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 Cell body Axon hillock Presynaptic cell Axon Synaptic terminals Synapse Postsynaptic cell Neurotransmitter 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, PO 4 and SO 4. Symbol is A -. Inside is NEGATIVE!
Outside of the cell Principal ion is Na + Outside is positive!
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. 48-10-2 Key Na + K+K+ +50 Action potential Threshold 0 1 4 5 1 –50 Resting potential Membrane potential (mV) –100 Time Extracellular fluid Plasma membrane Cytosol Inactivation loop Resting state Sodium channel Potassium channel Depolarization Undershoot 2 3 2 1 Notice, gates are closed! Some Na + gates open!
Fig. 48-10-3 Key Na + Na + gates open! K + +50 Action potential Threshold 0 1 4 5 1 –50 Resting potential Membrane potential (mV) –100 Time Extracellular fluid Plasma membrane Cytosol Inactivation loop Resting state Sodium channel Potassium channel 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 Key Na + K+K+ +50 Action potential Threshold 0 1 4 5 1 –50 Resting potential Membrane potential (mV) –100 Time Extracellular fluid Plasma membrane Cytosol Inactivation loop Resting state Sodium channel Potassium channel 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 Key Na + K+K+ +50 Action potential Threshold 0 1 4 5 1 –50 Resting potential Membrane potential (mV) –100 Time Extracellular fluid Plasma membrane Cytosol Inactivation loop Resting state Sodium channel Potassium channel Depolarization Rising phase of the action potential Falling phase of the action potential 5 Undershoot 2 3 2 1 3 4 Hyperpolarization K just keeps flowing 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_impul se.html
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
The Synapse Area between two neurons, between sensory receptors and neurons or between neurons and muscle cells or gland cells
Fig. 48-15 Voltage-gated Ca 2+ channel Ca 2+ 1 2 3 4 Synaptic cleft Ligand-gated ion channels Postsynaptic membrane Presynaptic membrane Synaptic vesicles containing neurotransmitter 5 6 K+K+ Na + http://glencoe.mcgraw- hill.com/sites/9834092339/student_view0/chapter44/transmission_acros s_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 NTs 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
Temporal summation occurs with repeated release of nts from one or more synaptic terminals before RP Spatial summation occurs when several different presynaptic terminals release NTs 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 IPSPs 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).
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 NTs 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 NTs at adrenergic synapses Many antidepressants block reuptake of serotonin so serotonin lingers longer in synaptic cleft.