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Field notes · chapter 42

The Nervous System

pp. 924–952 · Raven Part VII

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42.1

Nervous System Organization

pp. 924–927
42.2

The Mechanism of Nerve Impulse Transmission

pp. 927–932
  • Neuron function depends on building an electric potential across the plasma membrane and then deliberately disturbing it. Cells are aqueous, so charge is carried by ions, and ion gradients are controlled by transport proteins.
  • Ion channels are ion-specific protein pores. Leakage channels are always open. Gated channels open only when stimulated.
  • An electric potential is any separation of opposite charges and can do work, like a battery. In a neuron the membrane interior is the negative pole and the exterior the positive pole.
  • The resting membrane potential of vertebrate neurons ranges -40 to -90 mV (0.04–0.09 V). This chapter uses -70 mV as the standard value. The negative sign means the inside is negative relative to the outside. Watch Neurology | Resting Membrane, Graded, Action Potentials on YouTube, from Ninja Nerd
  • Three factors make the interior negative. (1) The Na⁺/K⁺ pump moves 2 K⁺ in for every 3 Na⁺ out, creating high K⁺ / low Na⁺ inside and high Na⁺ / low K⁺ outside. (2) The membrane has more K⁺ leakage channels than Na⁺ channels, so it is more permeable to K⁺, which diffuses out. (3) The membrane is impermeable to negatively charged proteins, nucleic acids, and organic phosphates, which stay trapped inside. Watch Neurology | Resting Membrane, Graded, Action Potentials on YouTube, from Ninja Nerd
  • The pump’s 3-out/2-in ratio by itself creates only a small charge imbalance. The bigger effect is the K⁺ concentration gradient the pump builds, which drives K⁺ out through leakage channels. Negative counter-ions cannot follow, so positive charge piles up outside and negative charge inside, and that electrical force pulls K⁺ back in. Where the outward diffusional force equals the inward electrical force is the equilibrium potential. Watch Neurology | Resting Membrane, Graded, Action Potentials on YouTube, from Ninja Nerd
  • The Nernst equation computes the equilibrium potential for one ion. For K⁺: E_K = 58 mV · log([K⁺]out / [K⁺]in). Watch Neurology | Resting Membrane, Graded, Action Potentials on YouTube, from Ninja Nerd
  • The calculated K⁺ equilibrium potential is -90 mV — close to the measured -70 mV. The Na⁺ equilibrium potential is +60 mV — nowhere close. The gap between -90 and -70 exists because a small amount of Na⁺ leaks in, pulling the resting potential up.
  • Resting potential is measured with a voltmeter and two electrodes, one outside the cell and one inside.
  • Neurons are not special for having a resting potential — they are special for the sudden, temporary, stimulus-triggered disruptions of it. Two kinds: graded potentials (small, continuous changes) and action potentials (transient, threshold-triggered signals that propagate along the axon).
  • The resting potential comes from leakage channels. Changes in potential come from gated channels. Ligand-gated channels open on a chemical signal and produce graded potentials. Voltage-gated channels open on a change in membrane potential and produce action potentials. Watch Neurology | Resting Membrane, Graded, Action Potentials on YouTube, from Ninja Nerd
  • Graded potentials occur mostly in dendrites, where ligand-gated channels respond to neurotransmitters. Opening a channel changes permeability, which changes potential through ion diffusion.
  • Depolarization = the potential becomes less negative (e.g. -70 → -65 mV). Hyperpolarization = it becomes more negative (e.g. -70 → -75 mV). Watch Graded Potentials, EPSPs, IPSPs, & Summation on YouTube, from Catalyst University
  • Graded potential size depends on stimulus strength or on how much ligand is available. They are local — they shrink with distance from their origin.
  • Depolarizing and hyperpolarizing potentials combine like merging waves, amplifying or canceling. That combining is summation, and it is essential for triggering action potentials. Watch Graded Potentials, EPSPs, IPSPs, & Summation on YouTube, from Catalyst University
  • Once depolarization reaches threshold — about -55 mV in some mammalian axons — an action potential is produced where the axon arises from the cell body. Watch The Nervous System, Part 2 - Action! Potential!: Crash Course Anatomy & Physiology #9 on YouTube, from CrashCourse
  • Action potential sequence: at rest -70 mV; a threshold stimulus opens chemically gated Na⁺ channels; at -55 mV voltage-gated Na⁺ channels open and Na⁺ rushes in — depolarization, the rising phase; the potential climbs to the peak at about +35 to +40 mV, where the neuron "takes action" and propagates the signal. Watch The Nervous System, Part 2 - Action! Potential!: Crash Course Anatomy & Physiology #9 on YouTube, from CrashCourse Watch 2-Minute Neuroscience: Action Potential on YouTube, from Neuroscientifically Challenged
  • Then Na⁺ channels close rapidly while K⁺ channels open, letting K⁺ diffuse out — repolarization, the falling phase. K⁺ channels stay open slightly too long, producing a small undershoot (hyperpolarization). The entire sequence takes about 1 millisecond. Watch The Nervous System, Part 2 - Action! Potential!: Crash Course Anatomy & Physiology #9 on YouTube, from CrashCourse
  • In gate terms: voltage-gated Na⁺ channels have activation gates that open at threshold and inactivation gates that slam shut at the peak. K⁺ gates open late and close slowly. Watch 2-Minute Neuroscience: Action Potential on YouTube, from Neuroscientifically Challenged
  • Action potentials are separate, all-or-none events. Below threshold nothing happens. Unlike graded potentials, they do not add together or interfere with each other. Watch 2-Minute Neuroscience: Action Potential on YouTube, from Neuroscientifically Challenged
  • After firing, Na⁺ channels stay inactivated until the inactivation gate reopens — the absolute refractory period, when the membrane cannot be restimulated at all. Then comes the relative refractory period, when stimulation is possible but produces a reduced-amplitude action potential. Watch The Nervous System, Part 2 - Action! Potential!: Crash Course Anatomy & Physiology #9 on YouTube, from CrashCourse
  • Producing an action potential is entirely passive ion diffusion. But each one leaves the cytoplasm with slightly more Na⁺ and slightly less K⁺, so the Na⁺/K⁺ pump must keep running to restore the gradients. Active transport is not needed for a single spike; it is needed to sustain firing.
  • Propagation is regeneration, not flow. Ions do not travel the length of the axon. The action potential starts at the axon base and is rebuilt fresh in each adjacent stretch of membrane: the Na⁺ influx of one patch depolarizes the next patch to threshold while the patch behind repolarizes. Watch 2-Minute Neuroscience: Action Potential on YouTube, from Neuroscientifically Challenged
  • The signal cannot travel backward because the Na⁺ channels that just fired are inactivated and refractory.
  • Action potentials do not shrink as they travel — the last one at the axon terminal is exactly the size of the first.
  • Two evolutionary speed-ups. Larger axon diameter lowers electrical resistance (resistance is inversely proportional to cross-sectional area), so positive charge spreads farther and pushes distant membrane above threshold sooner. This is mostly an invertebrate strategy — the squid giant axon drives the escape response and was the axon Hodgkin and Huxley used in their pioneering work.
  • Myelination is the other speed-up. Action potentials occur only at nodes of Ranvier; depolarization spreads passively and fast under the insulating myelin to trigger voltage-gated channels at the next node. The impulse appears to jump — saltatory conduction. Watch 2-Minute Neuroscience: Myelin on YouTube, from Neuroscientifically Challenged
  • Stadium-wave analogy: fans stand as their neighbors stand (depolarize), raise hands (peak), and sit (repolarize) — the wave moves but the people stay put. Saltatory conduction is that wave skipping whole empty sections, so it does not have to wait for every seat.
42.3

Synapses: Where Neurons Communicate with Other Cells

pp. 932–938
  • An action potential reaching the end of an axon and all its branches must cross to the next cell at a synapse — a junction where a presynaptic cell transmits and a postsynaptic cell receives. Watch The Nervous System, Part 3 - Synapses!: Crash Course Anatomy & Physiology #10 on YouTube, from CrashCourse
  • Electrical synapses are direct cytoplasmic connections through gap junctions. Potential changes, including full action potentials, pass directly and very rapidly. Common in invertebrates, less so in vertebrates. Watch The Nervous System, Part 3 - Synapses!: Crash Course Anatomy & Physiology #10 on YouTube, from CrashCourse
  • Chemical synapses are the vast majority of vertebrate synapses. Under a light microscope the cells look joined, but an electron microscope reveals a gap — the synaptic cleft. Watch 2-Minute Neuroscience: Synaptic Transmission on YouTube, from Neuroscientifically Challenged
  • Classic experiment: two frog hearts in saline. Stimulating the vagus nerve on the donor heart slowed it; transferring the fluid from around that nerve to a second heart with no nerve attached slowed that heart too. Conclusion — the vagus released a chemical signal. Synaptic signaling can be chemical.
  • The presynaptic axon terminal is swollen and packed with synaptic vesicles holding neurotransmitter.
  • Arriving action potentials open voltage-gated Ca²⁺ channels. The Ca²⁺ influx triggers vesicles to fuse with the plasma membrane and release neurotransmitter by exocytosis. Higher presynaptic firing frequency means more vesicles released. Watch 2-Minute Neuroscience: Neurotransmitter Release on YouTube, from Neuroscientifically Challenged
  • Released transmitter diffuses across the cleft and binds ligand-gated receptor proteins on the postsynaptic membrane, producing graded potentials there. Watch 2-Minute Neuroscience: Synaptic Transmission on YouTube, from Neuroscientifically Challenged
  • Because a chemical messenger sits inside a mostly electrical system, its action must be strictly time-limited. Transmitter is cleared by enzymatic digestion, reuptake into the presynaptic neuron, or uptake by glial cells. Watch 2-Minute Neuroscience: Synaptic Transmission on YouTube, from Neuroscientifically Challenged
  • Neurotransmitters can be excitatory (push toward an action potential) or inhibitory (prevent one). The same transmitter can do either, depending on the receptor the target cell carries. Watch The Nervous System, Part 3 - Synapses!: Crash Course Anatomy & Physiology #10 on YouTube, from CrashCourse
  • Acetylcholine (ACh) crosses the neuromuscular junction between a motor neuron and a muscle fiber. It binds receptor proteins that are themselves ligand-gated ion channels, letting Na⁺ into the muscle fiber. Watch The Nervous System, Part 3 - Synapses!: Crash Course Anatomy & Physiology #10 on YouTube, from CrashCourse
  • To let muscle relax, ACh must be cleared. Acetylcholinesterase (AChE), an enzyme in the postsynaptic membrane, cleaves ACh into inactive fragments — one of the fastest-acting enzymes known.
  • Nerve gas and the insecticide parathion are potent AChE inhibitors. In humans they cause severe spastic paralysis and death if the paralysis reaches the respiratory muscles.
  • ACh is not only a muscle transmitter — many neurons use it at synapses onto other neurons’ dendrites and cell bodies.
  • Amino acid transmitters: glutamate is the major excitatory transmitter of the vertebrate CNS. In Huntington disease some brain neurons become hypersensitive to glutamate, driving neurodegeneration.
  • Glycine and GABA are inhibitory. They open ligand-gated Cl⁻ channels; Cl⁻ flows in down its gradient and, being negative, drives the membrane more negative than resting — e.g. -70 to -85 mV. That hyperpolarization is an IPSP, and it matters for motor control and other brain functions.
  • Diazepam (Valium) is sedative because it enhances GABA binding to its receptors, boosting inhibition.
  • Biogenic amines: dopamine, norepinephrine, serotonin, plus the hormone epinephrine. Epinephrine, norepinephrine, and dopamine derive from tyrosine and form the catecholamine subgroup. Serotonin derives from tryptophan and is a biogenic amine but not a catecholamine.
  • Epinephrine is released into the blood as a hormone; norepinephrine is released at sympathetic synapses. Together they drive the fight-or-flight response: faster and stronger heartbeat, higher blood glucose, blood shifted to muscles and heart.
  • Dopamine is central to brain areas controlling movement. Degeneration of dopamine-releasing neurons causes the resting tremors of Parkinson disease, treated with L-dopa (a dopamine precursor). Excess dopamine activity elsewhere is linked to schizophrenia, helped by dopamine blockers like chlorpromazine (Thorazine).
  • Serotonin regulates sleep and is implicated in mood. Low serotonin activity may contribute to clinical depression; fluoxetine (Prozac) and other SSRIs block serotonin reuptake from the cleft.
  • Neuropeptides are polypeptides released at synapses. Some act as classic transmitters; others have subtler long-term effects and are called neuromodulators. An axon usually releases one transmitter type, though some release a transmitter and a neuromodulator together.
  • Substance P is released in the CNS by sensory neurons responding to painful stimuli. Perceived pain varies with circumstance — an injured athlete may feel nothing until the game ends — partly because of enkephalins and endorphins.
  • Enkephalins are released by axons descending from the brain into the spinal cord and inhibit pain signals traveling up. Endorphins are released by brain-stem neurons and also block pain perception. Opium, morphine, and heroin are analgesics because they are structurally similar enough to bind the same receptors — which is why enkephalins and endorphins are called endogenous opiates.
  • Nitric oxide (NO) was the first gas found to act as a regulatory molecule. It diffuses straight through membranes, so it cannot be stored in vesicles; it is made on demand from the amino acid arginine. In the PNS it is released by neurons serving the GI tract, penis, respiratory passages, and cerebral blood vessels, relaxing smooth muscle — engorging penile tissue causes erection. Sildenafil (Viagra) boosts NO release there. NO also acts as a brain transmitter in learning and memory.
  • One postsynaptic neuron integrates enormous input: a single spinal motor neuron can receive over 50,000 synapses, both excitatory and inhibitory.
  • Synaptic integration: EPSPs add together, bringing the potential closer to threshold; IPSPs subtract, holding it back. Because the action potential is all-or-none, the postsynaptic neuron behaves like a switch — on or off — though information can still be encoded in the pattern of firing over time. Watch Graded Potentials, EPSPs, IPSPs, & Summation on YouTube, from Catalyst University
  • Two routes to threshold. Spatial summation: simultaneous graded potentials from different presynaptic neurons add up. The inputs need not all be excitatory — only the net sum (EPSPs minus IPSPs) at the axon base has to exceed threshold. Watch Graded Potentials, EPSPs, IPSPs, & Summation on YouTube, from Catalyst University
  • Temporal summation: a single dendrite fires EPSPs close enough together in time to sum. A typical EPSP lasts about 15 ms, so the next impulse must arrive inside that window. Watch Graded Potentials, EPSPs, IPSPs, & Summation on YouTube, from Catalyst University
  • Analogy: filling a hole with soil. Many shovels working at once = spatial. One shovel working faster = temporal. Either way, when the hole is full the axon fires.
  • Prolonged constant stimulation makes cells lose responsiveness — habituation, like no longer noticing the chair you are sitting in.
  • If receptors face high transmitter levels for a long time, the postsynaptic cell reduces the number of receptor proteins in its membrane. That is normal efficiency feedback — but with drugs it means more drug is needed for the same effect: tolerance.
  • Cocaine makes abnormally large amounts of transmitter linger in synapses. It binds tightly to the transporter proteins on presynaptic membranes that normally clear dopamine from the cleft, so dopamine keeps firing receptors in the brain’s pleasure pathways (the limbic system).
  • Nicotine works differently: it has no affinity for transporters and instead binds directly to a postsynaptic receptor — one of a class that normally binds acetylcholine. Nicotine evolved in tobacco as a defense compound against herbivorous insect nervous systems; its fit to some human ACh receptors is an evolutionary accident.
  • Chronic nicotine makes the brain "turn down the volume" two ways: fewer nicotine-binding receptor proteins are built (RNA levels change too), and the receptors’ activation pattern and sensitivity are altered. That is why quitting is so hard.
42.4

The Central Nervous System: Brain and Spinal Cord

pp. 938–945
  • Among noncoelomate invertebrates, sponges are the only major phylum with no nerves at all. The simplest true nervous systems are the nerve nets of cnidarians — neurons linked in a web with no associative activity, no control of complex actions, and little coordination.
  • The simplest animals with associative activity are free-living flatworms. Two nerve cords run the body length with peripheral nerves to muscle, and the cords converge at the front into a mass of nervous tissue containing interneurons — a primitive "brain," a rudimentary CNS.
  • Everything later is elaboration on flatworm traits. Earthworms have a CNS plus peripheral nerves; arthropods concentrate coordination at the front of the nerve cord, adding interneurons and tracts — the major information highways of the brain. Concentrating nervous tissue at the head end is cephalization, and it tracks bilateral symmetry.
  • All vertebrate brains have three basic divisions, already visible in 500-million-year-old jawless fish braincases: hindbrain (rhombencephalon), midbrain (mesencephalon), forebrain (prosencephalon). Watch Central Nervous System: Crash Course Anatomy & Physiology #11 on YouTube, from CrashCourse
  • In fishes the hindbrain dominates. It contains the cerebellum, pons, and medulla oblongata and can be read as an extension of the spinal cord devoted to coordinating motor reflexes. Large axon tracts run up and down the cord to it.
  • The cerebellum ("little cerebrum") does much of that coordination and grows larger in more advanced vertebrates. In every vertebrate it processes limb position and movement, muscle contraction state, and overall body position relative to the world — movement and balance.
  • In fishes the midbrain is mainly the optic tectum, which receives and processes visual information, and the forebrain handles olfactory information. In terrestrial vertebrates the forebrain takes over far more processing.
  • Fish brains keep growing for life. Other vertebrates finish brain development early — the human brain develops through early childhood, and after that few new neurons form, except in the hippocampus, which decides which experiences get filed into long-term memory. How much adult neurogenesis really occurs is still debated.
  • From amphibians onward, and especially in reptiles, sensory processing shifts into the forebrain — the dominant trend in later vertebrate brain evolution.
  • The forebrain has two functionally distinct parts. The diencephalon = thalamus + hypothalamus. The telencephalon ("end brain") sits at the front, is devoted mostly to associative activity, and in mammals is called the cerebrum.
  • Thalamus = integration and relay center between incoming sensory information and the cerebrum. Hypothalamus = basic drives and emotions, and control of pituitary secretion.
  • Plotting brain mass against body mass splits vertebrates sharply: fish and reptiles have relatively small brains, birds and mammals much larger ones — most extreme in porpoises and humans. The mammalian increase is mostly cerebrum.
  • The cerebrum is the mammalian center for correlation, association, and learning. It receives sensory data from the thalamus and sends motor commands down the spinal cord via descending tracts. Ascending tracts carry sensory information up.
  • The human cerebrum is so large it appears to envelop the rest of the brain. It splits into right and left cerebral hemispheres joined by the corpus callosum, and each hemisphere has frontal, parietal, temporal, and occipital lobes.
  • Each hemisphere receives sensory input from and controls the contralateral (opposite) side of the body. A touch on the right hand goes mainly to the left hemisphere. Stroke damage on one side causes sensory loss and paralysis on the other.
  • The cerebral cortex is a gray-matter layer only a few millimeters thick on the cerebral surface, holding over 10 billion neurons — roughly 10% of all brain neurons. Its heavy folding triples the surface area. Watch Central Nervous System: Crash Course Anatomy & Physiology #11 on YouTube, from CrashCourse
  • Cortical activity is motor, sensory, or associative, and each region maps to a specific function.
  • The primary motor cortex lies along the gyrus at the posterior edge of the frontal lobe, just in front of the central sulcus. Each point controls movement of a different body part. Watch Central Nervous System: Crash Course Anatomy & Physiology #11 on YouTube, from CrashCourse
  • The primary somatosensory cortex lies just behind the central sulcus on the anterior edge of the parietal lobe. Each point receives skin and muscle sensation from a specific body part. Watch Central Nervous System: Crash Course Anatomy & Physiology #11 on YouTube, from CrashCourse
  • Cortical area is proportional to how finely a part is sensed or controlled, not to its physical size — hands, lips, tongue, and pharynx get disproportionately huge maps (the homunculus).
  • Auditory cortex sits in the temporal lobe, organized by sound frequency. Visual cortex sits in the occipital lobe, organized by retinal position.
  • Cortex not doing motor or sensory work is association cortex, the site of higher mental activity. It peaks in primates and makes up about 95% of the human cortical surface.
  • Basal nuclei are clusters of cell bodies and dendrites buried in cerebral white matter — islands of gray matter. They receive sensory input from ascending tracts and motor commands from cortex and cerebellum, and their output helps control movement. Damage to specific regions produces the resting tremor of Parkinson disease.
  • The thalamus is the primary site of sensory integration: visual, auditory, and somatosensory signals all synapse there with association neurons before relay to the occipital, temporal, and parietal lobes respectively.
  • The hypothalamus integrates visceral activity — body temperature, hunger and satiety, thirst, and (with the limbic system) emotional state. It controls the pituitary, which regulates many other endocrine glands, and links to the cortex and brainstem (midbrain + pons + medulla) control centers.
  • The limbic system — hippocampus + amygdala + hypothalamus — is an evolutionarily ancient set of linked structures deep in the cerebrum responsible for emotional responses. The hippocampus is also key to forming and recalling memories.
  • Sleep and arousal: the brainstem holds the diffuse reticular formation. Its reticular activating system (RAS) controls consciousness and alertness. All sensory pathways feed into it and it flags important stimuli; arousal raises activity across the brain. Anesthetics and barbiturates depress RAS pathways.
  • Darkness makes sleep easier because fewer visual stimuli reach the RAS. Serotonin also reduces RAS activity, lowering brain activity and inducing sleep.
  • EEG patterns: relaxed and awake with eyes closed = large slow alpha waves. Alert with eyes open = fast desynchronized beta waves. Theta and delta are very slow sleep waves. REM sleep, with rapid eye movements under closed lids, shows an EEG resembling an awake, relaxed person.
  • Lateralization of function: the hemispheres look alike but do different jobs. Language is the best-studied case — the left hemisphere is dominant for language in 90% of right-handers and about two-thirds of left-handers.
  • Wernicke’s area (parietal lobe, between the primary auditory and visual areas) handles language comprehension and turning thoughts into speech. Broca’s area (near the facial motor cortex in the frontal lobe) generates the motor output of speech.
  • Damage to these produces aphasias. Wernicke’s damage gives rapid, fluent, meaningless speech — "word salad."
  • The dominant hemisphere excels at sequential reasoning (building sentences). The nondominant hemisphere, usually the right, excels at spatial reasoning — puzzles, drawing — and is primarily responsible for musical ability. Someone with Broca’s damage may lose speech but still be able to sing.
  • Damage to the nondominant inferior temporal cortex causes prosopagnosia — inability to recall faces — while reading, writing, and comprehension stay normal; patients still recognize people by voice.
  • Memory appears dispersed, not stored at one cortical site: even extensive cortical damage does not selectively erase specific memories, and access often recovers gradually.
  • Short-term memory is transient, lasting moments, and can be erased by electrical shock while long-term memories survive — so it looks like a transient neural excitation. Long-term memory seems to involve structural changes in specific neural connections.
  • The hippocampus and amygdala, both temporal-lobe structures, handle short-term memory and its consolidation into long-term memory. Damage blocks converting recent events into lasting memories.
  • Synaptic plasticity is the cellular basis proposed for learning: long-term change in synaptic strength, in two directions.
  • Long-term potentiation (LTP) occurs at glutamate synapses on NMDA receptors. Repeated stimulation of that synapse — or of neighboring synapses — strongly depolarizes the postsynaptic membrane, which releases the Mg²⁺ block on the NMDA receptor. Glutamate binding then lets Ca²⁺ in, activating CaMKII, which inserts more AMPA receptors into the membrane. The synapse becomes more sensitive.
  • Long-term depression (LTD) is the mirror image: weaker NMDA stimulation and less depolarization activate a different Ca²⁺ pathway through calcineurin, which removes AMPA receptors. The synapse becomes less sensitive.
  • Alzheimer disease has two competing hypotheses. (1) The external protein beta-amyloid misfolds into plaques that damage nerve cells — weakened by the fact that plaques also turn up in people with no symptoms. (2) An abnormal form of the internal protein tau, which normally maintains transport microtubules, assembles into helical tangles that disrupt nerve cells. The tangle–neuronal death link currently has the stronger evidence.
  • The spinal cord is a neuron cable running from the brain down through the backbone, protected by the vertebral column and by membrane layers called meninges (which also cover the brain). Watch Central Nervous System: Crash Course Anatomy & Physiology #11 on YouTube, from CrashCourse
  • Spinal cord has two zones. Inner gray matter holds interneuron, motor neuron, and neuroglial cell bodies. Outer white matter holds axon tracts — sensory in the dorsal columns, motor in the ventral columns. Note this is inverted relative to the cerebrum, where gray is outside.
  • Besides relaying messages, the spinal cord runs reflexes directly — sudden, involuntary muscle movements. Reflexes are fast because sensory information goes straight to a spinal motor neuron with no higher processing. The blink reflex fires before the cerebrum even registers the danger. Watch Reflex action (& reflex arc) | Neural Control & Coordination | Class 11 | Biology | Khan Academy on YouTube, from Khan Academy India - English
  • The knee-jerk reflex is a monosynaptic reflex arc: a muscle spindle stretch receptor in the quadriceps fires a sensory neuron (cell body in the dorsal root ganglion) that synapses directly onto a spinal motor neuron, whose axon returns to the same muscle. No interneuron. Watch Reflex action (& reflex arc) | Neural Control & Coordination | Class 11 | Biology | Khan Academy on YouTube, from Khan Academy India - English
  • A cutaneous reflex is more complex: interneurons connect the sensory neuron to a motor neuron, and other interneurons inhibit motor neurons so the antagonistic muscle relaxes. Most vertebrate reflexes use just one connecting interneuron. Watch Reflex action (& reflex arc) | Neural Control & Coordination | Class 11 | Biology | Khan Academy on YouTube, from Khan Academy India - English
  • The same sensory neuron also contacts separate interneurons that carry signals up to the brain. That is why your hand jerks off the hot stove reflexively and then you consciously feel the pain.
  • Spinal cord regeneration: early nerve implants bridging a severed cord mostly failed — axons could grow through the implant but not into cord tissue beyond it, and the cord itself contains a nerve-growth-inhibiting factor.
  • After fibroblast growth factor was found to stimulate nerve growth, researchers glued nerve implants to rat spinal cords with fibrin plus FGF. Three months later those rats showed lower-body movement, and dye tracing confirmed regrowth from both sides of the gap. Caveats: most human spinal injuries are crushed, not cleanly severed, and even the successful rats could barely walk or stand.
42.5

The Peripheral Nervous System: Spinal and Cranial Nerves

pp. 946–949
  • The PNS receives information from the environment, relays it to the CNS, and carries responses out to effectors such as muscle cells. A nerve is a bundle of axons bound by connective tissue. Watch Peripheral Nervous System: Crash Course Anatomy & Physiology #12 on YouTube, from CrashCourse
  • At the spinal cord a spinal nerve splits. Sensory axons enter the dorsal surface as the dorsal root; motor axons leave the ventral surface as the ventral root. Watch Peripheral Nervous System: Crash Course Anatomy & Physiology #12 on YouTube, from CrashCourse
  • Cell body locations matter: sensory neuron cell bodies cluster outside the cord in the dorsal root ganglia; somatic motor neuron cell bodies sit inside the spinal cord, not in ganglia. Watch Peripheral Nervous System: Crash Course Anatomy & Physiology #12 on YouTube, from CrashCourse
  • Somatic motor neurons stimulate skeletal muscle contraction. Autonomic motor neurons innervate involuntary effectors — smooth muscle, cardiac muscle, and glands.
  • Somatic motor neurons release ACh. Nicotinic receptors on skeletal muscle bind it and open as Na⁺ channels, rapidly depolarizing the fiber — which is why skeletal muscle can act so fast.
  • When one muscle contracts, its antagonist must be inhibited. Flexing the arm needs the flexor stimulated and the extensor inhibited. Descending motor axons do this by producing IPSPs in the spinal motor neurons of the antagonistic muscle.
  • The autonomic nervous system has the sympathetic and parasympathetic divisions plus the medulla oblongata, which coordinates the whole system. Watch Autonomic Nervous System: Crash Course Anatomy & Physiology #13 on YouTube, from CrashCourse
  • Both autonomic divisions share a two-neuron efferent pathway. The preganglionic neuron has its cell body in the CNS, runs to an autonomic ganglion, and releases ACh. The postganglionic neuron has its cell body in that ganglion and runs to a smooth muscle, cardiac muscle, or gland cell. Watch Autonomic Nervous System: Crash Course Anatomy & Physiology #13 on YouTube, from CrashCourse
  • Transmitter at the second synapse is the giveaway: parasympathetic postganglionic neurons release ACh; sympathetic postganglionic neurons release norepinephrine. Watch Autonomic Nervous System: Crash Course Anatomy & Physiology #13 on YouTube, from CrashCourse
  • Sympathetic preganglionic neurons originate in the thoracic and lumbar spinal cord. Most axons synapse in two parallel ganglion chains just outside the cord — the sympathetic chain — which houses the postganglionic cell bodies that then innervate the viscera. Watch Autonomic Nervous System: Crash Course Anatomy & Physiology #13 on YouTube, from CrashCourse
  • Exception: some sympathetic preganglionic axons pass through the chain without synapsing and end in the adrenal medulla, whose cells secrete the hormone epinephrine into the blood while norepinephrine is released at postganglionic synapses elsewhere. Both raise metabolism and blood flow — the fight-or-flight package.
  • Parasympathetic preganglionic neurons originate in the brain and sacral spinal cord. Because of that split origin there is no parasympathetic chain. Their axons — many traveling in the vagus (cranial nerve X) — run to ganglia near or inside the target organs, where postganglionic neurons release ACh. Effects include slowing the heart and increasing digestive secretion and activity. Watch Autonomic Nervous System: Crash Course Anatomy & Physiology #13 on YouTube, from CrashCourse
  • G proteins explain how one transmitter does opposite things. ACh slows the heart because heart cells carry the muscarinic receptor, which activates a G protein that opens K⁺ channels; K⁺ diffuses out, hyperpolarizing the membrane and slowing the beat.
  • The same G-protein system excites elsewhere when the G protein acts on a different effector protein — parasympathetic nerves to the stomach increase gastric secretion and contraction.
  • Sympathetic effects are also G-protein-mediated: norepinephrine from nerve endings and epinephrine from the adrenal medulla both need G proteins to activate their target cells.
  • There are 12 pairs of cranial nerves, numbered I–XII in roman numerals, arising from the underside of the brain. Some are mixed (sensory and motor); others serve only a special sense — olfactory (I) for smell, optic (II) for vision. Watch Peripheral Nervous System: Crash Course Anatomy & Physiology #12 on YouTube, from CrashCourse
  • The vagus nerves (X) are the exception among cranial nerves: unlike the other eleven pairs they reach far past head and neck to innervate chest and abdominal organs. They arise from the medulla and carry mostly autonomic fibers central to homeostasis — heart rate, breathing, digestion, hormone release — branching to pharynx, larynx, heart, lungs, liver, stomach, spleen, pancreas, kidney, and intestines.
  • The olfactory pathway: receptor cells in the nasal cavity pass through the ethmoid bone to synapse in the olfactory bulb; their combined axons form the olfactory tract, collectively the olfactory nerve (I).