

Neuromodulators

chemicals secreted by neurons that have long term effects on groups of neurons

may alter the rate of neurotransmitter synthesis, release, reuptake, or breakdown

may adjust sensitivity of postsynaptic membrane

Nitric oxide

a simple neuromodulator

gas that enters postsynaptic cells and activates second messenger pathways (for example, relaxing smooth muscle)

neuropeptides

chains of amino acids that can act as neuromodulators

enkephalins and endorphins

neuropeptides that inhibit pain signals in the CNS - these neuropeptides are opioids

neural integration

the ability to process, store, and recall information and use it to make decisions

chemical synapses allow for decision making

brain cells are incredible well connected, allowing for complex integration

synaptic delay

makes information travel slower than it would if there was no synapse

excitatory postsynaptic potential (EPSP)

voltage change: from the RMP TOWARD threshold (depolarizing)

usual cause: Na+ flowing into the cell

neurotransmitters: Glutamate and aspartate in brain cells

Inhibitory postsynaptic potential (IPSP)

voltage change: more negative than at rest (hyperpolarizing)

usual cause: Cl- entering or K+ leaving the cell

neurotranmitters: Glycine and GABA

Summation

the process of adding up postsynaptic potentials and responding to their net effect

occurs in the trigger zone

Some incoming nerve fibers may produce EPSPs while others produce IPSPs – it will depend upon the movement of the ions into or out of the cell

• A neuron’s response depends on whether the net input is excitatory or inhibitory

• The balance between EPSPs and IPSPs enables the nervous system to make decisions

temporal summation

a single synapse generates EPSPs so quickly that each is generated before the previous one fades

allows EPSPs to add up over time to a threshold voltage that triggers an action potential

spatial summation

EPSPs from several different synapses add up to threshold at an axon hillock

Simultaneous input from multiple presynaptic neurons required for the postsynaptic neuron to fire

faciliation

a process in which one neuron enhances the effect of another

presynaptic faciliataion

occurs when one presynaptic neuron enhances one another

increases necessary synaptic transmission

example: facilitating neuron releases serotonin which makes voltage-gated calcium channels in axon terminal stay open longer

presynaptic inhibition

occurs when one presynaptic neuron suppresses another one

reduces or halts unwanted synaptic transmission

example: inhibition neuron releases GABA which prevents voltage gated calcium channels in axon terminal from opening and so little or no neurotransmitter is released

neural coding

converting stimulus information into meaningful pattern of action potentials

labeled line code

mechanism for transmitting qualitative information (type of stimulus)

depends on which neurons fire; for example, optic nerve input labeled as light

quantitative information

is encoded by firing frequency: weak stimuli cause a slower rate of action potentials, strong stimuli a higher frequency

all of non law

the strength of each action potential does not change with stronger stimuli - only the frequency changes

heavy metal poisoning

cause: chronic exposure to heavy metals damages neuroglia and causes demyelination

key facts: axons irreversible deteriorate

diptheria

cause: a bacterial toxin damages Schwann cells and destroys PNS myelin sheaths

key factors: Can lead to fatal paralysis. rare, thanks to the vaccine DT and DTaP

Multiple sclerosis

cause: autoimmune, inflammation of nerves triggered by immune cells (probably triggered by a virus or defective gene)

key factors: demyelination in the CNS; affects vision, speech, balance, and motor coordination. treated with corticosteroids and interferon to slow progression

Guillain-Barré syndrome

cause: autoimmune, triggered by a virus

key factors Demyelination disease affecting peripheral nerves

Sensation of weakness or tingling of legs that spreads to arms

• Progression of disease leads to paralysis (diaphragm also affected)

• Most fully recover, but some continue to have residual weakness