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

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, CO 2 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 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 Ca 2+ Increased Ca 2+ 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 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 Integration of multiple synaptic inputs

Figure 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 The structure of skeletal muscle

Figure The sliding-filament model of muscle contraction

Figure 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 P i 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 Ca 2+ which means it releases Ca 2+ –Sarcoplasmic reticulum – specialized ER that stores Ca 2+ Ca 2+ binds to troponin which frees binding site for myosin head

Figure 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 Ca 2+ binds to troponin, the shape of tropomyosin- troponin complex changes and frees binding site

Figure Hypothetical mechanism for the control of muscle contraction

Figure 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 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