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

Direction of impulse Dendrites Stimulus Presynaptic Nucleus cell Axon Fig. 48-4 Dendrites Stimulus Nucleus Presynaptic cell Axon hillock Cell body Direction of impulse Axon Synapse Synaptic terminals Postsynaptic cell Neurotransmitter

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 Inside is NEGATIVE! 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

Key Na+ Sodium- potassium Potassium Sodium pump channel channel K+ Fig. 48-6b Key Na+ Sodium- potassium pump Potassium channel Sodium channel K+ OUTSIDE CELL INSIDE CELL (b)

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.

Notice, gates are closed! Fig. 48-10-1 Key Na+ K+ +50 Action potential 3 Membrane potential (mV) 2 4 Threshold –50 1 1 5 Resting potential Depolarization –100 Time Extracellular fluid Sodium channel Potassium channel Plasma membrane Notice, gates are closed! Cytosol Inactivation loop Undershoot 1 Resting state

Notice, gates are closed! Fig. 48-10-2 Key Na+ K+ Some Na+ gates open! +50 Action potential 3 Membrane potential (mV) 2 4 Threshold –50 1 1 5 Resting potential 2 Depolarization –100 Time Extracellular fluid Sodium channel Potassium channel Notice, gates are closed! Plasma membrane Cytosol Inactivation loop Undershoot 1 Resting state

A lot of Na+ gates open! Fig. 48-10-3 Key Na+ Na+ gates open! K+ Rising phase of the action potential +50 Action potential 3 Membrane potential (mV) 2 4 Threshold –50 1 1 5 Resting potential 2 Depolarization –100 Time Extracellular fluid Sodium channel Potassium channel Plasma membrane Cytosol Inactivation loop Undershoot 1 Resting state

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.

Na closes, K opens Fig. 48-10-4 Key Na+ K+ 3 Rising phase of the action potential 4 Falling phase of the action potential +50 Na closes, K opens Action potential 3 Membrane potential (mV) 2 4 Threshold –50 1 1 5 Resting potential 2 Depolarization –100 Time Extracellular fluid Sodium channel Potassium channel Plasma membrane Cytosol Inactivation loop Undershoot 1 Resting state

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.

K just keeps flowing out. Hyperpolarization Fig. 48-10-5 Key Na+ K+ 3 Rising phase of the action potential 4 Falling phase of the action potential +50 Action potential 3 Membrane potential (mV) 2 4 Threshold –50 K just keeps flowing out. 1 1 5 Resting potential 2 Depolarization –100 Time Extracellular fluid Sodium channel Potassium channel Plasma membrane Cytosol Inactivation loop 5 Undershoot 1 Resting state Hyperpolarization

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. http://highered.mcgraw-hill.com/sites/0072495855/student_view0/chapter14/animation__the_nerve_impulse.html Action Potentials Video | DnaTube.com - Scientific Video Site

Requires the Na-K pump

Fig. 48-11-3 Axon Plasma membrane Action potential Na+ Cytosol Action K+ Na+ K+ Action potential K+ Na+ K+

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

What happens at the synapse? Fig. 48-15 What happens at the synapse? 5 Na+ K+ Synaptic vesicles containing neurotransmitter Presynaptic membrane Voltage-gated Ca2+ channel Postsynaptic membrane 1 Ca2+ 4 2 6 Synaptic cleft 3 Figure 48.15 A chemical synapse Ligand-gated ion channels http://glencoe.mcgraw-hill.com/sites/9834092339/student_view0/chapter44/transmission_across_a_synapse.html

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 potential opens 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 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 Affect ion channels 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.