Transcript nervous system

Neurons, Synapses, and Signaling
CHAPTER 48 and 50
Figure 48.1 Overview of a vertebrate nervous
system
NERVOUS SYSTEM
• Central nervous system (CNS) –
brain and spinal cord
• Peripheral nervous system (PNS) –
nerves that communicate motor and
sensory signals between CNS and rest
of body
BRAIN
• Brainstem
– Medulla oblongata – breathing,
heart rate, swallowing, vomiting,
digestion
– Pons – breathing
– Midbrain – receives sensory
information
• Cerebellum
– Coordination of movement, hand-eye
coordination, learning and remembering
• Diencephalon
– Hypothalamus, thalamus, and epithalamus
• Hypothalamus - regulates hunger, thirst,
sexual response, mating behaviors, fight or
flight, biological clock
–Contains the Suprachiasmatic nuclei –
make proteins in response to light/dark
(biological clock)
• Cerebrum
– Most complex integration
– Controls learning, emotion, memory,
and perception
– Divided into right and left hemispheres
– Cerebral cortex
• Most complex, most evolved, and
surface area is 0.5 m2 which is
~80% of total brain mass
– Corpus callosum – connects
hemispheres
Figure 48.20 The main parts of the human brain
Figure 48.20x1 Cerebral cortex, gray and white
matter
NEURON
• Functional unit of nervous system
• Relatively large cell body
• Processes:
– Dendrites – convey signals from tips to cell body;
often branched
– Axons – conduct signals away from body and
toward tip; often single
• Myelin sheath – protective, insulating layer that
covers many axons in vertebrates
– Made by Schwann cells in the PNS
– Made by oligodendrocytes in the CNS
• Axon ends at synaptic terminals
– Synapse – site of contact between
synaptic terminal and target cell (neuron or
effector cell – for example a muscle cell)
– Neurotransmitter – chemical messengers
between neurons and other cells
Figure 48.2 Structure of a vertebrate neuron
Figure 48.0 A neuron on a microprocessor
Figure 48.0x1 Aplysia neuron
Figure 48.5 Schwann cells
ORGANIZATION OF NEURONS
• Sensory neurons – communicate sensory
information from eyes and other senses
and internal conditions
– Senses, blood pressure, muscle tension, CO2
levels)
• Interneurons – integrate sensory input
and motor output; communicate only
between neurons; make up vast majority of
brain neurons
• Motor neurons – convey impulses from
CNS to effector cells (muscles and glands)
Figure 48.3 The knee-jerk reflex
MEMBRANE POTENTIAL
• Voltage measured across the membrane
(like a battery)
• Inside of cell more negative
• Typically –50 to –80 mV (resting
potential)
• Sodium-potassium pump keeps ionic
gradient (3Na+ out, 2K+ in)
Figure 8.15 The sodium-potassium pump: a specific case of active transport
Figure 48.6 Measuring membrane potentials
Figure 48.7 The basis of the membrane
potential
Charges Across Membranes
• Neurons have ability to generate
changes in their membrane potential
• Resting potential – membrane
potential of cell at rest (-60mV to -80mV)
• Gated ion channels control membrane
potential – open to different stimuli
– Hyperpolarization – increase in
electrical gradient
• Open K+ channel (K+ moves out)
• Cell becomes more negative
• No action potential because it makes
it harder to depolarize
– Depolarization – decrease in electrical
gradient
• Open Na+ channel (Na+ moves in)
• Cell becomes more positive
• Action potential generated if threshold
is reached (-50mV to -55mV)
–Massive change in voltage
• Threshold causes all-or-none event
–Action potential - massive change in
membrane voltage that can spread
along the membrane
Figure 48.8 Graded potentials and the action
potential in a neuron
Figure 48.9 The role of voltage-gated ion channels in the action potential
ROLE OF GATED CHANNELS
• Depolarizing – Na+ gates open rapidly so Na+
moves into cell
• Repolarizing – K+ gates finally open and K+ moves
out; Na+ gates close
• Undershoot (Refractory Period) - K+ still open
(they are slower to close) and Na+ still closed so cell
becomes even more negative than resting and
cannot be depolarized
• Stronger stimuli result in greater frequency of action
potentials and NOT from stronger action potentials
• Propagation
– Action potentials move in one direction due to
refractory period
Propagation of the action potential
Na+ moves into cell
starting action
potential.
Depolarization spreads
and K+ repolarizes
initial area. Prevents
action potential on that
side.
Figure 48.11 Saltatory conduction
• Voltage leaps from node to node
SYNAPSES
• Presynaptic cell – transmitting cell
• Postsynaptic cell – receiving cell
• Two types of synapses
– Electrical
• Need gap junctions (channels between neurons)
• No delays
– Chemical
• Narrow gap, synaptic cleft, between cells
• More common than electrical in vertebrates and
most invertebrates
• Require neurotransmitters (chemical intercellular
messengers)
• Depolarization of presynaptic membrane
causes influx of Ca2+
• Increased Ca2+ in cell causes synaptic
vesicles to fuse to cell membrane and
release neurotransmitters via exocytosis
• Neurotransmitters diffuse to postsynaptic
cell
• Postsynaptic membrane has gated
channels that open when
neurotransmitters bond to specific
receptors
Figure 48.12 A chemical synapse
• A single neuron may receive many inputs
simultaneously
• Neurotransmitters cause 2 different responses
depending on the gates that are opened
– Inhibitory
• (hyperpolarization)
– Excitatory
• (depolarization)
• Neurotransmitters are quickly degraded
• Excitatory postsynaptic potential (EPSP) –
Na+ in and K+ out = depolarization
• Inhibitory postsynaptic potential (IPSP) K+ out or CL- in = hyperpolarization
Figure 48.13 Integration of multiple synaptic
inputs
Figure 48.14 Summation of postsynaptic
potentials
NEUROTRANSMITTERS
• Acetylcholine
– one of the most common
– can excite skeletal muscle and inhibit
cardiac muscle
• Epinephrine and norepinephrine
– also function as hormones
• Dopamine
– Usually excitatory
– Excess dopamine can cause schizophrenia
– Lack of dopamine can cause Parkinson’s
• Sertonin
– Usually inhibitory
• Endorphins
– Natural painkillers (morphine and opium mimic
endorphins shape)
• Nitric Oxide (NO)
– Released during sexual arousal (increasing blood
flow)
– Nitroglycerin used to treat chest pain
SKELETAL MUSCLE
• Attached to bones and responsible
for their movement
• Consist of bundles of long fibers
• Each fiber is a single cell with many
nuclei
Figure 49.31x1 Skeletal muscle
• Each fiber made up of smaller
myofibrils
• Myofibrils made of 2 kinds of
myofilaments
–Thin myofilaments
•2 strand of actin with a
regulatory protein (tropomyosin)
–Thick myofilaments
•Staggered arrays of myosin
• Striated muscle due to repeating
light and dark bands
• Sarcomere – basic unit of muscle
• Contraction of sarcomeres results in
muscle contraction.
• Actin and myosin slide pass each
other to shorten the sarcomere.
Figure 49.31 The structure of skeletal muscle
Figure 49.32 The sliding-filament model of muscle
contraction
Figure 49.33 Myosin-actin interactions generate the
force for muscle contraction
• Sliding-filament model
• Myosin head phosphorylated by ATP making
the head energized
• Energized head attaches to actin making
cross-bridge
• ADP and Pi released from head so it goes
back to relaxed state, sliding the thin filament
toward center of sarcomere
• A new ATP binds to head releasing it from
actin
• Creatine phosphate – stores phosphate in
vertebrate muscles
How is skeletal muscle
contraction regulated?
• An action potential begins in the brain
and travels via nerve to muscle.
• The action potential causes neuron to
release acetylcholine
(neurotransmitter). This results in an
excitatory response in muscle.
• Acetylcholine triggers action
potential in T-tubules within
muscle
–T-tubules are infoldings of
muscle cell’s cell membrane
• T-tubules touch sarcoplasmic
reticulum and change is
permeability to Ca2+ which
means it releases Ca2+
–Sarcoplasmic reticulum –
specialized ER that stores Ca2+
• Ca2+ binds to troponin which
frees binding site for myosin
head
Figure 49.35 The roles of the muscle fiber’s
sarcoplasmic reticulum and T tubules in contraction
What’s troponin and tropomyosin?
• Tropomyosin blocks myosin
heads binding sites
• Troponin controls position of
tropomyosin
• When Ca2+ binds to troponin,
the shape of tropomyosintroponin complex changes and
frees binding site
Figure 49.34 Hypothetical mechanism for the control
of muscle contraction
Figure 49.36 Review of skeletal muscle contraction
• Summation and frequency of
action potentials determine
muscle tension
• One muscle cell only innervated
by one motor neuron, but one
motor neuron may innervated
many muscle cells
• More cells activated = more
tension
Figure 49.37 Temporal summation of muscle cell
contractions
Big Picture – Making a muscle contract
• Action potential generated in brain and travels down
nerve
• Action potential causes acetylcholine to diffuse across
synapse to muscle
• Acetylcholine causes excitatory responses (action
potential) that moves down T-tubules
• Change in membrane potential causes SR to release
calcium
• Calcium binds to troponin, which then moves
tropomyosin
• ATP used to bind myosin head to actin
• Sarcomere contracts and then ATP used to break
bridge