BI 315 Exam 1 Study Guide
BI 315 Exam 1 Study Guide BI 315
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This 15 page Study Guide was uploaded by JordanK on Saturday February 13, 2016. The Study Guide belongs to BI 315 at Boston University taught by Dr. Widmaier in Spring 2016. Since its upload, it has received 434 views. For similar materials see Systems Physiology in Biology at Boston University.
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Date Created: 02/13/16
BI 315 – Systems Physiology READING NOTES – CHAPTER 6 (Responsible for everything except pgs. 168170 but read GABA section) Key Terms Central nervous system (CNS): brain and spinal cord Peripheral nervous system (PNS): nerves that connect the brain and spinal cord with the body’s muscles, glands, sense organs, and other tissues Neuron: individual cell of the nervous system (Not a nerve!); generate electrical signals to other cells to communicate Nerves: groups of afferent and efferent neuron axons, myelin, connective tissue, and blood vessels Neurotransmitters: chemical messengers often released by neurons that communicate with cells Glial cells: nonneuronal cells that are important in supportive functions for neurons Section A (6.16.4) – Cells of the Nervous System Neuron structure (6.1) o Cell body (soma): contains nucleus and ribosomes o Dendrites: high branched outgrowths of cell that receive incoming information from other neurons Increases surface area to receive more signals (can have as many as 400,000 dendrites that branch into dendritic spines to receive many signals) o Axon (nerve fiber): long process that extends from cell body and carries outgoing signals to target cells; can be few microns to over a meter in length Initial segment (axon hillock): location where propagated electrical signals are generated Collaterals: branches on axon; more branches = more cells it can target May be covered by a myelin sheath, which speeds up conduction of electrical signals along axon and conserves energy CNS: myelin is formed by glial cell called oligodendrocyte PNS: myelin is formed by glial cell called Schwann cell Space between sections of myelin: nodes of Ranvier Axonal transport: movement of molecules from cell body to axon terminals, help from kinesins (anterograde movement to axon terminals) and dyneins (retrograde movement towards cell body) which use ATP to walk along microtubules o Axon terminal: site of neurotransmitter release o Varicosities: bulging areas where neurotransmitters are released along axon Functional classes of neurons (6.2) o Afferent neurons: convey info from tissues/organs towards CNS Sensory receptors: at peripheral ends of afferent neurons; respond to physical/chemical changes in environment by generating electrical signals Only have 1 process (axon) associated with cell body, which branches into a peripheral process (afferent terminal branches converge with receptor endings) and a central process (enters CNS to form junctions w other cells) o Efferent neurons: convey info from CNS to effector cells (muscles, glands, etc.) Cell bodies and dendrites generally in CNS, only axon is in periphery o Interneurons: connect neurons within CNS; most neurons in body (99%) for every afferent neuron, there is about 10 efferent neurons and 200,000 interneurons more interneurons between specific afferent and efferent neurons corresponds to complexity of action controlled (ex: millions involved in connecting a smell to a memory) o synapse: where signal is transmitted from one neuron to another by neurotransmitters; usually occurs at presynaptic axon terminal and goes to postsynaptic neuron glial cells (6.3) o accounts for half of cells in CNS o retain capacity to divide throughout life (unlike neurons) o oligodendrocyte: forms myelin sheath around CNS cells o astrocyte: regulates composition of extracellular fluid in CNS (removes K ions and neurotransmitters around synapses); stimulates formation of tight junctions between cells of walls of CNS capillaries forms bloodbrain barrier: selective filter for exchanged substances present in blood/other tissues provides glucose to neurons and removes ammonia guides CNS neurons to final destinations in developing embryos Very similar to neurons (ion channels, neurotransmitter receptors, etc.) o Microglia: perform immune functions in CNS; synapse remodeling and plasticity o Ependymal cells: line fluidfilled cavities in CNS; regulate production and flow of cerebrospinal fluid Neuron growth and regeneration (6.4) o Stem cells develop into neurons or glia in embryo in forming CNS After last cell division, neuronal daughter cells differentiate and migrate to final destination and send out processes (axons and dendrites) Growth cone forms on end of growing axons to help find final target; axon is attracting, supported, deflected from, or inhibited by many molecules in finding final destination o Alcohol, drugs, radiation, malnutrition, and viruses have effect on developing fetal nervous system when synapses are being formed o 5070% neurons (along with axons and synapses) formed in embryonic CNS undergo apoptosis o Plasticity: brain’s ability to modify its structure and function in response to stimulation or injury can generate new neurons or remodel synaptic connections; stimulated by exercise or cognitive challenge activities varies with age (visual synapses: first 2 years of life; language learning progressively decreases over life) synaptic contacts change throughout life due to growth, learning, aging o axons can repair themselves as long as it occurs outside of CNS and does not damage cell body piece of axon attached to cell body regenerates with new growth cone at about growth rate of 1 mm per day spinal injuries cannot be fixed if cell bodies die or lose myelin sheath (cannot transmit information effectively) Section B (6.56.7) – Membrane Potentials Basic principles (6.5) o two functions of a neuron: signal integration and celltocell communication o electrical potential (potential): potential defined by two separated electrical charges of opposite charge that could do work if allowed to come together; difference in amount of charge between two points o Ohm’s Law: current (movement of electrical charge) is equal to voltage divided by resistance water is a good conductor due to dissolved ions; ions can carry current lipids are insulators; regions of high electrical resistance separating intra and extracellular fluids Resting membrane potential (6.6) o Definition: potential across cell membranes normally; inside of cell is more negative than outside; typically 70 mV (represents difference between inside and outside only – not actual value of charge on either side of membrane) RMP in neurons is anywhere from 40 to 90 mV o Holds steady until an electrical current alters it o Excess of negative ions collect in thin layer on inside of plasma membrane (not distributed through cytosol) while excess of positive ions collect in thin layer on outside o Na , Cl are 1030 fold larger in concentration on outside of cell; K is 1030 fold larger in concentration on inside of cell + + + + Concentraton gradients for K and Na are established by Na /K ATPase pump; Cl concentration varies between cell types o Magnitude depends on differences in specific ion concentrations in intra and extracellular fluids and difference in membrane permeability to different ions and presence ion pumps o Membrane potential differences influences movement of ions across membrane Ex) Figure 6.10 and 6.11 o Equilibrium potential: the value to which each ion would bring the membrane potential if it were the only permeating ion (assuming unequal concentrations on either side of membrane) Depends on the concentration gradient for given ion across membrane (large concentration gradient = large equilibrium potential due to larger movement of ions to balance) Different ions have different magnitudes and directions of equilibrium depending on concentration gradient o Nernst equation: describes equilibrium potential for any ion 61 log C (out) Z ( C ¿ ) E(ion) for Na is +60 mV while for K it is 90 mV o The greater the permeability of a membrane of a specific ion, the greater of an impact that ion will have on membrane potential GoldmanHodgkinKatz (GHK) equation: accounts for concentrations of K/Na/Cl inside and outside of cell in membrane potential ( ) V m )=61log P K[ou( +P]Na Ku[ +( Cl)] K( ] ( P K[¿ +P]Na K(+P Cl ]utK ( ( )] ) + o K is most permeable to membranes, which is why RMP is close to its equilibrium potential Constantly moving down concentration gradient via leak channels (Na is also moving through fewer leak channels, which is why RMP does not exactly equal K equilibrium potential) ATPase pump moves ions back out (unequal 3 Na and 2 K establishes gradient in the first place = electrogenic pump) Graded potentials and action potentials (6.7) o Excitability: the ability to produce electrical signals that can transmit info between different regions of the membrane (excitable membranes) Includes all neurons and muscle cells Depolarized: membrane potential becomes less negative than RMP Overshoot: reversal of membrane potential; inside of cell becomes positive relative to outside Repolarized: depolarized membrane returns to RMP Hyperpolarized: potential is more negative than RMP o Graded potentials: changes in membrane potential confined to relatively small region of membrane Magnitude can vary based on magnitude of initiating event Includes receptor potentials, synaptic potentials, pacemaker potential Can be depolarizing or hyperpolarizing Important in signaling over short distances Local current is decremental: flow of charge decreases over distance from site of origin Can be summated o Action potentials Important in longdistance signals and with neuronal and muscle cell membranes; travels down axons Very rapid; can repeat at frequencies of hundreds per second Only occurs if stimulus can elevate membrane potential to threshold (all ornone) Stimuli that barely do that: threshold stimuli Same size regardless of strength of stimuli above threshold stimuli (signal information is dependent on frequency of action potential, not amplitude) Generation of action potentials is limited by local anesthetics (including procaine (Novocain) and lidocaine (Xylocaine)) by blocking voltage + gated Na channels (cannot open) no signal of pain is received Tetrodotoxin in puffer fish works the same way Cannot be summed due to refractory period needed + Absolute refractory period: when Na channels are already open or inactivated; cannot receive new action potential; reason why a signal only moves in one direction down an axon Relative refractory period: occurs during hyperpolarization; some Na channels have fully closed and can thus be reopened if strong enough stimulus allows threshold to be reached despite hyperpolarization o Types of ion channels (review from chapter 4) Ligandgated Mechanicallygated Voltagegated o Action potential mechanism: Begins with a depolarizing stimulus (less negative); stimulates opening of + some Na channels Once threshold potential is reached, depolarization becomes a positive feedback loop and all Na channels open; causing overshooting; + approaches Na equi+ibrium potential of +60 mV Inactivation of Na channels by inactivation gate prevents equilibrium potential from being reached; breaks positive feedback loop; K channels have finally opened (very slow compared to Na) + + K flux out of cell causes repolarization; causing Na hannels to close Membrane is momentarily hyperpolarized as K channels are slow to close in negative feedback loop (afterhyperpolarization); then RMP is restored o Action potential propagation can only occur if each point along the membrane is depolarized to its threshold potential as it moves down the axon New action potentials produce local currents of its own that depolarize the region adjacent to it, which causes an action potential in that region action potentials do not move, but sets off the next one Sequential opening and closing of Na and K channels along axon Action potential at end of axon is identical to initial one; they are not decremental Velocity depends on fiber diameter (larger = faster; less internal resistance and more ions can flow faster) and if it is myelinated (faster; less ion leakage and does not contain many Na channels so action potentials “jump” from nodes of Ranvier = saltatory conduction) o Generation of action potentials Afferent neurons: initial depolarization to threshold is achieved by a graded receptor potential generated in sensory receptors All other neurons: achieved by graded synaptic potential (generated by synaptic input) or pacemaker potential (spontaneous change in membrane potential) Section C (6.86.14) – Synapses Excitatory synapse: membrane potential of postsynaptic neuron is brought closer to threshold (depolarized) Inhibitory synapse: membrane potential of postsynaptic neuron is driven farther from threshold (hyperpolarized) or stabilized Convergence: many presynaptic cells affecting one postsynaptic cell Divergence: a single presynaptic cell affecting many postsynaptic cells Functional anatomy of synapses (6.8) o Electrical synapses Plasma membranes of pre and postsynaptic cells are linked by gap junctions to allow local current to flow directly across junction Advantage: communication is extremely rapid Function: synchronization of electrical activity among neurons clustered together in CNS and communication between glial cells and neurons Conductance modulated by membrane voltage, intracellular pH, Ca 2+ concentration o Chemical synapses Presynaptic axon terminals hold synaptic vesicles that contain neurotransmitters Postsynaptic membrane has postsynaptic density: a bunch of proteins that will receive neurotransmitters Synaptic cleft: region between pre and postsynaptic cells Mechanisms of neurotransmitter release (6.9) o Prior to activation, synaptic vesicles are docked on the presynaptic membrane at active zones by SNARE proteins o Release is activated when an action potential reaches presynaptic terminal membrane Depolarization activates influx of Ca channels o Ca ion help fusion of docked vesicles to membrane by binding to synaptotagmins on vesicle (causes conformation change in SNARE proteins), releasing neurotransmitters into cleft o Vesicles either fully fuse into membrane to be recycled or perform “kissandrun fusion” Activation of postsynaptic cell (6.10) o Fraction of released neurotransmitters will bind to receptors on postsynaptic plasma membrane Can be ion channels (ionotropic receptors), or indirectly influence ion channels via Gproteins/second messengers (metabotropic receptors) Binding of neurotransmitter causes change in membrane potential Reversible process; ion channels return to resting state when neurotransmitters are no longer bound o Unbound neurotransmitters are removed by active transport into presynaptic axon terminal for reuse (reuptake), transported to nearby glial cells for degradation, diffuse away from receptor site, or enzymatically transformed into inactive substances o Excitatory postsynaptic potential (EPSP): depolarizing graded potential that decreases in magnitude as it spreads; functions to bring postsynaptic membrane potential closer to threshold (occurs at excitatory chemical synapse) Opens channels for Na and K (net positive flow due to Na ) + o Inhibitory postsynaptic potential (IPSP): hyperpolarizing graded potential that lessens the likelihood that postsynaptic cell will reach threshold and generate an action potential Stabilization can also occur in place of hyperpolarization + Opens channels for Cl or K channels (net negative flow) Synaptic Integration (6.11) o Action potentials generally need more than one excitatory synapse event to occur Up to hundreds of excitatory synapses can be activated at once, adding together to cause a single action potential o EPSPs and IPSPs interact, which controls of an action potential occurs or not Temporal summation: input signals that were created at different times add together (the second occurs before the first is completely gone) Spatial summation: input signals created at the same time but from different locations add together An EPSP and an IPSP will cancel each other out o Different parts of the neuron will have different thresholds Initial segment of axon has a more negative threshold (less depolarization + needed) than dendrites or cell body higher density of Na channels o Neuronal responses almost always occur in bursts of action potentials, not just single, isolated events Synaptic strength (6.12) o Presynaptic mechanisms Release of neurotransmitters is not a constant amount; amount varies due to concentration of Ca in the cell (higher concentration = more release) The greater the release of neurotransmitters, the more ion channels opened in postsynaptic membrane, the greater the amplitude of EPSP or IPSP Neurotransmitters can bind to receptors on presynaptic membrane, causing more Ca in lux and more release Axoaxonic synapse: may be associated with presynaptic receptors; axon terminal of one neuron ends on axon terminal of another (ex: how A can affect C indirectly through B) Receptors can be ionotropic (rapid effect) or metabotropic (slow) Can result in presynaptic inhibition (A decreases amount that B releases on C) or presynaptic facilitation (A increases amount that B releases on C) Autoreceptors: presynaptic terminal is activated by neurotransmitters released by own axon terminal; important feedback mechanism for release (usually negative feedback) o Postsynaptic mechanisms A given signal transduction mechanism may be regulated by multiple neurotransmitters and may be associated with many secondmessenger systems Receptor desensitization: a receptor eventually fails to respond to the continued presence of a neurotransmitter (why tolerances exist) Cotransmitters can bind with neurotransmitters – more complexity in postsynaptic response (plasticity) o Modification of synaptic transmission by drugs and disease Recreational drugs alter synaptic mechanisms/strength by interfering with or stimulating normal processes in neurons controlling synthesis, storage, release of neurotransmitters and receptor activation (figure 6.34) Agonists: ligands that produce a response similar to normal activation Antagonists: ligands that bind to receptor but produce no response Agonists and antagonists can affect pre and postsynaptic receptors Tetanus toxin: results in tetanus, which destroys SNARE proteins in presynaptic terminal of inhibitory neurons; vesicles cannot fuse and release neurotransmitters; results in muscle contraction and rigid or spastic paralysis Botulism: destroys SNARE proteins in presynaptic terminal of excitatory neurons; results in reduced muscle contraction or flaccid paralysis Botox: low dose of botulinum toxin to reduce facial wrinkles, severe sweating, uncontrollable blinking, misalignment of eyes etc. Neurotransmitters and neuromodulators (6.13) o Neuromodulators: chemical messengers that cause complex responses that cannot be described as simply EPSP or IPSP Hard to distinguish sometimes; released with neurotransmitters Modify postsynaptic cell’s response to neurotransmitters (amplify or dampen effect of synaptic activity) May change presynaptic cell’s synthesis, release, reuptake, or metabolism of neurotransmitter Often bring changes in metabolic activity usually via Gproteins and secondmessenger systems; can occur over minutes or days (compare to neurotransmitters: elicit excitatory or inhibitory response immediately) Associated with slow events: learning, development, motivation o Acetylcholine (ACh) Major PNS neurotransmitter at neuromuscular junction and in the brain Neurons that release ACh: cholinergic neurons Acetylcholinesterase is responsible for degradation of leftover ACh in synaptic cleft; releasing choline and acetate Sarin: chemical weapon that inhibits AChase; buildup of ACh causes overstimulation of receptors = muscle contractions, desensitization, and paralysis Nicotinic receptors: respond to nicotine as well as ACh Present at neuromuscular junctions; important in cognitive function and behavior (attention, learning, memory) Present in reward pathways why nicotine is so addictive Muscarinic receptors: binds muscarine (poison in mushrooms) as well as ACh Metabotropic and coupled to Gproteins Present where PNS nerves are present in peripheral glands, tissues, organs (including heart) Atropine: natural antagonist; use in eye drops to relax smooth muscle of iris Alzheimer’s disease: degeneration of cholinergic receptors in brain Affects 1015% over 65 and 50% over 85 Lose of cholinergic receptors = decrease in ACh = loss of postsynaptic neurons that respond to ACh Associated with declining language and cognitive abilities, confusion, memory loss Associated with genetic mutations (ex: betaamyloid protein increase due to mutation on chromosomes 1, 14, and 21, which causes neuronal cell death) Environmentally affected (diet, exercise, mental stimulation) Drugs can slow progression o Catecholamines: catechol ring and amine group; derived from tyrosine (tyrosine Ldopa catecholamine; modulated by autoreceptors on presynaptic terminal) Forms dopamine, norepinephrine, and epinephrine Biogenic amines: small, charged molecules formed from amino acids Broken down in extracellular fluid and axon terminal by monoamine oxidase (MAO) MAO inhibitors increase amount of norepinephrine and dopamine in synapse (slows degradation); treats mood disorders Control consciousness, mood, motivation, direct attention, movement, blood pressure, hormone release In CNS, catecholamine receptors are found in brainstem and hypothalamus; released to all parts of body All receptors are metabotropic Norepinephrine and epinephrine are synthesized in adrenal glands Alphaadrenergic receptors: alpha 1 and alpha 2; inhibit norepinephrine release in presynaptic cells and stimulate or inhibit + K channels in postsynaptic cells Betaadrenergic receptors: beta 1, beta 2, and beta 3; act via G proteins to increase cAMP in postsynaptic cell o Serotonin: produced from tryptophan Works as neuromodulator (slow onset); serotonergic neurons innervate every structure in brain and spinal cord (operates through at least 16 different receptors) Excitatory effect when involved with control of muscles Inhibitory effect on pathways mediating sensation Lowest activity during sleep, highest during alert wakefulness Regulates food intake, reproductive behavior, emotional states (mood, anxiety) Paroxetine (Paxil): reuptake inhibitor; used in treatment of depression; side effects include decreased appetite and weight gain (drug affects many serotonin receptors) LSD: stimulates serotonin receptor in brain; produces intense visual hallucinations o GABA (gammaaminobutyric acid) major inhibitory neurotransmitter in brain modified form of glutamate can bind to ionotropic (increases Cl flux into cell; causing IPSP) or metabotropic receptors alprazolam (Xanax) and diazepam (valium): affects ionotropic receptors; reduce anxiety, prevent seizures, induce sleep ethanol stimulates GABA synapses and inhibits glutamate synapses, causing global depression of electrical activity in brain reduced cognitive ability and motor coordination, inhibition of hearing and balance, memory loss, impaired judgment, unconsciousness Neuroeffector communication (6.14) o Many PNS neurons do not end at synapses, but at neuroeffector junctions in muscles, glands, etc. Provides link between electrical activity of nervous system and effector cell activity o Evens at neuromuscular junction is similar to synapse events Neurotransmitter released diffuses to surface of effector cell, which can have ionotropic or metabotropic receptors Section D (6.156.19) – Structure of the Nervous System CNS: brain (6.15) o Key terms Pathway (tract): group of axons traveling together in CNS (NO nerves in CNS); includes long neural pathways (brain to spinal cord) and multisynaptic pathways (many neurons, branching axons) Commissure: group of axons that link right and left halves of brain Ganglion: a group of neuronal cell bodies with similar functions clustered together in PNS Nucleus: a group of neuronal cell bodies with similar functions clustered together in CNS o 3 regions of brain Forebrain: cerebrum and diencephalon Midbrain: heavily connected to pons and medulla oblongata (= form brainstem) Hindbrain: pons, medulla oblongata, cerebellum o Cerebral ventricles: 4 interconnected cavities filled with fluid to provide support to brain o Cerebrum Left and right hemispheres connected by corpus callosum; made up outer shell of gray matter (cell bodies) and inner layer of white matter (myelinated fiber tracts) = cerebral cortex Highly folded (ridges: gyri; grooves: sulci) for increase in number and integration of neurons for signal processing Collects basic afferent info from environment, processes info into meaningful perceptual images, controls refinement of skeletal muscles Subcortical nuclei underneath cortex Predominately basal nuclei; controls movement, posture, and complex aspects of behavior Contains frontal, parietal, occipital, and temporal lobes Pyramidal cells form major output cells; nonpyramidal cells mostly involved in receiving inputs and processing info Limbic system: gray and white matter found in frontallobe cortex, temporal lobe, thalamus, hypothalamus, fiber pathways Associated with learning, emotional experience, behavior, visceral and endocrine functions o Diencephalon Thalamus: collection of several large nuclei; integration center for most inputs in cortex Key function in general arousal, focusing attention Hypothalamus: below thalamus; master command center for neural and endocrine coordination Most important area in homeostatic regulation of internal environment, including behaviors needed for survival (eating/drinking/reproduction) Connected to and regulates pituitary gland (endocrine structure) Epithalamus: includes pineal gland; controls circadian rhythm through release of melatonin o Cerebellum Important center for coordinating movement, controlling posture and balance Receives info from joints, skin, eyes, etc. to do so o Brainstem (midbrain, pons, medulla oblongata) Reticular formation runs through core of brainstem; essential for life Involved in motor function (eye movement control, reflexive orientation of body), cardiovascular and respiratory control, sleep/wakefulness mechanisms, focus attention Most biogenic amine neurotransmitters released from here Consists of loosely arranged nuclei with bundles of axons Influences both afferent and efferent neurons Cranial nerves: peripheral nerves connected directly to brain and innervate muscles, glands, sensory receptors, thoracic and abdominal organs CNS: spinal cord (6.16) o Gray matter: interneurons, cell bodies and dendrites of efferent neurons, entering axons of afferent neurons, glial cells; forms butterflyshaped area Dorsal horns: gray matter projecting towards back of body Ventral horns: gray matter projecting towards front of body o White matter: myelinated axons surrounding gray matter; relays info from brain to spinal cord or from spinal cord to brain and also between different levels of spinal cord o Dorsal roots: groups of afferent fibers entering spinal cord from peripheral nerves; enters dorsal side of spinal cord Dorsal root ganglia: cell bodies of afferent neurons in dorsal root o Ventral roots: axons of efferent neurons leaving spinal cord on ventral side o Spinal nerve: dorsal and ventral roots from same level combine on each side of spinal cord; carries both afferent and efferent info PNS (6.17) o 43 pairs of nerves 12 pairs of cranial nerves (see Table 6.8) 31 pairs of spinal nerves connected with spinal cord (cervical, thoracic, lumbar, sacral, or coccygeal) (all nerves contain afferent and efferent fibers) Neurons at each vertebral level interact with nearby structures in that region (muscles, glands, sensory input) Cervical nerves (8 pairs) innervate neck/shoulders/arms/hands Thoracic nerves (12 pairs) associated with chest/upper abdomen Lumbar nerves (5 pairs) innervate lower abdomen/hips/legs Sacral nerves (5 pairs) innervate genitals/lower digestive tract Coccygeal nerves (1 pair) associated with skin over tailbone o Efferent division: carry signals from CNS to muscles, glands, tissues More complicated than afferent division Somatic NS: innervate skeletal muscle; cell bodies located in brainstem or ventral horn; release ACh Motor neurons: innervate skeletal muscle; only cause contraction (excitation) Autonomic NS: innervates smooth and cardiac muscle, glands, neurons in GI tract, etc.; can be excitatory or inhibitory o Afferent division: convey info from peripheral sensory receptors to CNS; first cells entering CNS in synaptically linked chains of neurons handling entering info Autonomic nervous system (6.18) o Enteric NS: autonomic neurons innervating a neuronal network in wall of GI tract o Consists of 2 neurons in series that connect CNS and effectors Autonomic ganglion: synapse between 2 neurons; outside CNS Preganglionic neurons: neurons passing between CNS and ganglia Postganglionic neurons: neurons passing between ganglia and effectors o Sympathetic division Fibers leave CNS from thoracic and lumbar regions of spinal cord Ganglia lie close to spinal cord; forms sympathetic trunks on either side of spinal cord Other ganglia in abdominal cavity Activation usually leads to bodywide response Uses ACh between pre and postganglionic neurons; uses norepinephrine between postganglionic neuron and effector Fightorflight response: increases heart rate and blood pressure and blood flow to skeletal muscles, heart, brain; liver releases glucose; pupils dilate; GI tract functions decrease o Parasympathetic division Fibers leave CNS from brainstem and sacral region of spinal cord Ganglia lie within or close to organs innervated by postganglionic neurons Activation leads to activation of specific organs finely tailored to physiological situation Uses ACh between pre and postganglionic neurons and also between postganglionic neuron and effector Restordigest response: opposite reaction of fightorflight responses o Postganglionic neurons are nonadrenergic or noncholinergic as well, which use nitric oxide or other neurotransmitters to regulate GI, respiratory, urinary, and reproductive functions o Most autonomic NS drugs affect ACh or norepinephrine receptors (including nicotine receptors in ganglia and muscarinic receptors in postganglionic neurons) o Adrenal medulla: endocrine gland in which postganglionic neurons do not develop axons Neurons release 80% epinephrine and 20% norepinephrine into blood (hormones) 2 hormones have different affects due to different affinities to receptors Epinephrine: beta 2 adrenergic receptors Norepinephrine: alpha 1 adrenergic receptors o Dual innervation: heart, glands, smooth muscles can be innervated by both sympathetic and parasympathetic fibers Usually have opposite effects on structure and usually reciprocally (increase in one activity has decrease in other activity) Parasympathetic and sympathetic divisions usually operate together Protective elements associated with the brain (6.19) o Meninges: membranous coverings between soft neural tissue and bone; protect and support CNS; circulate and support cerebrospinal fluid Dura mater: next to bone Arachnoid mater: in middle Pia mater: thin, next to nervous tissue Subarachnoid space: between arachnoid and pia maters, filled with cerebrospinal fluid (CSF) Meningitis: infection of meninges that occurs in CSF; results in intracranial pressure, seizures, loss of consciousness o Choroid plexus: specialized epithelial structure that produces CSF (replenishes it 3x a day); CSF circulates through interconnected ventricular system to brainstem o CSF can provide important diagnostic info for NS diseases; obtained through large needle inserted in spinal canal below second lumbar vertebra Provides shock absorption for brain and spinal cord Accumulation of CSF: hydrocephalus; can cause compression of blood vessels which can lead to neuronal damage and cognitive dysfunction o Most common form of brain damage is caused by decreased blood supply to brain Even a few minutes without nutrients or oxygen causes damage: stroke (neuronal death) Brain receives 1215% total blood supply o Bloodbrain barrier: exchange of substances between blood and extracellular fluid in CNS occurs here Complex mechanisms minimize the ability of harmful substances to reach the brain (including potentially therapeutic drugs) Formed by cells that line the smallest blood vessels in the brain; includes tight junctions, physiological transport systems Drugs that are not lipidsoluble get stuck in brain, leading to prolonged effects (ex: morphine) Nonlipidsoluble molecules (ex: glucose) can have rapid effects due to membrane transport proteins Drugs that are highly lipidsoluble have rapid effects in CNS (ex: barbiturates, nicotine, caffeine, alcohol) o CSF and extracellular fluid of CNS are in time, in diffusion equilibrium Restrictive, selective barrier mechanisms in capillaries and choroid plexus regulate extracellular environment of neurons of brain and spinal cord
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