51.0 Introduction

1. Nearly All Animals Possess Nerve Cell Networks
1. Gather Internal and External Information
2. Process and Integrate Information, Issue Commands
3. Neurons Connect Body Cells to Brain and Spinal Cord fig 51.1

51.1 The nervous system consists of neurons and supporting cells

1. Neuron Organization
1. Organization of a Nervous System
1. Animals respond to external stimuli
1. Requires sensory receptors to detect stimulus
2. Requires motor effectors to respond to stimulus

2. Nervous system links sensory receptors and motor effectors fig 51.2
1. Sensory (afferent) neurons carry impulses from sensory receptors
2. Motor (efferent) neurons carry impulses to effectors, muscles and glands

3. Association neurons (interneurons) are present in most nervous systems
1. Found in most invertebrates, all vertebrates
2. Located in central nervous system (CNS) composed of brain and spinal cord
3. Provide more complex reflexes, higher associative functions

4. Peripheral nervous system (PNS) is composed of sensory and motor neurons
5. Somatic motor neurons stimulate skeletal muscle contraction
6. Autonomic motor neurons regulate smooth and cardiac muscle, glands
1. Subdivided into sympathetic and parasympathetic systems
2. Act to counterbalance each other fig 51.3

2. Structure of a Neuron
1. Varied appearance, similar functional architecture fig 51.4
2. Cell body is an enlarged region containing nucleus
3. Dendrites extend from cell body
1. One or more branched cytoplasmic extensions
2. Motor and association neurons have multitudes of branched dendrites
3. Cell receives input from many sources simultaneously

4. Surface of cell body integrates information arriving at dendrites
5. If membrane excitation is enough it triggers impulse sent along axon
1. Electrical current travels outward from cell body
2. Generally only one for each cell body, may be quite long
3. Single axon in a giraffe may be three meters long

3. Neuron Support System
1. Provide structural and functional support
1. Called neuroglia in CNS
2. More numerous than neurons

2. Include Schwann cells and oligodendrocytes
1. Envelop axon, form myelin sheath
1. Schwann cells produce myelin in PNS
2. Oligodendrocytes produce myelin in CNS

2. Insulating material of multiple layers of neuroglial membrane fig 51.5

3. CNS composed of white and grey matter
1. White matter made of myelinated axons
2. Grey matter comprised of unmyelinated dendrites and cell bodies

4. PNS nerves composed of bundles of myelinated and nonmyelinated fibers
5. Myelin sheath interrupted at nodes of Ranvier fig 51.4

51.2 Nerve impulses are produced on the axon membrane

1. The Membrane potential
1. Plasma Membranes Possess Electrical Properties
1. Produce electrical impulses carried by neurons
2. Potential difference in electrical charge exists between two poles
1. Example battery terminals
2. One pole positive, other negative

3. Cells have potential difference across plasma membrane
1. Side of membrane exposed to cytoplasm is negative
2. Side of membrane exposed to extracellular fluid is positive

4. Potential difference called membrane potential
1. Resting membrane potential: Cell not producing impulses
2. Generally about 70 millivolts, written -70 mV

5. Cell membrane potential due to three factors, possessed by all cells
1. Action of sodium-potassium pumps
2. Different degrees of membrane permeability to different ions
3. Presence of fixed negatively charged anions
1. Include proteins and organic phosphates
2. Unable to leave cell

6. Action of sodium-potassium pump has lesser significance than other two
1. Pump three Na⁺s out for every two K⁺s pumped in fig 51.6
2. Primary active transport creates unequal charge distribution
3. Cell inside has fewer positive charges than outside

7. Fixed anions is most important factor in forming membrane potential
1. Anions attract positively charged cations from extracellular environment
2. Plasma membrane is differentially permeable to cations
3. Resting neuron membrane most permeable to K⁺

8. Examine actions if only K⁺ cations entered cell
1. Electrical attraction to fixed anions cause buildup of K⁺ inside cell
2. Higher K⁺ concentration produces diffusion gradient out of cell
3. Equilibrium state reached when two forces balanced each other out
1. Value is about -90 mV
2. Membrane potential called equilibrium potential for K⁺ tbl 51.1

4. Concentration of Na⁺ ten times higher on outside of cell than inside
5. Membrane potential must be positive on inside
1. Balances tendency for Na⁺ to diffuse inward
2. Value of +60 mV

6. Resting potential (-70mV) closer to equilibrium potential for K⁺ fig 51.7
1. Membrane is more permeable to K⁺
2. Resting potential slightly less than -90mV since some Na⁺ diffuses in
3. Some K⁺ diffuses out since -70 mV is less negative than -90 mV

7. Resting membrane potential viewed with oscilloscope

9. Cell membrane potential can change in response to stimulation
1. Depolarization: Shift in positive direction (-70 mV to -50 mV)
2. Hyperpolarization: Shift to more negative (-70mV to -85 mV)

2. Generation of Action Potentials
1. Action Potentials Associated with Gated Channels
1. Nerve and muscle cells Na⁺ and K⁺ channels have gates
1. Protein portion opens or closes pore with change in membrane potential
2. Called voltage-gated ion channels fig 51.8
3. Gates for Na⁺ are closed at resting membrane potential
4. Many K⁺ gates are open, membrane more permeable to K⁺ than Na⁺

2. Slight depolarization is upward deflection on oscilloscope, decays to initial value
3. If depolarization is strong enough action potential is generated
1. Typically -55 mV
2. Depolarization must reach cell's threshold level
3. Depolarization at this level opens both Na⁺ and K⁺ channels, Na⁺ first
1. Rapid diffusion of Na⁺ into cell shifts membrane potential toward equilibrium potential for Na⁺ (+60mV)
2. Membrane reverses polarity (+ sign) as Na⁺ rushes in
3. On an oscilloscope this shows a rising phase of a spike fig 51.9
4. Membrane potential does not reach +60 mV because Na⁺ channels close

4. At same time K⁺ channels open
1. Action potential peaks at +30 mV
2. K⁺ diffuses out of cell restoring resting membrane potential
3. Repolarization appears as falling phase on oscilloscope
4. Repolarization may slightly undershoot and be more negative for brief period

5. Entire sequence of events over in a few milliseconds

4. Action potentials have two distinguishing characteristics
1. When produced follow an all-or-none law
2. Are always separate events, can not add together or interfere with each other
1. Due to refractory period that exists after action potential is generated
2. New action potential cannot form for a brief period of time

5. Production of action potential results entirely from passive diffusion of ions
1. At end cytoplasm has a little more Na⁺ and a little less K⁺
2. Active transport returns cell to normal

3. Propagation of Action Potentials
1. Action Potentials Do Not Really Travel Along an Axon
1. Events are reproduced at different points along axon membrane
2. Propagation of action potential occurs for two reasons
1. Action potentials stimulated by depolarization
2. Action potential can serve as depolarizing stimulus
1. Reflects reversal in membrane polarity (-70 to +30 mV)
2. Positive charges depolarize next region of membrane to threshold
3. Region produces its own action potential fig 51.10

3. Previous region repolarizes back to resting potential

3. Analogy to the "wave" in a stadium
1. People stand up, in place (depolarize)
2. Raise hands (peak of action potential)
3. Sit down again (repolarize)

4. Action potential remains same along entire length, no strength lost
1. No change in amplitude
2. Last potential is same as first

5. Velocity of propagation dependent on fiber diameter and myelination tbl 51.2
1. Greater conduction velocity in larger fibers
2. Myelination dramatically increases velocity via saltatory conduction fig 51.11
1. Myelin sheath interrupted at nodes of Ranvier
2. Action potential jumps from node to node

51.3 Neurons form junctions called synapses with other cells

1. Structure of Synapses
1. Synapses Are Intercellular Junctions
1. Axon/dendrite junctions, sites on muscles or gland cells
1. Presynaptic cell: Side where axon transmits action potential
2. Postsynaptic cell: Opposite side of synapse

2. Synaptic cleft: Narrow gap between cells fig 51.12
3. Signals cross synaptic cleft chemically
1. Axonal ending on presynaptic side contain synaptic vesicles
2. Vesicles contain chemicals called neurotransmitters

4. In presence of action potentials, voltage-gated Ca⁺⁺ channels opened
1. Stimulates fusion of synaptic vesicle membrane with plasma membrane of axon
2. Vesicle contents released via exocytosis fig 51.13

5. Greater number of action potentials, more vesicles release contents
6. Neurotransmitters diffuse to other side of cleft, bind to receptor proteins
7. Different chemicals in different junctions permit varied responses

2. Neurotransmitters and their Functions
1. Acetylcholine (ACh)
1. Crosses neuromuscular junction, synapse between axon and muscle cell fig 51.12,13
2. ACh molecules bind to receptors in postsynaptic muscle fiber membrane
1. Open chemically regulated ion channels fig 51.14
2. Na⁺ diffuses into postsynaptic cell, K⁺ diffuses out
3. More Na⁺ enter faster than K⁺ leave
4. Produces excitatory postsynaptic potential (EPSP)
5. Opens voltage-regulated channels for Na⁺ and K⁺ responsible for action potentials
6. Stimulates muscle contraction

3. ACh must be destroyed for next transmission to occur or muscle remains contracted
1. Acetylcholinesterase (AchE) enzyme destroys acetylcholine
2. One of fastest acting enzymes known

4. Some chemicals inhibit acetylcholinesterase
1. Nerve gases, agricultural insecticide parathion
2. Produce continual neuromuscular stimulation, cause paralysis of respiratory muscles

5. Many other synapses use ACh as neurotransmitter
1. Postsynaptic membrane on dendrites or cell body of second neuron
2. EPSPs produced travel through dendrite or cell body to axon
3. First voltage-regulated channels located at axon membrane
4. First action potentials produced if EPSP depolarization is above threshold

2. Glutamate, Glycine and GABA
1. Glutamate
1. Major excitatory transmitter in vertebrate CNS
2. Produce EPSPs and action potentials in postsynaptic neurons
3. Normal amounts produce physiological stimulation
4. Excessive amounts cause neurodegradation, as in Huntington's chorea

2. Glycine and GABA (gamma aminobutyric acid)
1. Inhibitory neurotransmitters
2. Causes hyperpolarization and inhibition
1. Opens chemically-regulated gated Cl^– channel
2. Inward diffusion of Cl^– makes inside more negative fig 51.15

3. Membrane potential change called an inhibitory postsynaptic potential (IPSP)
4. Important for control of body movements, other brain functions
5. Associated with sedation effects of Valium (diazepam)
1. Enhanced binding of GABA to receptors
2. Increases effectiveness of GABA at synapse

3. Biogenic Amines
1. Chemicals derived from amino acids
1. Epinephrine, dopamine, norepinephrine derived from tyrosine
2. Serotonin derived from tryptophan

2. Epinephrine (adrenaline) is a hormone
3. Dopamine is a neurotransmitter found in the brain
1. Controls body movement and other functions
2. Degeneration of dopamine-releasing neurons causes Parkinson's disease
1. Produces resting muscle tremors
2. Treated with L-dopa, a dopamine precursor

3. Schizophrenia associated with excessive dopamine activity

4. Norepinephrine
1. Acts as neurotransmitter in the brain and some autonomic neurons
2. Complements actions of epinephrine hormone made by adrenal gland

5. Serotonin
1. Involved in regulation of sleep, implicated in various emotional states
2. Insufficient activity of serotonin-producing neurons results in clinical depression
3. Antidepressant drugs block elimination of serotonin from synaptic cleft fig 51.16
4. LSD blocks serotonin receptors in brain stem

4. Other Neurotransmitters
1. Neuropeptides released by axons at synapses
1. May have neurotransmitter function
2. May have long-term action on postsynaptic neurons, act as neuromodulators
3. Axons can release only one neurotransmitter, but also one neuromodulator

2. Substance P
1. Released at synapses in CNS by sensory neurons activated by pain stimuli
2. Perception of pain is varied in part by enkephalins and endorphins
1. Enkephalins released by axons from brain, inhibit passage of pain information
2. Endorphins released by neurons in brainstem, block perception of pain
3. Opium, morphine, heroin are similar in structure, bind to same receptors
4. Enkephalin and endorphin are endogenous opiates

3. Nitric oxide (NO)
1. First gas to act as regulatory molecule
2. Produced from amino acid arginine
3. Diffuses out of presynaptic axon and into cells, passes through lipid part of cell
4. In PNS, released by neurons that innervate smooth muscle organs
1. Include GI tract, penis, respiratory passages, cerebral blood vessels
2. Example: Produces engorgement of spongy tissues of penis, causes erection

5. Released as neurotransmitter in brain, implicated in learning and memory

5. Synaptic Integration Neuron can receive both excitatory and inhibitory synapses
1. EPSPs (depolarization) and IPSPs (hyperpolarization) from synapses reach cell body
2. Small EPSPs add together, bring membrane potential closer to threshold
1. IPSPs subtract from effects of EPSPs, keep membrane below threshold
2. Process called synaptic integration fig 51.17

6. Neurotransmitters and Drug Addiction
1. Cells exposed to constant stimulus lose ability to respond to stimulus
1. Nerve cells particularly prone to this loss of sensitivity
2. Receptor proteins exposed to neurotransmitters for prolonged period
3. Nerve cell response to put fewer receptor proteins into membrane
4. Normal functional feedback to increase cell efficiency

2. Cocaine
1. Neuromodulator that causes large amounts of neurotransmitter to remain in synapse
1. Effects nerve cells in brain's pleasure pathways (limbic system)
2. Cells use dopamine to transmit pleasure messages

2. Cocaine binds tightly to transport proteins in gaps between nerves
1. Proteins normally remove dopamine
2. If bound to cocaine, can't bind to and remove dopamine
3. Continued firing adds dopamine to gap, fires pleasure pathway fig 51.18

3. Exposure to prolonged dopamine causes nerves to lower number of receptor proteins
1. Nerve cells "turn down volume" of signal
2. Reduce number of targets available to hit

4. Cocaine user now addicted, needs drug to maintain normal activity fig 51.19

3. Is nicotine an addictive drug?
1. Radioactively labeled nicotine to discover protein carriers it attaches to
1. Ignored proteins in gap
2. Attached directly to specific receptor on receiving nerve cell surface
3. Nicotine not a normal brain chemical, unusual to have receptors

2. Nicotine receptors normally bind to acetylcholine
3. Normal function of receptor with ACh
1. Coordinate activities of other kinds of receptors
2. Fine tune sensitivity of wide variety of behaviors

4. Changes in receptors between smokers and nonsmokers
1. Changes in number of receptors
2. Changes in levels of RNA making the receptors

5. Brain "turns down volume" to prolonged exposure to nicotine
1. Makes fewer receptors to which nicotine can bind
2. Alters pattern of activation of receptors, the sensitivity to neurotransmitter

6. Nicotine changes level of activity of a wide variety of neurotransmitters
1. Includes ACh, dopamine, serotonin
2. Affects wide variety of pathways in brain

7. Addiction occurs with chronic exposure to nicotine, induces nervous system to adapt
1. Brain compensates by making other changes
2. Other adjustments made to restore normalcy, balance of activities

8. Attempts to stop smoking
1. Nicotine required for normal function and balance of activities
2. Level of signalling changes, level out if drug not reintroduced
3. Brain again makes compensatory changes
4. Over time receptor numbers, sensitivity and patterns return to normal
5. Pleasure pathways do not function normally until this point achieved

9. Use of patches changes one nicotine source for another
10. Ultimately, must eliminate drug altogether

51.4 The central nervous system consists of the brain and spinal cord

1. Evolution of the Vertebrate Brain
1. Nervous Systems of Simple Animals
1. Completely lacking in sponges
2. Simple nerve net in cnidarians fig 51.20
1. Lack associative activity
2. No control of complex actions, little coordination

3. First associative activity seen in free-living flatworms
1. Two nerve cords run length of body, extend to muscles
2. Cords converge at front end, from enlarged mass, primitive brain
3. Rudimentary CNS, more complex control of muscles than cnidarians

4. Elaboration of characteristics in other invertebrates
1. Earthworms CNS connected to body parts by peripheral nerves
2. Arthropod complex responses localized in from end of nerve cord
1. region progressively contained more associative interneurons
2. Developed tracts connecting associative elements

5. Early fossil agnathans vertebrate brains have characteristic divisions fig 51.21
1. Hindbrain = rhombencephalon
2. Midbrain = mesencephalon
3. Forebrain = prosencephalon

2. Basic Organization of the Vertebrate Brain
1. Hindbrain
1. Principal component of early brains
2. Primary component of present-day fishes
3. Composed of cerebellum, pons and medulla oblongata
4. Extension of the spinal cord, coordinates motor reflexes
1. Axons run along spinal cord to hindbrain
2. Integrates sensory signals from muscles
3. Coordinates pattern of motor responses

5. Cerebellum is coordinating center
1. Size increased in more advanced vertebrates
2. Involved in evaluating limb position, muscle state, general body position

2. Midbrain
1. Composed of optic lobes in fishes
2. Receive and process visual information

3. Forebrain
1. Compose olfactory lobes in fishes
2. Receive and process olfactory (smell) information

4. Brains of fishes continue to grow throughout lives
1. Not typical of other vertebrates
2. Development usually completed by infancy
3. Human brains develop through childhood, after which no new neurons are produced

3. The Dominant Forebrain
1. Further development in amphibians, more prominent in reptiles fig 51.22
2. Forebrain composed of two elements
1. Diencephalon: Thalamus and hypothalamus
1. Thalamus integrates sensory information
2. Hypothalamus participates in basic drives and emotions, controls pituitary secretions

2. Telencephalon
1. Located at front of forebrain
2. Devoted to associative activity
3. Called cerebrum in mammals

4. Expansion of the Cerebrum
1. Ratio of brain mass to body mass fig 51.23
1. Discontinuity between fish/reptiles and birds/mammals
2. Mammalian brains particularly large in comparison to body mass

2. Cerebrum is the center for correlation, association and learning
1. Receives sensory data from thalamus
2. Issues motor commands to spinal cord via descending tracts of axons

3. CNS composed of brain and spinal cord tbl 51.3
1. Responsible for most information processing
2. Composed of interneurons and neuroglia

4. Ascending tracts carry sensory information to brain
5. Descending tracts carry impulses from brain to motor neurons and interneurons in spinal cord that control body muscles

2. The Human Forebrain
1. Cerebrum fig 51.24
1. Split into two cerebral hemispheres
1. Hemispheres connected by nerve tract called corpus callosum
2. Hemispheres divided into frontal, parietal, occipital, temporal lobes

2. Each hemisphere receives information from opposite side of body
1. Controls motor activities on that side
2. Damage due to stroke results in loss of sensation, paralysis on opposite side

2. Cerebral Cortex
1. Outer layer of cerebral surface, location of most neural activity
2. Surface highly convoluted to increase surface area
3. Three categories of activity: Motor, sensory, associative
4. Primary motor cortex
1. Lies along posterior border of frontal lobe fig 51.25
1. Gyrus is convolution in surface
2. Sulcus is a crease in surface

2. Each point on surface associated with movement of a body part fig 51.26

5. Primary somatosensory cortex
1. Lies along anterior edge of parietal lobe, behind central sulcus
2. Each point receives input from sensory neuron on part of body

6. Auditory cortex
1. Lies within temporal lobe
2. Surfaces associated with different sound frequencies

7. Visual cortex
1. Lies on occipital lobe
2. Processes information from different positions on retina

8. Association cortex
1. Portion not occupied by any of the other motor/sensory cortexes
2. Site of higher mental activities, 95% of surface in humans

3. Basal Ganglia
1. Buried deep within white matter of cerebrum, produce islands of gray matter
2. Receive sensory information and motor commands from cerebral cortex
3. Output sent down spinal cord, participate in control of muscle activity
4. Damage produces tremor associated with Parkinson's disease

4. Thalamus and Hypothalamus
1. Thalamus
1. Primary site of sensory integration
2. Relays information from sensors to appropriate area of brain
3. Transfer of sensory information handled by aggregations of neuron cell bodies

2. Hypothalamus
1. Integrates visceral activities
2. Also helps regulate body temperature, hunger, thirst
3. Associated with limbic system and various emotional states
4. Controls pituitary gland, in turn regulates endocrine organs
5. Interconnected with cerebral cortex and brainstem control centers
6. Helps coordinate neural and hormonal responses to internal stimuli and emotions

3. Limbic system fig 51.27
1. Composed of hippocampus and amygdala
2. Linked structures involved with emotional responses
3. Hippocampus also involved with memory formation and recall

5. Language and Other Higher Functions
1. Arousal and sleep
1. Reticular system is a diffuse collection of neurons in brainstem
1. Reticular activating system controls consciousness and alertness
2. All sensory pathways feed into this system
3. When stimulated, increases level of activity in many parts of brain
4. Neural pathways depressed by anesthetics and barbiturates

2. Controls both sleep and waking states
1. Easier to sleep in darkened room due to fewer visual stimuli
2. Activity reduced by serotonin, causes level of activity to fall, induces sleep

3. Activity measured by an electroencephalogram (EEG)
1. EEG in relaxed, but awake state, eyes shut
1. Large slow waves, frequency of 8-13 Hertz
2. Called alpha waves

2. Alert subject, eyes open
1. EEG waves more rapid
2. Beta waves at 13-30 Hertz
3. More desynchronized due to multiple sensory inputs

3. EEG signals associated with sleep
4. Theta waves (4-7 Hertz) and delta waves (0.5-4 Hertz)
5. Slow-wave sleep associated with reduced body activities
6. Dreaming occurs in REM (rapid eye movement) phase of sleep

2. Language and spatial recognition
1. Dominant (left in most people) hemisphere specializes in language
1. Wernicke's area interprets language and formulates speech fig 51.28
2. Broca's area generates motor output resulting in speech
3. Damage to areas cause language disorders called aphasias

2. Specialization of the non-dominant (right) hemisphere
1. Involved with spacial relationships and musical activity

3. Facial recognition site
4. Consolidates memories of non-verbal experiences

3. Memory and learning
1. Memory not located in particular identifiable portions of the brain
2. Removal of portions of temporal lobe result in impaired memory
3. First stage of memory is transient, short-term memory
1. Can be removed from the brain by electrical shock
2. Long-term memories are preserved

4. Long-term memory based on structural change in neural connections in brain
5. Damage to temporal lobes, hippocampus and amygdala
1. Affects short-term memory and memory consolidation
2. Affects ability to process short-term into long-term memory

6. Long-term potentiation (LTP)
1. Synapses used intensively for short period have more effective transmission
2. Presynaptic neuron may release increased amounts of neurotransmitter
3. Postsynaptic neuron may become increasingly sensitive to neurotransmitter
4. May be responsible for some aspects of memory storage

6. Mechanism of Alzheimer's Disease Still a Mystery
1. Condition in which memory and thought processes become dysfunctional
2. Two hypotheses proposed about nature of disease and cause
1. Nerve cells killed from outside in
2. Nerve cells killed from inside out

3. First hypothesis: Outside to inside
1. External proteins, beta amyloid peptides, kill nerve cells
1. Protein processing mistakes produce abnormal form of protein
2. Forms aggregates or plaques

2. Plaques fill in brain, damage and kill nerve cells
3. Amyloid plaques also found in people without Alzheimers'

4. Second hypothesis: Inside to outside
1. Nerve cells killed by an abnormal form of internal protein
1. Tau protein normally maintains protein transport microtubules
2. Abnormal tau assemble into helical tangles, interfere with nerve function

5. Research continuing to determine if damage caused by plaques or tangles
6. Certain genes increase likelihood of developing Alzheimer's
7. Other genes cause it when mutated
8. Genes do not show up in all patients

3. The Spinal Cord
1. Structure of the Spinal Cord
1. Neurons extend from brain through backbone fig 51.29
2. Enclosed and protected by membrane layers called meninges
3. White versus gray matter
1. In spinal cord gray matter surrounded by tracts of white matter
2. Grey matter: Inner zone composed of interneurons and motor neuron cell bodies
3. White matter: Outer zone made of nerve cell axons and dendrites

4. Messages run up and down spinal cord "information highway"

2. Spinal Cord Also Involved with Reflex Actions
1. Reflexes are sudden involuntary muscle movements
1. Sensory neuron passes information to motor neuron in spine
2. No higher level processing used
3. Blinking in response to something approaching the eye is an example

2. Reflexes are fast, involve only a few neurons
1. Many never reach brain
2. Travel to spinal cord and back

3. Knee-jerk reflex is a monosynaptic reflex arc fig 51.30
1. Sensory cell synapses directly with motor neuron in spinal cord
2. Also example of a muscle stretch reflex
1. Muscle stretched by tapping patellar ligament
2. Muscle spindle apparatus also stretched
3. Activates sensory neurons
4. Synapse with somatic motor neurons in spinal cord

3. Motor neurons conduct action potential to skeletal muscle fibers, they contract
4. Simplest reflex since only one synapse crossed

4. Most reflexes involve one connecting interneuron between sensory and motor neuron
1. Example: Withdrawing hand from hot stove
2. Relays information from sensory neuron through one or more interneurons
3. Impulse goes to motor neuron that stimulates muscle to contract fig 51.31

3. Spinal Cord Regeneration
1. Early attempts used other nerves to bridge gap and provide guide for regeneration
2. Most failed
1. Bridges did not go from white to grey matter
2. Factor also inhibited nerve growth in spinal cord

3. Fibroblast growth factor stimulates nerve growth
1. Tried gluing on nerves from white to grey matter
2. Glue made of fibrin mixed with fibroblast growth factor
3. Positive results showed within three months
4. Spinal cord nerves grew from both ends of gap

4. Most spinal cord injuries involve crushed, not severed tissue

4. Components of the Peripheral Nervous System
1. Peripheral Nervous System (PNS) fig 51.32
1. Comprised of nerves and ganglia
1. Nerves are collections of axons of motor and sensory neurons
2. Ganglia are aggregations of cell bodies, outside CNS

2. Dorsal and ventral roots of spinal nerves
1. Spinal nerve separates into sensory and motor components at origin
2. Axons of sensory neurons enter dorsal surface of spinal cord in dorsal root
3. Motor neuron axons exit from ventral surface form ventral root

3. Dorsal root ganglia
1. Sensory neuron cell bodies grouped in ganglia at each level in spinal cord
2. motor neuron cell bodies located in spinal cord, not in ganglia

4. Somatic motor neurons stimulates skeletal muscle contractions
5. Autonomic motor neurons regulates activity of smooth and cardiac muscle, glands
6. Comparison of somatic and autonomic nervous systems tbl 51.4

2. The Somatic Nervous System
1. Somatic motor neurons stimulate skeletal muscles to contract
1. In response to conscious commands
2. As part of reflexes that do not require conscious control

2. Conscious control of skeletal muscles
1. Activation of tracts descending from cerebrum to specific level of spinal cord
2. Some directly stimulate spinal cord motor neurons
3. Others activate interneurons that further act on spinal motor neurons

3. Antagonistic control of the skeletal muscles
1. One muscle stimulated, antagonist must be inhibited fig 51.33
2. Descending motor axons produce inhibition
3. Cause hyperpolarization (IPSPs) of spinal neurons innervating antagonist

5. The Autonomic Nervous System
1. Composed of Multiple Elements
1. Sympathetic, parasympathetic divisions
2. Medulla oblongata of hindbrain coordinates system
3. In both divisions, efferent motor pathway involve two neurons fig 51.34
1. Preganglionic neuron cell body in CNS, axon goes to autonomic ganglion
2. Postganglionic neuron cell body in autonomic ganglion, axon goes to target organ

4. Ach is neurotransmitter at preganglionic synapse in both divisions
5. Neurotransmitters at postganglionic synapse
1. Ach in parasympathetic division
2. Norepinephrine in parasympathetic division

6. Sympathetic nervous system
1. Preganglionic neurons originate at thoracic and abdominal levels fig 51.35
2. Axons synapse in two parallel chains of ganglia just outside spinal cord
3. Structures called sympathetic chain of ganglia
4. Synapse with neurons whose axons innervate visceral organs

7. Exception to general pattern
1. Axons of some preganglionic sympathetic neurons pass through sympathetic chain
2. Do not synapse in chain
3. Terminate within adrenal gland medulla
4. Adrenal medulla secretes hormone epinephrine

8. With activation of sympathetic nervous system
1. Epinephrine released into blood as hormonal secretion
2. Norepinephrine released from postganglionic neurons
3. These two chemicals initiate flight-or-flight reaction tbl 51.5
1. Heart beats faster, stronger
2. Blood glucose concentration increases
3. Blood flow diverted to muscles and heart
4. Bronchioles dilate

9. Responses antagonized by parasympathetic nervous system
1. Preganglionic parasympathetic neurons extend from brain and sacral spinal cord
2. No chain of parasympathetic ganglia similar to sympathetic ganglia
3. Axons terminate in ganglia at or in internal organs
4. Regulate organs by releasing ACh at synapse
5. Response of parasympathetic neurons
6. Heart slows
7. Digestive functions stimulated

2. G-Proteins Mediate Cell Responses to Autonomic Nerves
1. Ach can have inhibitory and stimulatory effects
1. Slows heart rate
2. Causes potassium channels to open
3. Leads to outward diffusion of potassium, thus hyperpolarization

2. Parasympathetic effects of ACh produced indirectly via G-proteins
1. Regulated by GDP and GTP
2. Required since ion channels are located away from receptor proteins for ACh
3. G-proteins serve as connecting links

3. G-protein subunits
1. Designated alpha, beta, gamma
2. Bound together, attached to receptor protein for ACh

4. Ach released by parasympathetic endings fig 51.36
1. G-protein subunits dissociate
2. G-protein beta-gamma complex move within membrane to potassium channel
3. Cause channel to open
4. Produces hyperpolarization, slows heart

5. G-proteins have other effects in other organs
1. Parasympathetic nerves innervate stomach
2. Cause increased gastric secretions, contractions

6. Sympathetic nerve effects also involve G-proteins
1. G-proteins required for actions of norepinephrine and epinephrine
2. Norepinephrine released from sympathetic nerve endings
3. Epinephrine released from adrenal medulla