BIPN 100 Midterm 2 - Professor Catalina Reyes-Gonzalez PDF

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Professor Catalina Reyes-Gonzalez...

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Brain A. Folds: gyrus, sulcus & fissures B. Brain stem: controls basic body functions 1. Midbrain: initiation of movement, substantia nigra (nuclei; loss = Parkinson’s) 2. Pons: respiration 3. Medulla oblongata: heart C. Diencephalon: on top of the brain stem 1. Thalamus: relay station 2. Hypothalamus: homeostasis center 3. Pineal gland: produces melatonin (sleep) D. Cerebellum: coordination of movement E. Cerebrum: higher brain function (thought & action) 1. Cerebral cortex: allows higher brain functions a) Left & right hemispheres (1) Frontal: motor function, judgement (prefrontal: personality) (a) Broca’s area: production of speech (2) Parietal: somatosensory (touch, proprioceptors, pain, temperature) (3) Temporal: hearing (a) Wernicke’s area: comprehension of speech (4) Occipital: visual b) Basal ganglia: controls motor movement; white matter c) Limbic system (1) Cingulate gyrus: emotions & behavior (2) Hippocampus: memory (3) Amygdala: emotions & memory Sensory physiology A. Conscious 1. Special senses: vision, hearing, taste, smell, equilibrium 2. Somatic: touch, temperature, pain, itch, proprioception B. Subconscious 1. Somatic: muscle length, muscle tension, proprioception 2. Visceral: BP, blood glucose, temperature, osmolarity, pH, oxygen content Sensory receptors A. Sensory neuron w/ free nerve endings (smell = only special sense) B. Sensory neuron w/ nerve endings enclosed in connective tissue C. Sensory neuron w/ receptor that is separate (receptor synapses w/ sensory neuron) Types of sensory receptors A. Chemoreceptors: respond to chemical ligands that bind to the receptor B. Mechanoreceptors: respond to various forms of mechanical energy C. Photoreceptors: vision D. Thermoreceptors: respond to temperature Receptor potential (graded potential) A. Sensory neuron B. Epithelial sensory receptor cell: stimulus → receptor → depolarization → vesicle w/ nt → nt receptor → graded potential (dendrite) → AP C. Tonic receptors: adapt slowly; fire for the duration of a stimulus D. Basic receptors: adapt rapidly; stop firing even though stimulus still present Receptive fields (afferent) A. Somatosensory & visual neurons are activated by stimuli that fall within (receptive field) B. Primary (1st order sensory neuron): has its own receptive field C. Secondary (2nd order sensory neuron): a neuron into which all 1st order neurons converge; feels overlap of 1st order neurons, cannot pinpoint the location of stimulus D. Stimulus adds up on 2nd order sensory neuron (convergence) → AP → CNS E. More sensitive areas (eg. fingertips) have 1 primary to 1 secondary neuron F. Lateral inhibition: secondary neuron can inhibit another secondary neuron → can better

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pinpoint location of stimulus b/c one generates AP and the other doesn’t Somatosensory pathways (afferent) A. Somatosensory cortex (parietal lobe): the part of the brain that recognizes where descending tracts originate 1. *Dorsal white columns: touch, proprioception & pressure a) 1st order neuron (dorsal root ganglia/spinal cord) → synapses w/ 2nd order neuron & decussates (medulla/brainstem) → synapses w/ 3rd order neuron (thalamus) → somatosensory cortex/parietal lobe 2. *Spinothalamic tract: pain, feeling & temperature a) 1st order neuron (dorsal root ganglia/spinal cord) → synapses w/ 2nd order neuron & decussates (dorsal horn/spinal cord) → ascends contralaterally → synapses w/ 3rd order neuron (thalamus) → somatosensory cortex/parietal lobe 3. *Spinocerebellar tract: proprioception a) 1st order neuron (dorsal root ganglia/spinal cord) → synapses w/ 2nd order neuron → ascends ipsilateral → cerebellum Motor pathways (efferent) A. Sensory neuron = motor neuron 1. *Corticospinal tract a) Interneuron (frontal lobe/cortex) → crosses through the pyramids of the medulla/pyramidal tracts (medulla/brainstem) → synapses w/ 2nd order neuron (ventral horn/spinal cord) → ventral root → body (voluntary movement) b) Type of neuron innervated = alpha motor neuron (1) *Lateral corticospinal tract (a) Decussates in medulla (interneurons in cortex on one side controlling the opposite side of body) (b) Fine motor movement (2) *Anterior corticospinal tract (a) Decussates in spinal cord & synapses w/ motor neuron on contralateral/ipsilateral side (b) Bilateral movement & posture 2. *Extrapyramidal tract a) Does not cross through the pyramids; midbrain (not cortex) → medulla → spinal cord b) Involuntary movement Pathologies/injuries A. Parkinson’s disease 1. Abnormal movements (tremors), speech difficulties & cognitive changes 2. Loss of substantia nigra that release dopamine (necessary for basal ganglia) 3. Treatment: replacement of dopamine (L-DOPA) B. Trauma to the spinal cord: physical trauma, spinal meningitis/infection (arachnoid mater swells) & herniated intervertebral disk pushes spinal nerve PNS A. Somatic motor neurons vs. autonomic neurons (parasympathetic vs. sympathetic) B. Hypothalamus (homeostasis center), pons (respiration) & medulla (respiration) C. Exceptions to dual antagonistic innervation: sweat glands & smooth muscle in blood vessels (only innervated by sympathetic) D. Receptors: A1 & A2, B1 & B2 (1 = excitatory, 2 = inhibitory) E. ANS has 2 neurons vs. somatic has 1 neuron = alpha motor neuron 1. Preganglionic neuron: cell body inside the CNS → axon → 2. Postganglionic neuron: outside the CNS (autonomic ganglia) → target tissue a) Sympathetic chain

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(1) Autonomic ganglia come out through each side of spinal cord; thoracolumbar (2) Short preganglionic axons/neurons, long postganglionic b) Parasympathetic chain (1) Autonomic ganglia come out through brain stem & sacral region (2) Long preganglionic axons/neurons, short postganglionic 3. Both preganglionic neurons release ACh to nAChR (nicotinic neuronal cholinergic receptors) a) Sympathetic: postganglionic releases NE (synthesized from tyrosine) → A- & B-adrenergic receptors (G coupled-protein receptors) b) Parasympathetic: postganglionic releases ACh (acetyl CoA & choline) → nicotinic & muscarinic cholinergic receptors; AChe 4. Sympathetic a) Chromaffin cells (adrenal medulla) release E → bloodstream, slow 5. Autonomic synapses a) Necklace w/ separated beads b) Beads: varicosity (contains nt of postganglionic neurons that bind to receptors all over the tissue) 6. Norepinephrine release & removal at sympathetic neuroeffector junction a) AP → varicosity → depolarization opens calcium channels → exocytosis of synaptic vesicles → NE binds to adrenergic receptor b) Receptor activation stops when NE diffuses away from the synapse (1) NE can be taken back into synaptic vesicles for re-release or; (2) NE is metabolized by enzyme monoamine oxidase (MAO) 7. Parasympathetic (1, 3, 5 receptors = excitatory; 2, 4 = inhibitory) Endocrine system A. Endocrine release: hormone → blood B. Paracrine release: hormone → target nearby C. Autocrine: target is itself D. Neurocrine: hormone released by neurons (eg. chromaffin cells release E into blood) E. Types of hormones 1. Steroid a) Cholesterol-derived; made in adrenal cortex (cortisol, aldosterone) & gonads/placenta (estrogen, progesterone, testosterone) b) Lipophilic, can cross membranes (diffusion) c) Insoluble in plasma, needs to be bound to a protein carrier in order to travel through the blood (longer half-life) d) Bind to cytoplasmic or nuclear receptors → activates/represses genes e) Bind to cell membrane receptors (nongenomic responses) 2. Amines/amino acid-derived a) Tryptophan-derived (melatonin) b) Tyrosine-derived (1) Catecholamines = water-soluble; rings (2) Thyroid hormones T3 & T4 = lipid-soluble; rings 3. Peptides/proteins a) Water-soluble, cannot diffuse through bilayer, need to bind to membrane receptor (G-coupled protein) but can travel through blood (short half-life) b) Peptides: short chains of amino acids (ADH & oxytocin) c) Protein hormones: long chains of amino acids (insulin & HGH) 4. Eicosanoids a) Inflammatory, intensity/duration of pain/fever, induction of labor, BP control & clotting b) Produced from enzyme oxidation of arachidonic acid (1) Arachidonic acid → COX → prostaglandins →

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(a) Prostacyclins (vasodilation & prevent clotting) (b) Thromboxanes (vasoconstriction & clots) (2) Arachidonic acid → LOX → leukotrienes (mediate inflammation & bronchial constriction like asthma) c) Lipid-soluble but don’t, bind to G coupled-protein receptors 5. G-protein coupled signal transduction a) Gs: stimulatory hormone → GDP alpha unbinds from beta & gamma → binds/activates AC (GTP) → cAMP → phosphorylation b) Gi: inhibitory hormone → GDP alpha unbinds from beta & gamma → binds/inactivates AC (GTP) c) Gq: PLC converts phospholipid bilayer into messengers: (1) DAG (stays in membrane & activates PKC → phosphorylates L-type calcium channels & potassium channels) & (2) IP3 (moves to cytoplasm, binds to IP3 receptor in ER & activates receptor that is gate for calcium) 6. Termination of hormone action: hormones degraded into metabolites; uptake by specific receptors, enzymes in liver & kidneys & metabolites excreted in bile (hydrophobic) & urine (hydrophilic) F. Negative feedback loops 1. Parathyroid regulation of calcium a) Senses calcium concentration → releases parathyroid hormone → b) Bone resorption, kidney reabsorption & intestinal absorption of calcium 2. Pancreas regulation of glucose a) A-cells release glucagon → liver → glycogen into glucose (sympathetic) b) B-cells release insulin (parasympathetic) 3. Diabetes mellitus a) Type I: insulin is low b/c immune system destroys B-cells b) Type II: target cells become less sensitive to insulin G. Neurohormones 1. Adrenal medulla: catecholamines 2. Hypothalamic-pituitary axis (HPA): hypothalamus, PP & AP a) Neurohormones → PP (storage) → released into bloodstream b) Antidiuretic hormone (ADH)/vasopressin: water reabsorption in kidney c) Oxytocin: initiates contraction of uterus & ejection of milk 3. Neurohormones (hypothalamus) → AP → endocrine gland a) Tropic hormones: hormones that cause the release of a second hormone (hypothalamus & AP) b) Releasing/inhibiting hormones: produced by hypothalamus; purpose: to control the release of other hormones; exception: prolactin c) Long negative feedback loop: hormone 3 (endocrine gland) tells hypothalamus to stop d) Short negative feedback loop: hormone 2 (AP) tells hypothalamus to stop 4. Cortisol a) Hypothalamus releases CRH (corticotropin-releasing hormone) → AP releases ACTH (adrenocorticotropic hormone; short negative feedback loop) → adrenal cortex releases cortisol (long negative feedback loop) 5. Thyroid gland a) Low T3 & T4 → hypothalamus releases TRH (thyroid-releasing hormone) → AP releases TSH (thyroid-stimulating hormone) → thyroid releases T3 & T4 b) Hypersecretion: excess hormone: no negative feedback (1) Pathology in adrenal cortex (endocrine): primary (a) CRH levels - low (b) ACTH levels - low

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(c) Cortisol levels - high (2) Pathology in AP: secondary (a) CRH levels - low (b) ACTH levels - high (c) Cortisol levels - high (3) Pathology in hypothalamus: secondary (a) CRH levels - high (b) ACTH levels - high (c) Cortisol levels - high c) Hyposecretion: deficient hormone; no negative feedback (1) Receptor downregulation (slow): hormone ↑, # of receptors ↓ (2) Receptor upregulation (slow): hormone ↓, # of receptors ↑ (3) Desensitization (fast): hormone ↑, receptor response ↓ d) Diabetes insipidus: defects in ADH receptors or in secretion of ADH (1) Damage of PP or hypothalamus (2) Excretion of large volumes → dehydration e) Hypothyroidism: cause: low iodine; Hashimoto’s = autoimmune f) Hyperthyroidism: Grave’s disease = autoimmune (antibodies stimulate thyroid to produce extra T4), toxic adenoma (isolates itself, enlarges & produces extra T4), thyroiditis swelling = excess leaks into blood XII.

Skeletal muscle A. Contract only in response to NMJ/alpha motor neuron; neurogenic 1. Parallel fibers, grouped into fascicles 2. Sarcolemma: sheath/membrane that envelops skeletal muscle fiber 3. Sarcoplasm: cytoplasm inside muscle fiber 4. Myofibrils: function unit in muscle fiber a) Have proteins, mitochondria (ATP for contraction) & glycogen b) Each is wrapped by sarcoplasmic reticulum: stores calcium c) Enlarged ends of SR: terminal cisterna; close to T-tubules: extensions of sarcolemma; AP → sarcolemma → T-tubule → SR 5. Myofibril proteins a) Contractile proteins (1) Myosin: thick filament; two proteins intertwined; two heads (a) Heads have myosin ATPase: enzyme that hydrolyzes ATP (breaks the bond b/w ADP & P) (b) Heads have myosin-actin binding site: crossbridge (2) Actin: thin filament; like two beaded necklaces intertwined (a) Sarcomere: actin → middle → shortens sarcomere b) Regulatory proteins: regulate crossbridge (1) Tropomyosin: connected to actin & blocks binding site (2) Troponin C: troponin C + calcium → moves tropomyosin c) Accessory proteins (1) Titin: large, elastic protein; stabilizes position of actin & myosin; acts as a spring after stretching (2) Nebulin: inelastic protein, stabilizes actin (keeps actin straight) B. Excitation-contraction coupling & relaxation 1. AP → T-tubules (have DHP receptor/channel = L-type voltage-gated calcium channel) → activates ryanodine receptor 1 (RYR1) in SR 2. Calcium moves out of SR → cytosol → troponin C → tropomyosin → crossbridge a) Stopping DHP = no change b/c only needs change in conformation to activate RYR1, not calcium movement 3. Tension not b/c of shortening, but b/c of strong myosin & actin bond 4. End contraction (stop calcium): calcium ATPase pump (SERCA 1) in SR brings calcium in cytosol back → unbinds from troponin C → tropomyosin goes back

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C. Contraction-relaxation cycle: sliding filament theory at rest 1. ATP bound to myosin head in cocked position (perpendicular to actin) 2. ATP hydrolyzed by ATPase in myosin head (power stroke) → weak binding → increase in cytosolic calcium from SR → tropomyosin moves → crossbridge 3. Myosin head releases ADP molecule → rigor state: actin & myosin bound but no ATP (still calcium) → maintains connection until denaturing 4. Once ATP binds again, myosin head releases actin & can hydrolyze ATP & position itself in cocked position (ready to bind to another actin) D. Excitation-contraction coupling 1. Muscle twitch: a single contraction-relaxation cycle 2. Latent period: short delay b/w the muscle AP & beginning of muscle tension development; the time required for calcium release & binding to troponin 3. Summation: twitch on twitch, muscle doesn’t completely relax → greater tension 4. Tetanus: increase frequency of AP → summation → max tension → unfused tetanus (tiny relaxation) v. complete tetanus E. Motor units 1. 1 alpha motor neuron & muscle fibers; contract in unison 2. Recruit muscle fibers next (medium) in threshold & next → increases tension 3. Asynchronous recruitment avoids fatigue; take turns to maintain tension 4. Higher ratio of muscle fibers to motor neuron for leg than arm F. Muscle mechanics 1. Isotonic contractions (same tension) a) Maintain maximum tension, shorten muscle (eg. holding purse) 2. Isometric contractions (same length) a) Change tension, cannot shorten muscle; elastic elements at ends stretch G. Length-tension relationship 1. Passive tension: stretching muscle (elastic elements, not contractile proteins) 2. Active tension: AP → twitch → total tension curve 3. Too short/long = too much/little overlap (optimal = max cross bridges) H. Muscle fatigue 1. Central & peripheral fatigue 2. Less nt release = less receptor activation 3. SR calcium leak, less calcium release, less calcium-troponin interaction 4. Depletion of PCr, ATP, glycogen & accumulation of lactate (acidic) I. Fast-twitch & slow-twitch muscle fibers 1. Slow-twitch fibers (type I) a) Oxidative phosphorylation (aerobic metabolism) b) Low myosin ATPase activity → don’t fatigue as quickly c) Low contraction speed & low tension (eg. posture) d) A lot of mitochondria to generate ATP & myoglobin (binds oxygen) 2. Fast-twitch fibers (type II) a) Develop tension faster & hydrolyze ATP more quickly b) Pump calcium into SR more rapidly c) Fatigue faster b/c hydrolyze ATP at faster rate (1) Fast-twitch glycolytic fibers (white muscle) (a) Anaerobic glycolysis → lactic acid → fatigue (b) Faster, look pale b/c less myoglobin (2) Fast-twitch oxidative-glycolytic fibers (red muscle) (a) Oxidative & glycolytic metabolism (aerobic & anaerobic) (b) Slower, look red b/c more myoglobin, more mitochondria Smooth muscles A. Differences from skeletal muscles 1. Single nucleus centrally located 2. Less myosin; entire surface covered w/ myosin heads (stretch, but cross bridges)

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3. More actin; extensive cytoskeleton (keeps the actin in place) 4. No troponin & no T-tubules 5. Slower b/c AP takes longer w/ L-type calcium channels (LTCC) Smooth muscle contraction 1. No troponin so calcium binds to calmodulin (CaM) → increases activity of myosin ATPase & myosin light-chain kinase (phosphorylates/moves phosphate group from ATP to myosin light-chain of myosin head) → crossbridge Smooth muscle relaxation 1. Calcium & calmodulin complex regulates itself & other things a) Inhibit calcium L-type channels b) Increase SERCA (calcium ATPase pump) activity → sequesters calcium c) Sodium-calcium exchanger pump: sodium in, calcium out d) Calcium-dependent potassium channels → repolarization 2. Calcium unbinds from calmodulin → decreases activity of myosin light-chain kinase & increases activity of myosin light-chain phosphatase (dephosphorylates/removes phosphate group from myosin head) Smooth muscle classification 1. By location 2. By contraction pattern a) Phasic smooth muscles (relaxed most of the time; eg. esophagus) b) Tonic smooth muscles (contracted most of the time; eg. bladder) 3. By communication w/ neighboring cells a) Single-unit smooth muscle or visceral smooth muscle (1) In most hollow organs (2) Cells communicating through gap junctions (3) Release more calcium into cytosol b/c all muscles acting as one b) Multi-unit smooth muscle (1) Not connected by gap junctions (eg. eye) (2) Contraction of one muscle does not mean contraction of another (3) Release more calcium into cytosol or recruit more fibers Smooth muscle contraction 1. Myogenic: some spontaneously depolarize b/c of calcium channels 2. Hormones & paracrine a) Histamine constricts smooth muscle of airways (asthma) b) NO relaxes smooth muscles of blood vessels (dilation) Smooth muscle control 1. ANS a) Parasympathetic (nt = acetylcholine) (1) Receptor: m3AChR (muscarinic 3 acetylcholine receptor) (2) Effect: excitatory (contraction); Gq pathway (3) Effector: bladder, uterus, bronchioles b) Sympathetic (nt = norepinephrine) (1) Receptor: A1 (E1, NE); Gq pathway & B2 (E); Gs pathway (2) Effect: excitatory & inhibitory, respectively (3) Effector: blood vessels & bronchioles, respectively 2. Local effects: stretch (air bubbles activate calcium) causes contraction 3. Metabolic state: low oxygen & high CO2 when exercising → NO → dilation 4. Hormones a) Angiotensin II: vasoconstriction b) Oxytocin: uterus contraction c) Epinephrine: effect depends on receptor d) NO: relaxation...