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Transcript
Chapter 48: Nervous Systems
I.
Overview
A. Close interaction between endocrine and nervous systems
1. Nervous system can integrate vast amounts of information
2. Nervous system communicates with targets more quickly and directly
B. Serves three overlapping functions (fig. 48.1)
1. Sensory input–requires sensory receptors
2. Integration–occurs in central nervous system
a. Central nervous system (CNS)–brain and spinal cord
b. Peripheral nervous system (PNS)–sensory and motor neurons that connect to CNS
c. Nerve–ropelike bundles of neuronal axons
3. Motor output–requires effector cells (muscle and gland cells)
C. Cells of the nervous system
1. Neurons–functional unit of nervous system that transmits information throughout body
a. Structural details depend on the type of neuron (fig. 48.4)
b. Common features (fig. 48.2)
i. Cell body–contains nucleus and cellular organelles
ii. Dendrites–fiberlike processes specialized to receive input from other neurons
iii. Axons–fiberlike processes specialized to conduct information toward synapse
iv. Axon hillock–conical region of axon that joins the cell body
c. Myelin sheath–insulating layer surrounding the axons of some neurons
d. Synaptic terminals–site at the end of axons where neurotransmitters are released
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e. Synapse–narrow gap between synaptic terminal and effector cell
f. Information flow = presynaptic cell to postsynaptic cell
2. Glia–supporting cells that assist, structurally support, protect, and insulate neurons
a. Outnumber neurons by 10-50 fold
b. Radial glia–form tracks along which neurons migrate (developing embryo)
c. Astrocytes–provide structural and metabolic support
i. Induce formation of blood-brain barrier
ii. Chemically communicate with each other and neurons
d. Oligodendrocytes (CNS) and Schwann cells (PNS)–form myelin sheath (fig. 48.5)
D. Reflex arc–simplest nerve circuit (e.g., knee-jerk reflex; fig. 48.3)
1. Neuronal classes
a. Sensory neurons = sensory receptors –> CNS
b. Interneurons = neurons –> neurons
i. Often absent in reflex arcs
ii. Constantly active and talking to one another
c. Motor neurons = CNS –> effector cells
2. Ganglia–clusters of cell bodies from nerves of the PNS
3. Nuclei–clusters of cell bodies from nerves of the CNS
4. Patterns of neuronal circuits
a. Convergent
b. Divergent
c. Circular
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II.
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Electrical properties of neurons
A. Membrane potential (Vm)–voltage difference across the plasma membrane of a cell
1. Vm = -50 to -100 mV in most animal cells (inside of cell is more electronegative)
2. Factors contributing to membrane potential (fig. 48.7)
a. Relative distribution and concentration of ions and charged molecules
i. Extracellular: [K+]e = 5 mM, [Na+]e = 150 mM; [Cl-]e = 120 mM
ii. Intracellular: [K+]i = 150 mM, [Na+]i = 15 mM, [Cl-]i = 10 mM, [A-]i = 100 mM
b. Relative permeability of plasma membrane to these ions and charged molecules
c. Electrochemical forces drives ions through channels
3. Equilibrium potential–Vm caused by the concentration gradient of a single ion
a. EK = -90 mV
b. ENa = +60 mV
4. At rest, membrane is approximately 50 times more permeable to K+ than to Na+
5. Sodium-potassium pumps use ATP to maintain the ionic gradients (fig. 48.7b)
B. Excitable cells–capable of generating large changes in their membrane potentials
1. Resting potential–Vm of unexcited cell (Vm ≈ -70 mV)
a. Depolarization–Vm becomes less negative
b. Hyperpolarization–Vm becomes more negative
2. Changes in Vm are due to changes in ion conductances
a. Ungated-ion channel–channels remain open all the time
b. Voltage-gated ion channel–voltage change triggers change in channel permeability
c. Chemically-gated ion channel–ligand binding triggers change in channel permeability
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d. Note: each ion channel is permeable to only one type of ion
3. Graded potential–change in Vm proportional to amount of stimulation (fig. 48.8)
C. Action potential–an all-or-none electrical event that propagates down axons
1. Axons propagate action potentials once Vm exceeds a threshold potential (≈ -50 mV)
2. All-or-none event (i.e., amplitude of action potential does not vary!)
3. Generation of action potential (fig. 48.9)
a. Vm exceeds threshold potential at axon hillock
b. Triggers fast-acting voltage-gated Na+ channels to open causing depolarizing phase of
action potential
c. Also triggers slow-acting voltage-gated Na+ channels to close and slow-acting voltagegated K+ channels to open causing repolarizing phase of action potential (delayed
response to Vm > threshold)
d. Continued opening of voltage-gated K+ channels causes “undershoot”
e. Voltage-gated K+ channels slowly close and Vm returns to resting state
4. Refractory period–short interval following an action potential during which axon cannot
be stimulated to fire another action potential
a. Occurs during undershoot phase when voltage-gated Na+ channels are resetting
b. Limits the firing rate of neurons (fmax = 500 spikes/sec)
c. Ensures that action potentials are propagated in only one direction!
5. Neurons encode information by the pattern/frequency of trains of action potentials
6. Propagation of action potentials down axon (fig. 48.10)
a. Initiated at axon hillock
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b. Continuously regenerated along the length of the axon
c. Factors influencing the speed of propagation
i. Axonal diameter (↑diameter = ↑velocity)
ii. Presence of myelin (nodes of Ranvier) = saltatory conduction (fig. 48.11)
III.
Communication across synapses
A. Electrical synapses
1. Action potentials spread from presynaptic cell to postsynaptic cell via gap junctions
2. Extremely rapid mode of communication
B. Chemical synapses (fig. 48.12)
1. Synaptic cleft–separates presynaptic and postsynaptic cell
2. Electrical signal –> chemical signal –> electrical signal
a. Presynaptic membrane depolarizes (due to arrival of action potential)
b. Depolarization triggers an influx of Ca2+
c. Ca2+ influx causes synaptic vesicles to fuse with presynaptic membrane
d. Vesicles release neurotransmitter into synaptic cleft
e. Neurotransmitters bind to receptors in postsynaptic membrane
f. Binding triggers chemically-gated ion channels to open/close (changes Vm)
g. Neurotransmitter molecules are inactivated
3. Most neurons release only one neurotransmitter, but neurons may receive signals from
multiple neurotransmitters
4. Binding of neurotransmitter triggers electrical events in postsynaptic cell
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a. Excitatory postsynaptic potential (EPSP)–causes postsynaptic cell to depolarize
b. Inhibitory postsynaptic potential (IPSP)–causes postsynaptic cell to hyperpolarize
c. EPSPs and IPSPs are examples of graded potentials (fig. 48.8)
5. Anatomy of synapse ensures one-way flow of information
C. Integration of synaptic information
1. Dendrites of a single neuron receive information from thousands of neurons (fig. 48.13)
a. Changes in Vm reflect a weighting of all of the EPSPs and IPSPs that dendrites receive
i. EPSPs and IPSPs cause waves of electrical activity starting from site of stimulation
ii. EPSPs and IPSPs decay with time
iii. EPSPs and IPSPs decay with distance (relative to axon hillock)
b. If voltage at axon hillock exceeds threshold, then action potential is fired
2. Summation–ADDITIVE effect of EPSPs and IPSPs (fig. 48.14)
a. Temporal summation–additive effects of PSPs from a single synapse
b. Spatial summation–additive effects of PSPs from multiple synapses
3. Note: action potentials are all-or-none; PSPs are graded potentials
D. Neurotransmitters (table 48.1)
1. Like hormones, a single neurotransmitter often triggers different responses in target cells
a. May activate chemically-gated ion channels directly (fast)
b. May activate complex signal transduction pathways (slow)
2. Acetylcholine (ACh)–released at neuromuscular junctions (skeletal muscles)
3. Biogenic amines (neurotransmitters derived from amino acids)
a. Norepinephrine and epinephrine
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b. Dopamine–affects sleep, mood, attention, and motor skills
c. Serotonin–also affects sleep and mood
4. Amino acids
a. GABA (γ-amino butyric acid)–inhibitory
b. Glycine–inhibitory
c. Glutamate–excitatory
d. Aspartate–excitatory
5. Neuropeptides (short chains of amino acids)
a. Substance P–mediates pain perception
b. Endorphins–natural analgesics
6. Gases
a. Nitric oxide (NO) and carbon monoxide (CO)
b. Aren’t stored and released from vesicles
IV. Evolution and diversity of nervous systems
A. Nervous systems have been evolving for billions of years
B. Comparison of different designs (fig. 48.15)
1. All neurons function similarly, but may be organized in very diverse ways
2. Invertebrates
a. Sponges–lack nervous system
b. Nerve net–branching system of nerves (e.g., hyrda)
c. Radial symmetry–radial nerves (e.g., sea star)
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d. Bilateral symmetry (most animals)
i. Cephalization–concentration of organs, sensors and neurons in anterior end (CNS)
ii. Nerve cord–thick bundle of nerves extending longitudinally through body
iii. Brains evolved from anterior enlargements of nerve cord
e. Cephalopods have most sophisticated nervous systems of any invertebrates
3. Vertebrates
a. Exhibit high degree of cephalization
b. CNS–brain and spinal cord (fig. 48.16)
i. White matter–bundles and tracts of myelinated axons
ii. Grey matter–nerve cell bodies and dendrites
iii. Central canal and ventricles–filled with cerebrospinal fluid
iv. Cerebrospinal fluid–passes nutrients and hormones to brain; cushions brain
c. PNS–paired cranial nerves, ganglia outside CNS, and paired spinal nerves
i. Cranial nerves–12 pairs (mammals); innervate head and upper body
ii. Spinal nerves–31 pairs (mammals); innervate entire body
iii. Most cranial nerves and all spinal nerves contain both sensory and motor neurons
C. Divisions of vertebrate PNS (fig. 48.17)
1. Sensory division–afferent neurons that convey information to CNS from sensory receptors
2. Motor division–efferent neurons that convey information from CNS to effector cells
a. Somatic nervous system–carries signals to skeletal muscle in response to external
stimuli (“voluntary control”)
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b. Autonomic nervous system–conveys signals to smooth and cardiac muscles that
regulate the internal environment (“involuntary control”) (fig. 48.18)
i. Parasympathetic division–enhances activities that conserve energy
ii. Sympathetic division–enhances activities that increase energy consumption and
arousal of individual
iii. Enteric division–regulates gastrointestinal activity
c. Somatic and autonomic nervous systems work together to maintain homeostasis
D. Development of vertebrate brain
1. Develops from three bilaterally symmetrical bulges of the nerve cord (fig. 48.19)
2. Forebrain
a. Telencephalon –> cerebrum
b. Diencephalon –> thalamus and hypothalamus
3. Midbrain –> mesencephalon –> midbrain
4. Hindbrain
a. Metencephalon –> pons (part of brain stem), cerebellum
b. Myelencephalon –> medulla oblongata (part of brain stem)
V.
Brain structure and functions
A. Brainstem–stalk and caplike swellings at anterior end of spinal cord
1. Medulla oblongata (medulla)–contains centers that control visceral functions (e.g.,
breathing, heart and blood vessel activity, swallowing, vomiting, etc...)
2. Pons–regulates medulla; site of extensive data conduction
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3. Midbrain–relay for sensory information (inferior and superior colliculi)
B. Reticular system–mediates arousal and sleep (fig. 48.21)
1. Reticular formation–system of 90 separate nuclei that extends through brainstem
2. Electroencephalogram (EEG)–technique for monitoring electrical activity of brain
a. Synchrony of waves correlates with reduction in mental activity
b. Wave patterns and the stages of sleep (fig. 48.22)
c. Rapid eye movements (REM) occur during dreaming
3. Why do we sleep?
C. Cerebellum–coordination of automated movements and balance
D. Diencephalon
1. Thalamus–important relay center for sensory and motor information
2. Hypothalamus–site of homeostatic regulation (e.g., thirst, hunger, temperature)
a. Suprachiasmatic nuclei (SCN)–region that regulates biological rhythms
b. Circadian rhythm–biologically rhythm whose period is about a day (fig. 48.23)
E. Cerebrum–most highly evolved integrating center in CNS (fig. 48.24)
1. Divided into right and left cerebral hemispheres
2. Each hemisphere consists of outer gray matter, internal white matter and a basal nuclei
a. Basal nuclei (ganglia)–important centers for motor coordination
b. Cerebral cortex–outer portion of cerebrum; largest and most complex part of brain
i. Region of brain that has changed the most during vertebrate evolution
ii. Neocortex (outer layer of cortex)is unique to mammals
iii. Relative size (surface area) of neocortex correlates with complexity of behavior
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c. Corpus callosum–thick band of fibers connecting right and left hemisphere
d. Each hemisphere regulates the opposite side of the body
3. Regions of the cerebrum are specialized for different functions (fig. 48.24)
a. Cerebral cortex is comprised of four lobes (frontal, parietal, temporal and occipital)
b. Information flows from primary cortical areas to more advanced associative areas
c. Proportion of cortex devoted to a task is correlated with its importance (fig. 48.25)
d. Increase in size of neocortex reflects an increase in size of association areas
4. Lateralization of brain function
a. Left hemisphere–language, math, logic operations and processing serial sequences of
information
b. Right hemisphere–pattern recognition, face recognition, spatial relations, parallel
processing, art and music
5. Language and speech (fig. 48.26)
6. Emotions (48.27)
a. Limbic system–includes parts of thalamus, hypothalamus and inner portions of cerebral
cortex
b. Amygdala–major organizer of emotional information and memories
7. Memories and learning
a. Short-term vs. long-term memory
b. Memory transfers are enhanced by practice and previous associations
c. Fact memory vs. skill memory
d. Hippocampus and amygdala are crucial sites of memory formations
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e. Role of long-term depression (LTD) and long-term potentiation (LTP)
8. Consciousness represents an emergent property of whole-brain patterns of activity
VI. Recent advances in neuronal development and neural stem cells
A. CNS, unlike PNS, cannot repair itself when damaged
B. Nerve cell development
1. Factors that help developing axons know which way to grow (fig. 48.28)
a. Growth cone of axon responds to gradients of signal molecules
b. Interactions of cell adhesion molecules on growth cone with molecules from other cells
c. Nerve growth factors and other growth promoting proteins
C. Neural stem cells
1. Brain is capable of producing some new brain cells
2. Source of these cells is neural progenitor cells (stem cells) (fig. 48.29)
3. How can these stem cells be coaxed into differentiating into specific types of neurons?
Hmm.... This would make an excellent exam question!
Clearly explain how changes in ion conductances give rise to the action potential. What is the
refractory period? What causes it and what important functional role does it serve?
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