Nervous System

AP Biology Chap 48

Neuron

The basic structural unit of the nervous system

The job of the neurons

Neurons transfer long-distance information via electrical signals and usually communicate between cells using short-distance chemical signals.

• The higher order processing of nervous signals may involve clusters of neurons called ganglia or most structured groups of neurons organized into a brain.

Types of neurons

• Sensory (afferent) – receive stimulus

• Motor (efferent) stimulate effectors which are target cells, muscles, sweat glands, stomach, etc.

• Association (interneurons) located in spinal cord or grain integrate or evaluate impulses for appropriate responses.

• The transmitting cell is called the presynaptic cells

• The receiving cell is the postsynaptic cell

Neuron Structure

• Cell body which contains the nucleus and organelles and numerous extensions

• Dendrites receive signals• Axon longer, transmits signals• Ends of axons end in synaptic terminals

which release neurotransmitters across a synapse

• Glial cells nourish and support the neurons

Fig. 48-4

Dendrites

Stimulus

Nucleus

Cellbody

Axonhillock

Presynapticcell

Axon

Synaptic terminalsSynapse

Postsynaptic cellNeurotransmitter

Direction of impulse

Glial Cells• Nourish neurons

• Insulate axons

• Regulate the extracellular fluid around the neuron

Nerve conduction

• In order to conduct an electrical nerve impulse, a voltage or membrane potential, exists across the plasma membrane of all cells.

• For a typical non-transmitting neuron, this is called the resting potential and is between -60 and -80 mV.

Membrane Potential

• Principal cation inside of cell K

• Principle anion inside of cell:

negatively-charged proteins, amino

acids, PO4 and SO4. Symbol is A-.

Inside is NEGATIVE!

Outside of the cell

• Principal ion is Na+

• Outside is positive!

Measuring membrane potential

How is the membrane potential established?

• Ion channels

• Concentration of ions

• Size of particles (proteins too large – semipermeable nature of membrane)

• Na-K pump maintains Na outside and K inside

Fig. 48-6b

(b)

OUTSIDECELL

Na+Key

K+

Sodium-potassiumpump

Potassiumchannel

Sodiumchannel

INSIDECELL

What causes the generation of a nerve

signal?• Neurons and muscle cells are excitable

cells – they can change their membrane potentials due to gated ion channels* – can be chemically gated which respond to neurotransmitters or voltage-gated which respond to a change in membrane potential.

* Found only in nerve cells

• Upon receiving a stimulus, Na+  channels open and Na+ flows into the cells and thus they become more positive inside and

more negative outside and the charge on the membrane becomes depolarized.

• The stronger the stimulus, the more Na

gated Ion channels open.

Production of an Action Potential

• Once depolarization reaches a certain membrane voltage called the threshold level (-50 mv), more Na gates open and an action potential is triggered that results in complete depolarization.

• This stimulates neighboring Na gates, further down the neuron, to open. The action potential is an all or none event, always creating the same voltage spike once the threshold is reached.

Fig. 48-10-1

KeyNa+

K+

+50

Actionpotential

Threshold

0

1

4

51

–50

Resting potential

Mem

bra

ne

po

ten

tial

(mV

)

–100Time

Extracellular fluid

Plasmamembrane

Cytosol

Inactivation loop

Resting state

Sodiumchannel

Potassiumchannel

Depolarization

Undershoot

2

3

1

Notice, gates are closed!

Fig. 48-10-2

KeyNa+

K+

+50

Actionpotential

Threshold

0

1

4

51

–50

Resting potential

Mem

bra

ne

po

ten

tial

(mV

)

–100Time

Extracellular fluid

Plasmamembrane

Cytosol

Inactivation loop

Resting state

Sodiumchannel

Potassiumchannel

Depolarization

Undershoot

2

3

2

1

Notice, gates are closed!

Some Na+ gates open!

Fig. 48-10-3

KeyNa+

Na+ gates open!K+

+50

Actionpotential

Threshold

0

1

4

51

–50

Resting potential

Mem

bra

ne

po

ten

tial

(mV

)

–100Time

Extracellular fluid

Plasmamembrane

Cytosol

Inactivation loop

Resting state

Sodiumchannel

Potassiumchannel

Depolarization

Rising phase of the action potential

Undershoot

2

3

2

1

3

A lot of Na+ gates open!

• In response to the inflow of Na, the gated K channels begin to open, allowing K to rush to the outside of the cell. Na gates close. This creates a reverse charge polarization, (neg outside, positive inside) called repolarization.

Fig. 48-10-4

KeyNa+

K+

+50

Actionpotential

Threshold

0

1

4

51

–50

Resting potential

Mem

bra

ne

po

ten

tial

(mV

)

–100Time

Extracellular fluid

Plasmamembrane

Cytosol

Inactivation loop

Resting state

Sodiumchannel

Potassiumchannel

Depolarization

Rising phase of the action potential Falling phase of the action potential

Undershoot

2

3

2

1

3 4

Na closes, K opens

In fact more K ions go out than is actually needed to return to threshold, resulting in an increased negative charge inside called a hyperpolarization or undershoot.

This keeps the direction of the nerve impulse going one way and not backing up.

Fig. 48-10-5

KeyNa+

K+

+50

Actionpotential

Threshold

0

1

4

51

–50

Resting potential

Mem

bra

ne

po

ten

tial

(mV

)

–100Time

Extracellular fluid

Plasmamembrane

Cytosol

Inactivation loop

Resting state

Sodiumchannel

Potassiumchannel

Depolarization

Rising phase of the action potential Falling phase of the action potential

5 Undershoot

2

3

2

1

3 4

Hyperpolarization

K just keepsflowing out.

Refractory Period

• After the impulse, the Na channels remain inactivated

• Since the neuron cannot respond to another stimulus with the reversal of charges, the Na-K pump has to restore the original charge location. This is called the refractory period.

Action Potentials Video | DnaTube.com - Scientific Video Site

http://highered.mcgraw-hill.com/sites/0072495855/student_view0/chapter14/animation__the_nerve_impulse.html

Requires the Na-K pump

Fig. 48-11-3

Axon

Plasmamembrane

Cytosol

Actionpotential

Na+

Actionpotential

Na+

K+

K+

ActionpotentialK+

K+

Na+

Properties of an Action Potential

• Are all or none depolarization – once threshold is reached (-50 mV) – always creates the same voltage spike regardless of intensity of the stimulus.

• The frequency of the action potentials increases with intensity of stimulus.

• Action potentials travel in only ONE direction!

• The greater the axon diameter, the faster action potentials are propagated.

Importance of myelin

• Acts as insulators.

• Gaps in the myelin are called nodes of Ranvier and serve as points along which the action potential is propagated, increasing the speed.

• This is called saltatory conduction.

The myelin sheath is composed of Schwann cells (PNS) or oligodendrocytes (CNS) that encircle the axon in vertebrates.

Saltatory Conduction

• Voltage channels concentrated at the nodes of Ranvier - jumping action potentials

http://www.blackwellpublishing.com/matthews/actionp.html

Multiple Sclerosis

http://www.youtube.com/watch?v=o4YkqRUErPY

The Synapse

• Area between two neurons, between sensory receptors and neurons or between neurons and muscle cells or gland cells

Fig. 48-15

Voltage-gatedCa2+ channel

Ca2+12

3

4

Synapticcleft

Ligand-gatedion channels

Postsynapticmembrane

Presynapticmembrane

Synaptic vesiclescontainingneurotransmitter

5

6

K+Na+

http://glencoe.mcgraw-hill.com/sites/9834092339/student_view0/chapter44/transmission_across_a_synapse.html

What happens at the synapse?

Types of synapses

• Electrical – via gap junctions such as in giant axons of crustaceans

• **Chemical – electrical impulses changed into chemical signals

• Arrival of action potential opens Ca+ channels (membrane signaling cAMP), causes synaptic vesicles full of NT’s to fuse with membrane and pop open

Post-synaptic Responses

EPSP - excitatory post-synaptic potential     --> open Na channels --> inside +

May generate an AP

IPSP - inhibitory post-synaptic potentialopens Cl channels -  Cl-in  -> 

more neg  >  no AP                                                  

-->  opens K channels - K-out ->  more  neg  >  no AP   

EPSP and IPSP

Integration of impulses

summation

• Through summation, an IPSP can counter the effect of an EPSP

• The summed effect of EPSPs and IPSPs determines whether an axon hillock will reach threshold and generate an action potential

Summation of impulses

Temporal and Spatial Summation

• Temporal summation occurs with repeated release of nt’s from one or more synaptic terminals before RP

• Spatial summation occurs when several different presynaptic terminals release NT’s simultaneously

Assume a single IPSP has a negative magnitude of -0.5 mV at the axon hillock and that a single EPSP has a positive magnitude of +0.5 mV, for a neuron with initial membrane potential of -70 mV, the net effect of 5 IPSP’s and 2 EPSPs spatially would be to move the membrane potential to? Would the impulse continue?

-85 mV

Neurotransmitters

(a) Affect ion channels

(b) Affect signal transduction pathways

How? Involve cAMP, cAMP protein kinases, GTP, GTP binding proteins

• After release, the neurotransmitter

– May diffuse out of the synaptic cleft

– May be taken up by surrounding cells

– May be degraded by enzymes

Neurotransmitters

• The same neurotransmitter can produce different effects in different types of cells

• There are five major classes of neurotransmitters: acetylcholine, biogenic amines, amino acids, neuropeptides, and gases

a. ACETYLCHOLINE

• Found in vertebrate neuromuscular junctions

- excitatory at skeletal muscles

- inhibitory at heart

b) Biogenic Amines (derived from amino acids)

• epinephrine, norepinephrine (fight or flight),

• dopamine, serotonin (involved in sleep, mood, attention, and learning).

Blocking epinephrine

c) Amino Acids

• Types:

GABA – most common inhibitor

Glutamate - excitatory

d) Neuropeptides (short chains of amino acids)

Types

• Endorphins – inhibitory, relieves pain

• Opiates – mimic endorphins

e) Gaseous signals

• Gases such as nitric oxide and carbon monoxide are local regulators in the PNS

How do drugs work?

• Agonists – mimic drugs such as in nicotine mimicking acetycholine

• Antagonists – block action of NT’s such as atropine and curare (poisons) – block acetylcholine and thus prevent nerve firing in muscles – leads to paralysis and death

• Cocaine and amphetamines block the reuptake of NT’s at adrenergic synapses

• Many antidepressants block reuptake of serotonin so serotonin lingers longer in synaptic cleft.