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CHAPTER 12
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  1. CHAPTER 12 Nervous Tissue

  2. Structures of the Nervous System • Brain • Nerves • bundles of axons plus their associated CT & blood vessels • follow defined path & innervate specific regions/structures • Spinal cord • connects to brain thru foramen magnum • protected by vertebral column • Ganglia • masses of nervous tissue outside brain & spinal cord • closely associated with cranial/spinal nerves • Sensory receptors = dendrites • monitor changes in internal/external environments

  3. Functions of the Nervous System • Sensoryfunction • receptors sense changes in internal & external environments • AFFerent neurons carry sensory info TO brain/spinal cord • Integrativefunction • processes sensory info by analyzing sensory information & makes decisions regarding appropriate behaviors • interneurons have short axons that contact neurons in brain/spinal cord; participate in integration • Motorfunction • after integration of sensory info, nervous system elicits appropriate response • EFFerent neurons carry motor response away from spinal cord to effector organs/glands

  4. NERVOUS SYSTEM DIVISIONS CENTRAL NERVOUS SYSTEM PERIPHERAL NERVOUS SYSTEM • Brain & Spinal Cord ONLY!!! • Integrates sensory input from PNS & • sends output back • to PNS Autonomic Somatic • MotorSensory • Stimulates ●Input from • skel. musc. somatic • only receptors • (voluntary) to CNS • MotorSensory • Info from CNS ●Input from • to viscera viscera to • (involuntary) CNS SympatheticParasympathetic ●”fight or flight” ●“rest and digest”

  5. Divisions of the Nervous System • Central nervous system (CNS) = brain & spinal cord ONLY! • Peripheral nervous system (PNS) = all nervous tissue outside CNS • Somatic (voluntary) nervous system (SNS) • neurons from cutaneous and special sensory receptors to the CNS • motor neurons to skeletal muscle tissue • Autonomic (involuntary) nervous system • detailed in Chapter 15 • sensory neurons from visceral organs to CNS • motor neurons to smooth & cardiacmuscle and glands • sympathetic division (speeds up heart rate) • parasympathetic division (slow down heart rate)

  6. NERVOUS TISSUE HISTOLOGY • Neurons = nerve cells • electrically excitable  can convert stimulus to electrical signal (action potentials) • parts of neuron • cell body • nucleus surrounded by cytoplasm & organelles • rough ER & free ribosomes for protein synthesis • dendrites = sensory (input) portion of neuron • axons =output portion of neuron • carry impulses away from cell body to effector cell • attaches to cell body @ axon hillock • axon collaterals = branches of axon • synapse = point of communication btwn neuron & cell • serves as site of control of nerve impulses • prevents “backwards” transmission of impulses

  7. NERVOUS TISSUE HISTOLOGY • Neuroglia = supporting cells of nervous tissue • actively take part in nervous tissue functions • do not generate a.p. but can reproduce  site of brain tumors (gliomas) • CNS neuroglia (4) • astrocytes • processes contact capillaries, neurons, pia mater • strong  support neurons by holding in place • processes around capillaries isolate neurons from blood-borne toxins  help establish blood/brainbarrier • oligodendrocytes form & maintain myelin sheath around CNS axons • microglia function as phagocytes  remove debris

  8. NERVOUS TISSUE HISTOLOGY • CNS neuroglia (c’td) • ependemyal cells produce, monitor & circulate the cerebrospinal fluid (CSF) which is ISF of CNS • PNS neuroglia (2) • Schwann cells • surround PNS axons • myelinate single axon • facilitate regeneration of PNS axons • can enclose several unmyelinated axons • satellite cells • surround cell bodies of PNS ganglia • provide structural support • regulate exchange of materials btwn neurons & ISF

  9. Myelination • Some axons covered by multilayered lipid & protein covering called myelin sheath • Provides electrical insulation which allows nerve impulse to travel faster • Produced by Schwann cells in PNS & oligodendrocytes in CNS • Neurolemma = cytoplasm & nucleus of Schwann cell • ***found only in PNS! • Nodes of Ranvier = gaps in myelin sheath that appear @ intervals along axon • one Schwann cell found between two nodes

  10. Myelination in the CNS • Oligodendrocytes myelinate axons in the CNS • one oligodendrocyte myelinates several axons • broad, flat cell processes wrap around CNS axons • No neurolemma is formed • probably results in lack of regrowth after injury (because PNS axons can regenerate)

  11. Gray and White Matter • White matter = primarily myelinated axons • Gray matter = unmyelinatedstructures • nerve cell bodies, dendrites, axon terminals, bundles of unmyelinated axons and neuroglia • In spinal cord, white matter surrounds inner core of gray matter • In brain • thin layer of gray matter covers surface • found in clusters called nuclei deep within CNS ***A nucleus is a mass of nerve cell bodies and dendrites inside the CNS.***

  12. Electrical Signals in Neurons • Neurons are electrically excitable due to the voltage difference across their membrane • graded potentials participate in localized cellular communication • action potentials can communicate a signal over long or short distances • The difference in voltage across a membrane is referred to as the membrane potential • resting membrane potential is the voltage difference that exists when a cell is at rest (not being stimulated) • Plasma membrane of neurons contains ion channels that open/close in response to stimuli

  13. Ion Channels • Allow movement ofspecificions across the membrane & down their electrochemical gradient • positively charged ions move to a negatively charged area (lower concentration of positive charge) • negatively charged ions generally are too large to leave the cell, thus the tendency is for positively charged ions to flow into the cell • Four types of channels • leakage channels randomly alternate btwn open/closed conformation • more K+ channels than Na+ K+ is “leakier” • membrane is more permeable to K+ • voltage-gated channels open in response to a change in voltage across the membrane  function in generation of action potentials

  14. Ion Channels • Channels c’td • ligand-gated channels open/close in response to specific chemical messenger (ligand) • ligand can be NT, hormone or an ion • two modes of operation • direct activation by binding of ligand to receptor • indirect activation of channel via 2nd msgr system • mehanically gated channels open/close in response to mechanical stimuli • stretching of muscle • vibrations within ear

  15. Resting Membrane Potential (RMP) • Results from unequal distribution of ions btwn ECF & ICF • buildup of negative ions in cytosol (PO4-3, amino acids) • buildup of positive ions outside membrane (Na+) • Separation of charges represents a form of potential energy • the greater the charge difference across membrane, the greater the potential (voltage) • potential energy difference at rest is -70 mV (this is RMP) • Resting potential exists because • concentration of ions different inside & outside • extracellular fluid rich in Na+ and Cl- • cytosolfull of K+, PO4-3 & amino acids

  16. Resting Membrane Potential (RMP) • Resting potential exists because • membrane permeability differs for Na+ and K+ • 50-100x greater permeability for K+ • inward flow of Na+ can’t keep up with outward flow of K+ • ***Na+/K+ ATPase pump maintains R. M. P.*** • w/o this pump, ion concentrations would reach equilibrium and the membrane potential (excitability) would be destroyed • K+ has a natural tendency to leak out of cell and Na+ tends to flow into the cell (down their respective gradients) • pump returns 3 Na+ to ECF and 2 K+ to cytosol

  17. Graded Potentials • Local changes (of varying magnitudes) in membrane potential • Any stimulus that opens a gated channel produces a graded potential • Make cell more or less polarized • hyperpolarization = membrane has become more negative • depolarization = membrane has become less negative • “Graded” means they vary in amplitude (size), depending upon strength of stimulus • Are decrementalbecause they die out as they travel further from their origin • Occur most often in dendrites and cell body of a neuron • Graded potentials occurring in response to NT are called postsynaptic potentials

  18. How do Graded Potentials Arise? • Source of stimuli • mechanical stimulation of membranes with mechanical gated ion channels (pressure) • chemical stimulation of membranes with ligand gated ion channels (neurotransmitter) • Graded/postsynaptic/receptor or generator potential • ions flow through ion channels and change membrane potential locally • amount of change varies with strength of stimuli • Flow of current (ions) is local change only

  19. Generation of an Action Potential • Action potential = sequence of rapidly occurring events that briefly reverse membrane potential due to rapid changes in membrane permeability • depolarization = membrane becomes less negative inside • repolarization = restoration of RMP (-70 mV) • threshold potential = -55 mV • potential at which an action potential is generated • all-or-none principle: if stimulus causes depolarization to threshold, action potential is generated • no “large” or “small” a.p. • stronger stimulus will not cause a larger impulse • Action potentials can travel over long distances w/o dying out

  20. Depolarizing Phase of Action Potential • In resting membrane, Na+inactivation (inner) gate open & activation (outer) gate is closed (Na+ cannot get in) • Depolarizing graded potential or some stimulus initiates movemt of Na+ into cell (↓ potential) • This further depolarization activates Na+-gated channels which open & allow rapid influx of Na+ until threshold reached • @ threshold (-55mV), both Na+ gates open & Na+ enters & membrane becomes several hundred times more permeable to Na+ • more channels open in adjacent regions of membrane (positive FB) • influx of Na+ makes inside less negative (up to +30 mV) • @ +30 mV, Na+ inner (inactivation) gates close

  21. Repolarizing Phase of Action Potential • As Na+ gates close (at +30 mV), K+ gates are activated & membrane permeability to K+ is increased • K+ flows out of cell (down its gradient) until RMP is reached • If the cell “overshoots” K+ efflux, hyperpolarization results • -90 mV  cell further from threshold no a.p. can occur • K+ channels close and the membrane potential returns to the resting potential of -70mV via action of Na+/ K+ ATPase pump

  22. Refractory Period of Action Potential • Period of time during which neuron cannot generate another action potential • Absolute refractory period • even very strong stimulus will not produce another a.p. • inactivated Na+ channels must return to the resting state before they can be reopened • Na+ inner gates closed & cannot reopen • Relative refractory period • 2nd a.p. can be generated by very strong stimulus • Na+ channels have been restored to resting state, but K+ channels are still open • Allows unidirectional transmission of impulses • Axons w/ large diameter have greater membrane surf. area & shorter abs. refract. periods than small-diameter axons

  23. Propagation of Nerve Impulses • Continuous conduction (local current flow) • starts @ axon hillock where membrane is most sensitive to changes in potential • step-by-step depolarization of adjacent segments of membrane • membrane polarity is reversed (out becomes (-) & in becomes (+) • inactive area of membrane (downstream) has resting polarity  opposite charges attract  (+) “pulls” (–) • this opens voltage-gated channels in adjacent regions of membrane & a.p. moves along axon • occurs in muscle fibers & unmyelinated axons

  24. Propagation of Nerve Impulses • Saltatory conduction • in myelinated axons only • depolarization occurs in similar way @ nodes of Ranvier where voltage-gated channels are concentrated • current flows thru aqueous cytosol & ECF of Schwann cells • nerve impulses appear to jump from node to node • much quicker/more energy efficient • open fewer voltage channels • less use of Na+/K+ pump  less ATP used • Axon diameter • large fibers are all myelinated  fastest • medium fibers myelinated, but slower (b/c less surf. area) • small fibers unmyelinated & slowest (longest abs. refr. per.)

  25. Encoding of Stimulus Intensity • How do we differentiate a light touch from a firmer touch? • Perception of intensity results from frequency of impulses (not the magnitude of an impulse) • frequency of impulses • firm pressure generates impulses at a higher frequency • number of sensory neurons activated • firm pressure stimulates more neurons than does a light touch

  26. SIGNAL TRANSMISSION AT SYNAPSES • Presynaptic neuron = neuron sending the signal • Postsynaptic neurono = neuron receiving chem/elec signal • Electrical synapses • ionic current spreads to next cell through gap junctions • advantages • faster transmission of impulses  a. p. jumps directly from pre-synaptic to post-synaptic neuron • capable of synchronizing groups of neurons as in the contraction of cardiac & visceral smooth muscles

  27. SIGNAL TRANSMISSION AT SYNAPSES • Chemical synapses • Synaptic cleft separates pre/post-syn neurons  chem signals can’t “jump” from one neuron to next • Presynaptic neuron releases NT into cleft; NT binds receptor on post-synaptic neuron • Binding of NT produces graded (postsynaptic) potential • Repeated binding eventually produces a.p. • Synaptic delay = time required for events to occur @ chemical synapse

  28. Mechanism of Chemical Synapse • Action potential reaches end bulb and voltage-gated Ca+2 channels open • Ca+2 flows inward & triggers release of neurotransmitter • NT crosses synaptic cleft & binds to ligand-gated receptors • ligand-gated channels activated & ions flow across membrane • ion flow can change postsyn. potential • If Na+ in  depolarization • If Cl- in or K+ out  hyperpolariz • If depolarizing potentials reach threshold, a.p. is triggered

  29. Excitatory & Inhibitory Potentials • If NT causes depolarization excitatory postsynaptic potential (EPSP) is generated • excitatory = a.p. generated if sum of EPSPs exceeds -55mV • usually results from cation channels opening • partial depolarization makes cell more excitable • If NT causeshyperpolarization inhibitory PSP (IPSP) • inhibitory because membrane is further from threshold • usually result of K+ or Cl- channels opening

  30. Removal of Neurotransmitter • Diffusion: NT diffuses away from cleft & is no longer effective • Enzymatic degradation • EX: acetylcholinesterase breakdown of ACh • Cellular uptake • Uptake by nearby neuroglia • Re-uptake by secreting axon • Clinical application: some drugs block uptake process • EX: Prozac = SSRI  blocks serotonin reuptake  serotonin’s effects are prolonged

  31. Summation of PSPs • Summation = integration of synaptic inputs • Spatial summation results when several presynaptic neurons secrete NT that affects single postsynaptic neuron • Temporal summation results from repeated release of NT from single presynaptic neuron • One postsynaptic neuron can receive numerous excitatory/inhibitory inputs • Sum of inputs determines postsynaptic response • EPSP: excitatory input > inhibitory input • above threshold  a.p. generated • below threshold  cell more sensitive b/c partial depolarized • IPSP: inhibitory input > excitatory input • membrane is hyperpolarized & no a.p. occurs

  32. Summation of PSPs • Clinical relevance: strychnine poisoning • Under normal conditions: inhibitory neurons in spinal cord release glycine (a NT) which inhibits XS contractions of skeletal muscle • Strychnine binds & inactivates glycine receptors • inhibitory effects of glycine are removed • uncontrolled muscle contraction results • diaphragm remains fully contracted  death ensues via suffocation

  33. Small-Molecule Neurotransmitters • Acetylcholine (ACh) • excitatory effect @ NMJ via direct ligand-channel binding • inhibitory @ some parasympathetic synapses • indirect activation of receptors via G-protein • slows heart rate • inactivated by acetylcholinesterase • Amino Acids • excitatory: glutamate & aspartate • inhibitory: GABA & glycine • generate IPSP via opening of Cl- channels • Valium enhances GABA effects • prolongs effects of GABA • acts as anti-anxiety drug

  34. Small-Molecule Neurotransmitters • Biogenic Amines • catecholamines • norepinephrine (NE) & epinephrine (Epi) • also act as hormones when released from adrenal gland • dopamine: responsible for emotions, addictive behaviors • Regulates skeletal muscle tone • Parkinson’s disease result of degeneration of dopamine-secreting neurons • serotonin responsible for mood control, appetite, sleep induction • SSRIs prevent reuptake • Zoloft, Prozac for treatment of depression

  35. Small-Molecule Neurotransmitters • Nitric oxide (NO) • potent vasodilator: increases blood flow in regions where it is released • unique because is formed on demand & acts immediately • first recognized as vasodilator that helped lower blood pressure • extremely toxic in high quantities • metabolic pathway = target of Viagra

  36. Neuropeptides • 3-40 amino acids linked peptide bonds • Can be excitatory or inhibitory • Brain has receptors for binding opiate drugs • Enkephalins have potent analgesic effect (200x morphine) • Opiod peptides = body’s natural painkillers • Dynorphins • Endorphins: responsible for “runner’s high” experienced after exercise • Substance P transmits pain-related input from PNS to CNS • Enhances perception of pain • Suppressed by enkephalins & endorphins

  37. Modifying Effects of NTs • NT synthesis can be stimulated or inhibited • Parkinson’s patients benefit from L-dopa b/c it boosts dopamine production for limited time • NT release can be enhanced or blocked • Amphetamines promote release of dopamine & NE • Botulinum toxin inhibits release of Ach  paralysis • NT receptors can be activated or blocked • Agonists activate: Isoproterenol activates NE & Epi receptors dilate airways during asthma attack • Antagonists block: Zyprexa blocks dopamine/serotonin receptors  treatment of schizophrenia • NT removal can be stimulated or inhibited • Cocaine blocks dopamine reuptake  euphoric feeling