EXAM 1 MATERIAL
EXAM 1 MATERIAL NROSCI 1000 - Intro to Neuroscience
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3. Brain and Spinal Cord Anatomy Subdivisions and Components of the CNS Know this chart (more in Neural Development): Cranial Nerves and Their Functions: 1. Olfactory: sensory; sense of smell 2. Optic: sensory; vision 3. Ocularmotor: motor; eye movements 4. Trochlear: motor; eye movements 5. Trigeminal: both sensory and motor; somatic sensation from face, mouth, cornea, chewing muscles 6. Abducens: motor; eye movements 7. Facial: both sensory and motor; sensation from posterior tongue and pharynx, 8. Vestibulocochlear: sensory; hearing and sense of balance 9. Glossopharyngeal: both sensory and motor; sensation from tongue and pharynx, 10. Vagus: both sensory and motor; autonomic functions of gut; sensation from larynx and pharynx, muscles of vocal cords, swallowing 11. Spinal Accessory: motor; shoulder and neck muscles 12. Hypoglossal: motor; movements of tongue Required Anatomy: precentral gyrus, central sulcus, postcentral gyrus cerebellar hemisphere lateral (Sylvian) ﬁssure cingulate sulcus cingulate gyrus corpus callosum lateral ventricle midbrain fourth ventricle pons thalamus medulla oblongata hypothalamus optic chiasm longitudinal ﬁssure olfactory tract olfactory bulb 5. Lipid Bilayer, Membrane Potential, Ions and Current & Action Potential Aplysia, “Gill withdrawal reﬂex" similar to the knee jerk sensory neuron is activated, uses glutamate (all sensory neurons do), sends an excitatory signal and activates interneurons and motor neuron, interneuron also helps activate the motor neuron theres also an inhibitory interneuron that inhibits the motor neuron (don’t need it for this particular reﬂex) Plasma membrane phospholipid bilayer hydrophobic head region + hydrophilic tail region impermeable to water none of the ions or molecules dissolved in water can get through either Lipid bilayer forms the entire cell membrane dendrites - receptor proteins embedded cell body axon axon terminals - releases chemical signals, special proteins for that the membrane potential is created by the separation of ionic charges across the lipid bilayer membrane how much charge could travel if the ion channels opened creates a diﬀerence - an electric potential between the two sides sodium is driven to go inside, inside is more negative (Na+ wants to go to the negative side) more K+ on the inside, driven to go out because of the concentration gradient, but driven to stay in because it’s negative. under normal conditions most ion channels are closed but there are potassium leak currents; little bit of K+ is leaving (follows its concentration gradient and its charge gradient) Cl- is not attracted to the inside so it stays on the outside. resting membrane potential: separation of charge across neural membrane when neuron is not electrically active (usually -40 to -90 mV) measure: how much more negative is the inside from the outside negative because its the inside relative to the outside Separation of charge creates membrane potential when the ions move the charge changes -> current at equilibrium thats the resting potential know which ions are more concentrated on the inside and the outside: more K+ on the inside more Na+ on the outside, driven inside more Cl- on the outside, stays there energy is spent running this pump helping to keep the resting membrane potential at -60-90 mV A neuron’s resting membrane potential is maintained actively by the sodium potassium pump (requires ATP energy) Leakage happens (Na+ leaking in, K+ leaks in and out) the pump is designed to bring K+ back inside the cell and Na+ back outside to maintain the resting potential Na+/K+ pump uses active transport both sodium and potassium ions are moving against its concentration gradients (why it takes energy), area of low concentration to high concentration Ion pumps vs. Channels pump=active, requires energy channel=passive, diﬀusion, ions won’t pass through unless prompted by their gradient Types of Membrane Potentials Resting Potential In a resting neuron, few channels are open, lets some ions leak out, but the resting potential is still pretty constant (-45 to -70), but jitters a little because of the leaking. K+ will leak in or leak out Na+/K+ pump helps regulate the resting potential exchanges Na+ for K+ takes sodium back out of the cell brings potassium back in at rest, the inside of the cell is negatively charged what drives the ion movement is what’s available right next to the membrane the most readily available ions close to the membrane are the ones that go in or out through the pump separation of charge exists down the entire neuron (axon, dendrites, etc) when the ion channel is open = current ﬂow Receptor Potential touch receptors due to sensory receptors being stimulated; converting environmental signal to neural signal (weak or strong) Pacinian corpuscle: sensory neuron specialized to detect pressure in skin neuron at rest, membrane potential increases (becomes less negative - less separation of charge - ion channels open, positive ions rush in, then ion channels close, and we go back down toward the resting potential receptor potential: sensory receptor is activated graded potentials - they can be small or larger produced by sensory stimulus stimulus may or may not lead by activation in this particular example this cell was not activated sensory neurons in the knee-jerk reﬂex: when we tap the knee the sensory neuron wrapped around the muscle that is stretched generates the receptor potential pain, olfactory stimuli, optics/visual (sensory stimulus = light) all have receptor potentials Synaptic Potential activate synapse not enough to activate neuron (usually) synaptic potentials are graded potential in the receiving (postsynaptic) neuron or muscle cell = produced by synaptic input Action Potential neuron takes a signal it receives and delivers it stimulated enough to cross a threshold for activation change in voltage that races down the axon through the axon terminal motor neuron is activated (injecting current, putting in Na+) - depolarizes action potential: gotten above the threshold all or none phenomenon, either begins or it doesn’t, if it does, travels all the way down the axon “all or none” potentials in neurons produced by a sensory stimulus or by synaptic inputs that always produce neural activation and signal transmission to that neuron’s target all neurons have to be activated to ﬁre an action potential inhibitory neurons ﬁre action potentials too - just inhibit their targets instead of activating them PHASES: 1. resting potential 2. rising phase massive inﬂux of sodium causes an increase in voltage 3. overshoot phase inactivation opening of slower potassium voltage gate channels cell = positive potassium is driven out 4. falling phase potassium brings back down to resting potential sodium potassium pump continues working to restore resting conditions 5. undershoot phase more K+ exits the cell and brief hyperpolarization 6. recovery K+ ions diﬀuse back into the cell through leak channels and Na+/K+ pump rests the proper extracellular/intracellular ionic concentrations required for signal transmission Action potential requires that the neuron reach threshold passive conductance: no spike for action potential not enough current; not enough depolarization ap conduction has both active and passive components passive sets it up for the active component ions leaking in passively causes it to push into action potential Membrane polarization terms Polarization – the normal resting membrane potential, produced by the normal separation of charges (ions) Depolarization – less separation of charge across the membrane promotes “excitation” of the neuron, more likely to become activated (i.e., to ﬁre an action potential) has anything to do with receptor potential? excitatory Hyperpolarization – more separation of charge across the membrane promotes “inhibition” of the neuron, less likely to become activated to ﬁre an action potential inhibitory Repolarization – restoration of normal polarization after a period of de- or hyper-polarization restorative Passive and Active Currents passive currents: “graded” currents ion channels opening further away you get, the smaller the charge will be fade away as ion channels close not ampliﬁed receptor potentials active currents begin when the sum of graded currents produces a membrane depolarization that is large enough to initiate an Acton potential large enough to open voltage-gated Na+ channels open when membrane becomes depolarized enough stimulation electrode injects ions/current to change the separation of charge across the membrane Passive conduction decays over time no “action potential” - not enough current, not enough depolarization Action conduction is constant over distance the “action potential requires both passive and active conduction passive current spread is enough to depolarize the next segment active segment comes after the active part is due to opening of voltage-gated ion channels action potential has to travel down the axon; there’s some delay between the beginning and the end (dominos) ion channels are in the nodes of ranvier between the myelin; action potential skips from node to node; Na+ passively rush in; action potential moves down the axon much more quickly myelin speeds up the action potential when the ion channels open Na+ rushes in Why kids have low reaction time (throw a ball and they reach out to catch it too late): myelin hasn’t formed yet, makes the signal a lot slower The functional state of voltage-gated ion channels (i.e., open or closed) depends on membrane potential, detected by voltage sensors on the channel voltage sensors are pushed out by depolarization (opens channel) pulled in by hyper (or re- )polarization (closes channel) Na+ channel opens with depolarization, inactivates, membrane potential is still depolarized, and as soon as it gets back close to the resting potential, the channels close meanwhile, K+ channel stays closed until higher separation of charge, then opens, K+ rushes out passage of these ions forms the basis of the membrane potential? Membrane potential changes during an action potential Can a hyper polarizing current ever be an active current, or will it always be a passive current? always be passive: active currents are action potentials 4. Neural Development Fertilization and Implantation ovary becomes fertilized as the egg moves down the fallopian tube 6th day: about to implant; already have a mass of cells (developing embryo) egg implants in the lining of the uterus and begins to develop inner cell mass = developing embryo initial development is the nervous system Neural Development 1. Gastrulation (ﬁrst step - not really on the exam): blastula becomes gastrula the developing embryo midline section/structure develops into the nervous system nervous system develops on the midline cell layers: ectoderm: outer layer mesoderm: middle layer endoderm: inner layer process of gastrulation is the folding of the midline to form the three germ layers (above) the notochord forms at the midline of gastrulating embryo derived from the mesoderm don’t confuse notochord with spinal cord!! notochord is part of the mesoderm, and all of the nervous system comes from the ectoderm notochord (forms at the midline of the embryo) deﬁnes the embryonic midline; deﬁnes an axis of symmetry also induces the formation of the nervous system; delivers signals to the ectoderm to become the nervous system notochord eventually disappears; job is to induce the ectoderm to form neural ectoderm neural ectoderm gives rise to the nervous system; other ectoderm gives rise to skin, hair, and teeth, etc. 2. Neurulation neurulation is the formation of the nervous system: how the ectoderm becomes neural ectoderm and how the neural ectoderm gives rise to the central and peripheral nervous system 18 days after fertilization: already have the three major layers of the developing embryo all of the outer tissue is ectoderm but only the midline portion is going to form the neural plate neural ectoderm is beginning to become the brain and the spinal chord the mesodermal areas on the side give rise to body segments and parts neurulation: ectoderm becomes neural ectoderm the neural ectodermal precursor cells give rise to the neural plate; neural plate will become the whole nervous system same thing as the neural ectoderm 20 days after fertilization: neural plate is now a groove = neural groove (still neural ectoderm) groove extends along the midline pre-somitic mesoderm (future body segments) the very top of the groove is called the neural crest the neural crest is going to get pinched oﬀ; gives rise to the entire PNS and the rest of the neural groove will close oﬀ and become the CNS at this stage, same structure all from neural ectoderm Neural crest gives rise to mesenchymal cells that generate all peripheral neurons and glia, plus some other body tissue cell neural crest comes entirely outside the neural tube neural crest is dividing and becoming PNS diﬀerent path: adrenal gland and pigment cells, cartilage, and some bone (separate paths) somites are developing along with them initially when the embryo is developing, the nervous system and the somites are developing in close proximity (sprouting of axons connecting to muscles, everything is close together so the initial axon doesn’t have to grow a long distance, the muscle is right there) 22 days: neural tube is closed, but as you get closer to the edge, the neural tube looks more like a plate; the center of the neural ectoderm is developed ﬁrst the middle of the developing embryo develops ﬁrst; continues developing rostrally and caudally top of the neural tube is going to develop into the brain the upper spinal cord will develop ﬁrst lower spinal cord hasn’t closed yet walls of neural tube will be the brain, tissue, etc space in the middle of the neural tube, inner wall of the neural tube is going to become the ventricles (pre-pre-pre ventricular space) edges of the ventricular space is where the new neurons and glia are going to be born 24 days: more of the neural tube is closed most of the brainstem is closed up most of what will become the spinal cord is closed up neural crest → PNS sensory ganglia will eventually be receiving sensory feedback Regional Speciﬁcation of CNS forebrain - lateral (telencephelon) & third ventricles (diencephalon) midbrain - cerebral aqueduct hindbrain - fourth ventricle spinal cord - central canal chambers will become the ventricles and the walls of the ventricles will become diﬀerent regions of the brain If a portion of the neural tube doesn’t close: neural plate never becomes a neural tube spina biﬁda → the bottom of the spinal cord doesn’t develop anencephaly → the upper portion of the brain (forebrain) does not develop because the neural tube never closed can be partially hereditary (gene through families) or environmental - deﬁciency in folic acid (change the way that genes are functioning, enough folic acid makes things go normally) After Neurulation: Still immature cells, still have the ability to develop into other cells Migrate out to ﬁll tissue space to become connected and occupy a space in the nervous system Undergoing diﬀerentiation due to its unique pattern of gene expression – which genes are expressed determine which cell they become. Hundreds of subtypes – due to gene expression diﬀerences. Neural circuits are formed by various neurons (few or thousands) that are synaptically connected, involved in processing information (knee jerk=very simple circuit, circuit used to navigate things in your room in the dark = complex) For circuits to form you need axon and dendrites to grow and form to create synapses Neurogenesis, Gliogenesis (stem cells) can become a variety of things neural stem cells are derived from neural ectoderm (NSC) will become the neurons and glia of the CNS done dividing → blast cell, can diﬀerentiate into neural progenitors glial progenitors progenitor cells → blast cells? Induction One set of cells induces a response in another set of cells e.g. notochord induces the ectoderm nearby to become neuroectoderm changes gene expression in these developing cells - leads to speciﬁcation and specialization of the neurons neurons and glia arise from pluripotent neural stem cells (NSC) neurogenesis/gliogenesis: begins right after neural tube forms Migration once the cell has been born, needs to ﬁnd its way in the neural tube to its ﬁnal resting spot in CNS cells born in the hindbrain stay in the hindbrain forebrain neurons migrate out to form forebrain neurons do not translocate between regions once they leave the wall of the neural tube they can travel laterally/radially, migrating along radial glia (immature astrocytes) goal → get out of proliferative zone into ﬁnal CNS destination proliferate zone is right next to the lumen of the ventricle place they have to go might not exist yet; they may take up residence while other cells join them migrating cell will “shimmy” its way up a glial cell (immature astrocyte) scaﬀold migrating cells are guided by the radial glia radial glia are present in the tube after birth too sometimes, but as the tissue matures these glia will disappear/mature to live on as astrocytes diagram: oldest cells at the bottom, newest at the top Cortical Lamination (Layering) wall of neural tube is much thicker prefrontal (1) lobe, occipital (4) lobe Neural Migration Disorders (NMDs) disorders of the nervous system arising from failure of neurons to properly migrate Lissencephaly = smooth brain migration defects in developing CNS and other body tissues neural tube never became thick enough - nothing to cause folding to occur amount of tissue dedicated to the cortex is signiﬁcantly less lateral ventricles are a lot bigger than normal - in the developing neural tube the ventricular space is relatively large - walls of the neural tube didn’t get thicker but the skull still grew - so ventricles are large to ﬁll its space corpus collosum is really small - axon of neurons in the cortex, fewer neurons → fewer axons Down syndrome NMD extra 21st chromosome why does that cause downs syndrome? we don’t know cell migration problems, physical features, mental retardation, intellectual slowing, sometimes mild sometimes severe Diﬀerentiation unique patterns of gene expression that determine the cell type even though all cells were born in the same small region, they will go on to become many diﬀerent kinds of cells express a set of genes for a speciﬁc function of a cell new neurons being born every day (after birth) Circuit Formation: Neuronal polarization Growth of dendrites, axons, synapse formation ﬁrst axon growth cone, then synapse formation all cells will only have one axon and (most) have multiple dendrites neurons are a special type of polarized epithelial cells absorb and secrete molecules, and have special regions for intercellular communication neurons apical domain: becomes an axon (specialized for secretion - neurotransmitter release) - secretes at the very tip basal domain: becomes a dendrite (specialized for receiving signals - via receptors) - expresses receptors to receive chemical signals from other neurons Apical domain generates one axon Basal domain generates one or several “minor neurites”, some or all of which will become dendrites (others will retract) Neuronal polarization is the ﬁrst step in circuit formation protein-protein interactions within the neuronal cytoskeleton Axon Growth Cone sense signals based on whether they go toward or away from something OtV = where eye will end up labeled growth cones growth cone represents the decision point, where the developing axon is deciding to make a synapse to grow around a region and then continue on its target, or to be attracted by a cel growth process requires ATP diﬀerent types of axons will grow toward diﬀerent targets - leads to the speciﬁcation of the synapse Continuing principle events in CNS Development Circuit Formation growth of dendrites, axons, synapse formation branching of axons, formation of axon terminals At early stages of development, chicken embryo looks similar to human’s; experiments done to test hypothesis that motor neurons developing in the spinal chord are targeting the wing bud and some are going to send axons out to the limb bud. Is it just because of proximity? Or is it something else? experiment: took region of developing spinal chord and ﬂipped it; neurons that would’ve been leg going to leg muscle are in the more rostral area going toward the wing, and the wing neurons going to the wing were more caudal and going toward the leg. the neurons did ﬁnd their correct target even though they were far away innervate: to provide axonal inputs (motor neuron innervates muscle) what does this mean? how did it work/how was the motor neuron able to ﬁnd its correct target? Developmentally, after synapses form, will they persist? Many neurons are born, migrate, and grow their dendrites and axons, but then are eliminated Many synapses form, and then are eliminated “pruning” – based on competition, elimination of extra inputs optimizing signal transfer/function not every neuron that is made survives - the ones that make the right connections will survive Synapse number and innervation patterns are adjusted during early development Synaptic competition continues after birth neurons that “lose” the competition withdraw their synaptic contacts (axon terminals) the “losing” neurons might ﬁnd an appropriate alternate synaptic target nearby or they might wither away and die Target-derived trophic support regulates neuronal survival motor neurons are overproduced before limbs are innervated cut oﬀ limb bud 1 week later, neurons on that limb are gone (missing limb) in normal development, pruning occurs; there is an overabundance and some are eliminated neurons went away because they didn’t compete appropriately for the target bigger target, would they have survived? if you add a limb to a chicken embryo, they won’t die donor chicken embryo, took its limb oﬀ, and put it on another the side with an extra limb has its extra neurons survive, because all the neurons are able to interact with something so they all survive. but on the side with the normal limb, only half the neurons survived (like usual) Which principle(s) of development is/are demonstrated by the”ﬂipping chick spinal chord” experiment? Axons follow pre-determined cues in order to innervate the correct target what is it about the wing or leg bud that is attracting those axons? growth cones seek out factors that attract them or repel them - nerve growth factor - those are chemical factors Which principle is demonstrated by the extra limb experiment? neurons that fail to innervate their correct target will not survive Postnatal Human Brain Development In a human infant in the cortex, there is going to be a massive amount of dendritic growth, etc, after birth. by 2 years of age there aren’t more neurons, just more dendrites and axons. by 6 years, the number of neurons is the same, but some of the dendrites have retracted and axons have been eliminated early in development: huge up-ramp, lots of synapses being formed followed by a period of pruning (age 1-10) lose some synapses then stabilizes 6. Synaptic Transmission & Signal Integration Knee Jerk Reaction the sensory and motor axons are myelinated; that’s why the reaction is so fast, the signal can travel really quickly the motor neurons’ cell bodies are in the spinal cord the signal enters very quickly and the motor command reaches the receptor very quickly (because of myelin) Multiple Sclerosis (MS) attributed to a loss of myelin (CNS and PNS; aﬀects shwann cells and oligodendrocytes) autoimmune? muscle weakness and slow reﬂexes; knee-jerk reﬂexes and other reﬂexes can diminish or disappear Divergent Circuit: one cell or two cells diverge; one sensory neuron will ultimately impact hundreds of neurons to be able to perceive a signal Converging circuit: typical in motor circuits; many neurons tell one motor neurons to contract muscle The Synapse 1. transmitter is synthesized back in the cell body, shipped down in vesicles to axon terminals (the enzymes) transmitters are synthesized in the axon terminals synthesis can occur in the cell body or the teminal gets put into synaptic vesicles (contain molecules of neurotransmitter substance; must be in a vesicle to be released) 2. action potential originated up at the axon hillock or sensory receptor, travels down to invade the axon terminal huge wave of depolarization 3. depolarization opens the voltage gated ion channels 4. calcium ﬂows through the channels 5. this causes vesicles to fuse with presynaptic membrane 6. transmitter is released into synaptic cleft via exocytosis 7. transmitter binds to receptor molecules present in membrane neurotransmitter receptor: opened by a ligand; something has to bind to them in order to open them (that something = neurotransmitter) diﬀerent neurotransmitters can be released into the synaptic cleft when the transmitter binds to the receptor: receptor changes shape and opens the ion channel 8. Opening or closing of postsynaptic channels neurotransmitter does NOT ﬂow through the channel - just opens it the charge carrying ions ﬂow through; sodium, potassium, chloride 9. when those charges move through, do they cause a depolarization or hyperpolarization depolarization: chance to activate the cell hyperpolarization: more separation of charge; chance to inhibit the cell 10. removal of neuron-transmitter by glial uptake or enzymatic degradation neuron ﬁres a lot of action potentials more vesicles and more transmitters can slowly come down to help reﬁll Step 4 in more detail: Neurotransmitter release is calcium ion-dependent measuring current for calcium (tracing the positive ions) positive ions come in = depolarization excitatory phase calcium came in and caused neurotransmitter release when you block the calcium current calcium does not come in no postsynaptic potential, because no neurotransmitter was released no excitatory phase all postsynaptic potentials need calcium ﬂow into the cell Step 7 Transmitter chemicals will bind to receptor molecules in the postsynaptic membrane ligand-gated channels: opened by a ligand glucose binds to a receptor site; ion channel opens calcium binds, potassium can go through Neurotransmitter Criteria deliver a chemical signal that will depolarize or hyperpolarize a cell must be present within the presynaptic neuron must be released in response to depolarization of presynaptic membrane in a Ca 2+-dependent manner must engage speciﬁc receptors present on the postsynaptic target Small-molecule neurotransmitters synthetic enzymes made in cell body enzymes transported to axon via microtubules neurotransmitter synthesis (from precursor molecules) completed and packaged into vesicles within axon terminal transmitter released from vesicles at synapse precursor molecules taken up into axon terminal precursors used for enzyme-mediated synthesis of new transmitter molecules (which also may be taken back up and recycled) Neuropeptides much bigger (many amino acids) examples: substance P, opioids, somatostatin, oxytocin Neurotransmitter precursor proteins and cleavage enzymes made in cell body Enzymes and precursors packaged into vesicles that are transported along microtubules to axon terminal Enzymes modify precursors within vesicles to produce ﬁnal peptide transmitter Transmitter released from vesicles at synapse Neurotransmitter degraded by proteolyticenzymes, (or may be taken back up and recycled) some things get reused and some things get degraded Postsynaptic Membrane responses depend on ion movement which ion channels does it open? which receptor bound molecule and what ion channels are opened as a result ions carry their charges with it: postitive ions ﬂow in = depolarization sodium in and less potassium out = net positive current = smaller depolarization sodium in, potassium out = no net current = no change potassium out = losing positive charge = hyper-polarized Diﬀerential activity-dependent release of neurotransmitters from the same axon terminal clear vesicles = small molecule transmitters small molecule transmitters; vesicles are smaller; closer to the axon presynaptic membrane (these are the vesicles that will preferentially get released) dense core vesicles = peptide transmitters hang back, not right at the presynaptic membrane; not going to get released if only a little calcium comes in when more calcium comes in, interaction with design core vesicles Neurotransmitter Receptors Two main families of receptor proteins: ionotropicreceptors (a.k.a. ligand-gated ion channels) ions move through channel in direct response to ligand binding (the receptor is part of an ion channel) Initiate very rapid postsynaptic eﬀects (millisecond scale) Example: ACh acting at neuromuscular junction metabotropic receptors (a.k.a. G-protein-coupled receptors) Functionally coupled ion channels open in response to initiation of metabolic events (the receptor does not include an ion channel) Initiate slower postsynaptic eﬀects (seconds to hours) Example: adrenaline (epinephrine) acting on visceral smooth muscle not for instantaneous signal transfer (longer timescale) Glial Cell astrocyte neurotransmitter molecules encounter the glial cells outside the synapse glial cells regulate “Neural threesome”,“Tripartite Synapse" 1. astrocytes wrap around the gaps of synapses between neurons 2. neuron releases neurotransmitter; some can be taken up by the astrocyte 3. astrocytes can become activated or just sop it up and get it out of the synapse 4. calcium levels can increase 5. astrocytes themselves can release signaling molecules that can aﬀect the way the synapse works *inject calcium current into astrocyte - actively signal and create communities of electrical signaling 1. Introduction to the Nervous System Important early innovators that helped found neuroscience Golgi most famous for his technique (his theories turned out to be wrong); developed silver impregnation/stain; revealed structure of neurons and glial cells Golgi stain only labels a subset of neurons (randomly), which helps you see them better No explanation as to why this happens This is valuable because if you look at a block of a Golgi stained tissue, you can see the individual cell bodies, dendrites, axons At this time they thought neuron signals traveled through the shared cytoplasm; communication through a shared network He developed a technique to prove himself wrong; he wasn’t able to make that intellectual leap Cajal Golgi’s adversary Cajal used Golgi’s technique against him/improved it, and used it to prove the neuron doctrine: each neuron is an individual independent cell, and communicates with other cells but not through shared cytoplasm, but through gaps between cells linked by synapses. Work followed up by Charles Sherrington who further reﬁned the neuron doctrine Both Sherrington and Cajal are credited for the doctrine Cells in the nervous system 2 main types of cells in the nervous system neurons (nerve cells) glia (glial cells): support cells for the nervous system oligodendricites make myelin (insulating tissue) microglia are scavengers astrocytes participate in the blood brain barrier and buﬀer the pH and osmotic content of the extracellular ﬂuid vascular endothelial cells make up the blood vessels of the brain hundreds of thousands of miles of blood vessels in the brain capillaries make up more bulk of tissue than any other type in the brain “Brainbow" cassette will express the primary colors; random expression of colors (some cells are red, some are blue, etc) Nervous system has two major components central (CNS) - brain & spinal chord - brain protected by skull and spinal chord is protected in the vertebral column peripheral (PNS) - not protected by bone (everything else) cranial nerves, spinal nerves, peripheral ganglia in heart/pancreas, autonomic nervous system one exception to the rule: the retina; the origin of the optic nerve. not protected by bone. Major components of the nervous system CNS: areas that are primarily motor; control how to make the body move sensory components: bring information from the outside world AND from within the body into the brain (internal and external environmental signals that travel through sensory pathways into the system) motor components will control skeletal muscles or smooth muscles of the bladder/uterus/heart (autonomic) cranial nerves are in charge of the head and neck the spinal nerves are in charge of the shoulders down exception: vagus nerve is a cranial nerve but controls some things below the neck General neuron categories sensory neurons take environmental signals (temp, pressure, sound waves, photons of light) and traduces them into neural signals that neurons can understand. they are aﬀerent neurons because they bring information into the nervous system motor neurons contract muscles to move the body around, or to control visceral functions (glands, hormone secretion, cardiac muscle). they are eﬀerent neurons because they take information out of the CNS and into the body. some of the motor neurons are endocrine neurons because they secrete hormones (control the release of hormones) interneurons communicate signals between neurons usually between the same region of the nervous system/close by. sharing information with a neuron of group of neurons nearby. projection neurons have long axons within the CNS (if they left they’d be motor neurons), and communicate with other neurons located in a distant area in the nervous system. how far away is the signal going to be delivered? close = interneuron; distant = projection neuron. mass of nerves at the end of spinal chord reﬂex arc: knee jerk reﬂex tests the transition of signals from sensory receptors in a tendon in the knee and a sensory signal that can travel up to the spinal chord through a long nerve impact the ﬁring activity cause the activation of motor neurons that project back out down to the muscles that move the knee. knee jerk reﬂex is an example of the sensory in, motor out. common neurological test of function for injury in nerve pathway or spinal regions, myelin is appropriate, etc. tap the patellar tendon, physically stretches and pulls on incense muscle, turns on sensory neuron send its signal that enters the spinal chord, and the signal gets delivered to interneurons and motor neurons in the spinal chord. motor neuron gets excited; becomes activated and sends a neural signal to control a muscle; muscle is stretched and tells the motor neuron to ﬁre and contract a muscle; back to its original place; knee jerks. interneuron is also excited and silences the opposing muscle. turns the other motor neuron oﬀ (the one that keeps your leg from ﬂailing). so the motor neuron excites and activates the jerk muscle, and the interneuron excites and activates the opposing muscle. neurons are diﬀerent every neuron is unique; like trees every oak tree has morphological features, but no two trees are identical. birch, oak, maple; many diﬀerent types/categories of neurons. diﬀerent types with diﬀerent functions. shape, size, structure, location, dictates function of neurons things they have in common: cell bodies, all (exceptions) have dendrites dendrites are involved with receiving signals; increase the surface area for receiving input of a neuron. they would not have as many diﬀerent inputs with just the cell body. every single aspect of the dendrite is available to receive synaptic input; neuron can now receive more complex input. only one axon that comes oﬀ the cell body (but the axon can branch): axon delivers the signal to another target, to another neuron or a group of neurons, or if its a motor neuron it might be to muscle. as many axon branches as there are that will provide a way for an individual neuron to target diﬀerent neuron or muscle targets. neurons’ major features neurons are made to communicate by electrical and chemical signaling (unique bc they do both) intracellular signaling (within neurons) intercellular signaling (between neurons) cell body is called the soma lots of ribosomes because they are so highly specialized to secrete neurotransmitters, making so many proteins, so they have extra ribosomes dendrites all along the dendrites there are many instances of axon terminals (synapse) and it has the ability to signal to the dendrite axon only one that leaves the cell body but will often branch; delivers signals to other targets close or far away; covered in insulation called myelin to increase the speed of the electrical signal being sent axon terminal; synaptic ending this is a synapse; the point of contact; very thin space; cleft; membrane of axon terminal and membrane of the dendrite; synapse is a point of chemical signaling 2. Glia, Meninges, Ventricles, & the Blood Brain Barrier Glial cells - cells in the brain that support the neurons CNS contains 3-4x more glial cells than neurons; for every neuron there are 3-4 glial cells types of glial cells astrocytes oligodendrocytes (CNS) shwann cells (PNS) microglia/macrophages macrophages are derived from bone marrow macrophages diﬀerentiate into microglia ependymoglia cells that line the ventricles; interface between cerebral spinal ﬂuid and Astrocytes in close proximity with the blood vessels; usually where you will ﬁnd them restricted to CNS they help maintain the proper extracellular chemical environment necessary for neural signaling calcium regulating “end feet” that come into contact with capillary endothelial cells to maintain their tight junctions; these junctions comprise the blood brain barrier the astrocytes interacting with the tissue that forms the tight junctions also have a special role during early embryonic development astrocytes become radial glia cells; neuron Oligodendrocytes and Schwann cells - the glia that make myelin CNS: oligo PNS: shwann each glial cell lays down multiple layers of myelin (lipid membrane) to “insulate” myelinated axons Each oligodendrocyte myelinates several parts of several CNS axons Each Schwann cell myelinates one part of a single PNS axon (like beads on a chain) Microglia smallest glial cells multifunctional originally from the bone marrow - don’t develop as part of the brain/spinal chord, develop in the Periphery, and migrate to the CNS primary function: scavenger change their form back and forth multiple times (can become phagocytic and return to resting state) e.g. infection/stab wound: migrate in and help out, transform in many directions as necessary bacteria being gobbled up by macrophages with lysosomes that have enzymes that digest them down microglia secrete cytokines (signalling molecules) to call more macrophages into the area while the local microglia react to the situation they call macrophages to help out (via cytokine secretion) change the fastest, have the most plastic structure Ependymoglia line the inner surface of the ventricles not just providing the barrier; long processes that go into the tissue probably signaling into brain tissue in that area especially in the hypothalamus specialized form interacts with capillary cells and forms the choroid plexus choroid plexus is a vascularized tissue this secretes the cerebral spinal ﬂuid into the ventricular system Meninges encases the CNS (brain and spinal chord), protects it from trauma, maintains a ﬂuid cushion around the nervous system three protective layers of tissue surrounding the CNS 1. dura mater: hard, tough, can’t break through it dura mater comes oﬀ with the skull 2. arachnoid mater: spider like subarachnoid space 3. pia mater: tender matter, fragile and thin, completely covers everything, impossible to peel oﬀ, really thin and ﬁne pia layer folds in with all the gyri subarachnoid space between arachnoid and pia layers this space is ﬁlled with ﬂuid and also is occupied by major arteries and veins on the surface of the CNS left the ventricular system and entered the subarachnoid space meningitis: infection of the meninges; causes swelling and subsequent compression of the skull, leads to seizures and stroke viral meningitis bacterial meningitis (more serious, often fatal; immunization available) Ventricular System series of interconnected, ﬂuid-ﬁlled spaces within the core of the brain and spinal cord ﬁlled with cerebrospinal ﬂuid (CSF) 1. derived from the choroid plexus - a specialized capillary/ependymoglia tissue within the walls of ventricles; ﬁlters capillary blood and secretes the CSF product into the ventricles 2. Enters the lateral ventricles, third ventricle, through cerebral aqueduct into fourth ventricle 3. CSF leaves ventricles through several foramina to enter the subarachnoid space surrounding the brain/spinal cord 4. CSF then drains out of subarachnoid space through the arachnoid villi/granulations into subdural sinuses, then back into the general venous blood circulation Blockage in cerebral aqueduct can lead to swelling of the head due to swelling of the brain thin aquaduct is blocked, that ﬂuid has no where to go, ventricles swell and push the brains out usually happens in infants because their skulls haven’t fully formed yet called hydrocephalus blockage and build up of spinal ﬂuid Blood-brain Barrier NOT the role of the meninges, meninges BBBarrier = walls of the blood vessels in the brain Formed by the tight junctions between vascular (capillary) endothelial cells inside the brain and spinal cord these tight junctions are induced by astrocytic “end feet” which contact vascular endothelial cells Brain capillaries are NON-FENESTRATED (no windows) capillaries in the rest of the body’s tissues are FENESTRATED (with windows because they lack tight junctions/barriers) A few small, special brain regions do contain fenestrated capillaries . . . specialized for detecting toxins, hormones, etc. Circumventricular organs (on brain midline, adjacent to ventricles) area postrema near the fourth ventricle allow entry of other molecules that the rest of BBB will not keeps out proteins, hormones, toxins, bacteria, blood cells allows in oxygen, carbon dioxide, gases, glucose, insulin, amino acids, alcohol, nicotine, cocaine
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