Neuroanatomy & Function of Nervous System: Spinal Cord, Reflexes & Sensory Systems - Prof., Study notes of Biology

Download Neuroanatomy & Function of Nervous System: Spinal Cord, Reflexes & Sensory Systems - Prof. and more Study notes Biology in PDF only on Docsity! Lecture 11 – Subcortical Structures – Memory Subcortical Structures: Structures below cortex that control different functions Basal Nuclei: (Ready, GET SET, Go) – Collection of 5 structures on each side of the brain; Below cortex to the sides of the thalamus; connected to each other and to the cortex Posture control is not conscious – Feedback loops correct posture variations Decreased dopamine linked to Parkinson’s. Decreased dopamine = schizophrenic Thalamus: “Gatekeeper”: Sensory info passes through to synapse Receives sensory input from the opposite side About 98% of input blocked from reaching cortex; cortical focus allows input through thalamus – one time of autism due to lack of thalamic editing Hypothalamus: detects but doesn’t solve problems Monitors homeostatic functions: temperature, thirst, milk release, hunger, reproductive urges, circadian rhythms, and increase in emotional feelings Limbic system: Ring of structures underneath cortex of cerebrum Detects emotions and memory formation Hippocampus: part of the limbic system where emotions are processed Emotions: feelings about things – reproductive drive, rage, fear, motivation Can’t make emotions go away – it just takes time Cortical control doesn’t control emotions but controls responses 30/1/14 Neurotransmitters: Norepinephrine, Dopamine, and Seratonin are NTs in the limbic system Altered concentrations of NTs have been associated with depression (Anti-depressants use receptors for these NTs) Excess dopamine has been linked to Schizophrenia – limits L-Dopa Parkinson’s treatment Memory: Retention, storage and ability to recall information. Memory traces: sequences of neural activations Declarative Memory – Facts: events, words, language, rules – hippocampus and temporal lobe for storage Procedural memory: Unconscious – Physical skills, habits, tasks – Cerebellum plays a major role Short Term Memory: Seconds to hours, alter activity in existing neurons in hippocampus – can be erased and replaced Long Term Memory: Creation of new synapses and memory traces Makes multiple copies of important memories over years Retain youthful memories as you age Transfer from hippocampus to cortex Working Memory: In the Pre-Frontal Association Cortex Compares newly acquired short term data and stored long term data Determines relevance of new material, organizes, and prioritizes Amnesia: inability to recall – REPRESSED MEMORY DOESN’T EXIST IN PHYSIOLOGY Retrograde Amnesia: Fairly common: RA caused by trauma – loss of short term memory No long term memory formation of traumatic events Anterograde Amnesia: RARE: Hippocampal damage – Can’t for new LT memories No Loss of previous LT memory, Memory stuck on day of damage Lecture 12 – Cerebellum – Sleep – Spinal Cord Cerebellum: Structure on back of brainstem, controls coordinated movements and learned movements Balance: maintains balance and controls eye movements Coordination: Connected to motor cortex, received “motor plan” Afferent input gives current muscle position Coordinated function with “aim” ie movement matches motor plan As practice occurs, motor cortex, parietal lobe, and cerebellum take over Planning is reduced, initiation of activity is faster and smother input to cortex Input to cortex: Brain stem: Medulla, pons, and midbrain Interface between spinal cord and higher brain centers Cranial nerves supply sensory and motor function to head and neck Different center in brainstem control heart rate, breathing, wakefulness Reticular Activating System – RAS Neural net, awareness of surroundings Cortical, pain, auditory, visual input Output to cortex and thalamus  all cortex Controls consciousness/sleep Sleep: Low frequence activity in hypothalamus + thalamus  sleep Reason needed? UNKNOWN Adaptation: decreases action potential number despite prolonged stimulus. Phasic Receptors: adapt over time – rate is variable Touch receptors adapt quickly Pain, Blood Pressure receptors adapt slowly Taste is Phasic Tonic Receptors: Virtually do not adapt – few true tonic receptors: smell receptors Postural receptors in trunk are near tonic Sensory Specificity: Normal stimulus produces a response that the brain interprets Different stimulus needs more strength for a response brain still interprets as “normal” response – see “stars” Pain: Survival value, protection from harm. Anticipation of pain activates pain areas and cortex Nociceptors – pain receptors – chemical and physical Fast pain: sharp, localized, passes quickly Fast, myelinated afferents – glutamate neurotransmitter Slow pain: diffuse, dull, long lasting Slow, unmyelinated afferents – substance P neurotransmitter Substance P: presence suspected before discovery Neurotransmitter unique to afferent, slow pain neurons Opioid Receptors: natural analgesics block pain by binding to opioid receptors Activation alters ion channels and membrane Enkephalins/Endorphins – types of natural opioids Peptides, multiple types, different sizes Short half life, 25 seconds Morphine – effective for hours Chemical senses: Molecular binding to receptor Flavor: combination of smell and taste Taste: Molecules dissolve in saliva and reach taste bud receptors to be tasted Taste buds: receptors at taste pore Tight junctions keep saliva away from the rest of taste bud Surrounding epithelial cells  basal cells  receptor cells Turnover is roughly 10 days for taste buds Neural tracts: Sensory neurons send taste information Neurons to thalamus: parietal lobe, “what” taste Neurons to limbic system – “like” it? Taste Receptors: Salty – Na+ Sweet – organic sugars Acid, sour – H+ Bitter, basics (quinine – cations, poisons, most sensitive receptor Umami – glutamate (MSG) Smell: Olfactory mucus membrane on roof of nasal cavity > 1000 different odor receptors Largest gene family, >1% of human genome Molecules must diffuse through mucus (H2O soluble) Olfactory Receptors: Part of dendrites of olfactory neurons – covered by mucus Neurons turn over every few weeks Unusual: dendrites as receptors, new neurons Olfactory adaptation: Unusual: Reception primarily tonic Unusual: Most adaptation in CNS – brain can overcome adaptation Adaptation to one smell does not affect others Lecture 14 – VISION Eye: designed to receive light and produce electrical signals Cornea: clear, non-cellular front of the eye Light passes through, not refracted (bent) Lens: Ciliary body Lens refracts light to focus on retina Ciliary body has muscles parallel to lens Muscles contraction allow lens to round up – focus near Muscles relax for distance vision Iris: open/closes pupil Smooth muscle – contractions adjust to light level Aqueous humor: between cornea and lens – constanct production and drainage Glaucoma: Decrease drainage or excess production causes an increase in pressure causing retinal damage Beta blockers decrease production, cholinergic agonist increase drainage Vitreous Humor: Gel-like – bulk of eye volume Between lens and retina – maintenance of eyeball shape No refraction Retina: visual receptors at the back of the eye Multiple cell layers Choroid: highly pigmented layer behind retina Absorbs light – no reflection – no signal Refraction: bending light waves Glycoproteins in lens refract light, focus it on the retina Retina: light passes through bipolar and ganglion cells to reach photoreceptor cells Bipolar and ganglion cells pulled back at fovea Fovea has best color vision – dense cone concentration Photoreceptors: Rods – shades of gray – most photoreceptors Cones – color receptors – fewer overall receptors Rods and cones produce receptor potentials – no Action potentials Bipolar cells: generate potentials – activated by rods/cones No Action potentials – synapse with ganglion cells Edge effect – center/surround on/off effects MAKE edges appear sharp Ganglion cells: reach threshold and fire Aps that leave eye for CNS Carry visual information to lateral geniculate, part of thalamus  cortex Optic nerve: bundle of ganglion cell axons Creates blind spots as axons pass through the retina Need cochlear implant to treat Frequency deafness: loud, repetitive sounds at one frequency pull out hair cells in one place – selective hearing loss Equilibrium: Vestibular apparatus: detect changes in motion Rotational Acceleration: 3 semicircular canals at right angles to one another Fluid filled – as fluid lags motions, fluid pulls on hair cells. Semicircular canals: hair cells imbedded in cupula – intertia Generates graded potential   action potential When hard rotation stops, 25-30 seconds to reequilibriate Linear acceleration: hair cells imbedded in gel with otoliths Acceleration pulls on hair cells Gravity constant  MOST tonic signal, know the position of the head Utricle - Saccule Detect linear a cerlation U: Horizontal motion, S: vertical motion Mismatch of signals  motion sickness Excess (rides) or loss (space flight) Lecture 16 – Efferent Nervous System Sympathetic Structure – part of the Autonomic nervous system Sympathetic chain ganglia parallel spinal cord Impur from cord, medulla, hypothalymus No direct corticol control Preganglionic Neurons: Short neurons Use Acetylcholine (Ach) as neurotransmitter to post ganglionic neurons in ganglia Postganglionic Neurons: Long neurons Activated by preganglionic neurons Use Norephinephrine (NE) as neurotransmitter Adrenal medulla behaves like Post-g neuron Sympathetic responses: respond to emergencies Flight-or-fight response: designed to remove danger Increased blood flow to skeletal muscle and heart Concurrent activation of motor units Decrease activity of digestive and related functions Receptor types: adrenergic Receptors All bind norepinephrine from post-ganglionic neurons Alpha adrenergic receptors: Cause increase in tissue activity Alpha 1  Increase IP3 increase Ca++ release from SR increased Ca++ Alpha 2  decrease in cAMP  decreased Ca++ pump  net increase Ca++ Beta 1 adrenergic receptors: Increase Ca++ in heart – open Ca++ channels Increase heart activity Beta 2 adrenergic receptors: increase cAMP  increase Ca++  decrease Ca++ Decrease blood vessel contraction and decrease lung bronchiole constriction = more blood, more air Parasymphatic structure: Part of autonomic nervous system 2 neuron series – all use Ach as Neurotransmitters Cholinergic activation controls day-to-day homeostatic maintenance Preganglionic Neurons: long neurons, spinal cord to organ Synapse at ganglia on organs with postganglionic neurons Postganglionic Neurons: short neurons – travel from ganglia to cells Parasympathetic responses: Decrease in heart rate Increase GI contractions and secretions Increase pancreatic secretions Contracts urinary bladder Relaxes internal anal and urinary sphincters Agonists/Antagonists: Pharmeceuticals can mimic or antagonize autonomic nervous system Para: increase or decrease digestive activity, etc. Sym: increase blood pressure in shock, decrease blood pressure in hypertensions Motor Neurons: Alpha motor neurons gets multiple inputs – up to 10,000! Input from: stretch receptors, withdrawal reflexes, cerebellum (learned activities), cortex (conscious control) Both IPSPs and EPSPs to alpha motor neurons – threshold? PUT IN NOTES FROM TRISH, YA DUMB. 18/2/2014 Lecture 19 – Muscle Metabolism and Control Muscle energy use: Progressive use of energy resources Phosphocreatine: Supports about 20 seconds of full activity PCr + ADP  ATP + Cr by creatine kinase reaction ATP  ADP + Pi by myosin ATPase PCr  Cr + Pi net reaction – NET REACTION Pi inhibits myosin ATPase (M*ADP*Pi M + ADP + Pi) Glycolysis – 10 Rxs, ~ 2 min of energy use Glucose and glycogen in muscles  pyruvate  lactate No Oxygen use Oxidative Phosphorylation: Krebs and electron transport ~ 2 hours of energy support Pyruvate  C02 Oxygen used Carbohydrate Loading increases glycogen storage, increased by up to 30% Fiber types: Variation in fiber type even within same muscle Controlled by motor neuron – most muscles are mixed Red Fibers: Also called slow oxidative High mitochondria levels – slow myosin ATPase – slow speed High energy capacity, low energy use – no fatigue White fibers: also called fast glycolytic Few mitochondria – fast myosin ATPase – fast speed Low energy capacity – high energy use – easily fatigued Hypertrophy: Larger cells, not hyperplasia (more cells) High intensity, high force exercise needed for maximum effect Filament Number: High intensity exercise causes microdamage to filament Disassembly of tangled filaments increases free myosin and causes pain Free myosin causes increase in expression of filament forming enzymes – more filaments, bigger cells Young – 48 hour cycle (24 disassembly, 24 assembly) Elderly – 72 hour cycle, risk? Testosterone Dependence: Filament production optimized by testosterone Females with normal hormones cannot maximize muscle size