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Midterm 2 - Review Notes (Lec 14-21) PSYCH 2NF3
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Department
Psychology
Course
PSYCH 2NF3
Professor
Gautam Ullal
Semester
Winter

Description
PSYCH 2NF3 2013 Midterm 2 – March 7, 2013 Alzheimer’s Disease  Amyloid-Precursor Protein (APP) – transmembrane protein important for normal development and plasticity of synapse o Cleaved by secretases; NH2-------β ---- α -- | -- γ - | ----- COOHcytoplasm o Amyloid Peptide (Aβ) – toxic and detrimental to dendrites, axons and synapse; coupled β and γ cleavage  Amyloid Plaques deposited in synapse  Neurofibrillary Tangles (abnormal helical precipitates; tau-aggregates) formed inside axon  Cell and neuronal death  Risk Factors for AD o Age – risk increases with each decade of adult life; 20-40% of >85 years have AD  Late Onset and Sporadic AD  95% of cases (sporadic = no clear pattern of incidence; here-and-there)  Apolipoprotein E – important for cholesterol transport, maintaining synaptic function, clearing amyloid deposits and neurofibrillary tangles  Apo E4 – variant apolipoprotein E allele; associated with increased risk of amyloid deposits; toxic; associated with late-onset and sporadic AD o Family history of AD o Head injury o Low educational attainment o Family history of Down’s syndrome o Gender (females more prone)  Tau-aggregation (tangles beta-amyloid plaques) o Taupathy in polymodal areas sensitive to Beta-Amyloid Plaques beta-amyloid in polymodal areas enter taupathy  Polymodal areas – cortical sensory areas that integrate various sensations (eg/ touch, vision etc)  Distribution of Neurodegenerative Changes in AD – Braak stages follow a Domino-pattern” of tau-deposition in axons o Entorhinal cortex (major input into hippocampus; first see tangles)  Hippocampus  Posterior parietal/polymodal neocortex (sensory areas)/association cortex (after several years)  Frontal cortex ( Prefrontal cortex)  Primary sensory and Primary motor areas (last and least; sensory and motor loss)  Amyloid plaque formation and neurofibrillary tangle deposition – follows similar progressive neuroanatomical pathway o Stage I and II – transentorhinal; subclinical; no clinical signs o Stage III and IV – progressed to limbic cortex  Mild cognitive impairment – anterograde amnesia (inability to form new memories), loses way, spatial memory affected (because of hippocampal involvement)  Right hippocampus – particularly activated in spatial recall (spatial learning and orientation (navigation)); eg/ Morris Water Maze  Left hippocampus – particularly activated in word recall o Stage V and VI – progressed to association neocortex, prefrontal lobe, language areas, primary sensory and motor areas  Impairment in abstract thinking, language, personality changes, retrograde amnesia, social issues, motor paralysis  Eg/ HM – severely epileptic for several years, not controlled with medicines; bilateral temporal lobe resection controlled seizures – after seizure; anterograde amnesia, normal memory for events prior to surgery, normal IW, normal language and normal social behaviour  Pittsburgh A (amyloid) Compound – marker for amyloid plaque (protein marker); used in PET studies – amyloid plaques detected in patient with mild cognitive impairment; progressive trend observed  Drug Therapy – no definite treatment o Cholinesterase inhibitors (increases acetylcholine) o Vaccines against insoluble A-β-P – effective in reducing amyloid and progression in mice (human trials cause severe meningoencaphalitis (inflammation of entire brain) o Drugs that dissolve tangles are being developed Frontotemporal Dementia  Frontotemporal Dementia – degeneration in the form of beta-amyloid plaques and tangles start from frontal lobe to temporal lobe; begins with disturbance in personality and reasoning (unlike AD); more common in men; hard to diagnose  Structural-Functional Correlates o Sulca (depression//fissure) prominence and atrophy in prefrontal regions (identified by MRI; axial-T1 weighted MRI); dorsolateral and dorsomedial prefrontal regions; mild periventricular/subcortical nonspecific white matter changes noted o Reduced metabolism in prefrontal and temporal areas (fluorodeoxyglucose PET imaging) Glial Cells  Gliobalstoma Multiforme – malignant glial tumor; can grow along white matter tracts and nerve bundles; may destroy blood vessels and cause swelling; difficult to remove (can use radiation and various drugs to suppress it) o Pressing on hypothalamus and amygdala – associated with emotional response and outbursts  Glioma – glial tumors are the most common tumors of the brain (>70%; benign and malignant); highly invasive (invades neighboring and distant areas) o Astrocytoma – most common glial tumor; most are malignant in adults  Glia – 90% of cells in nervous system (10% neurons)  “glue cells” o Microglia (10% of glial cells) o Macroglia (90% of glial cells)  Central Nervous System – astrocyte, oligodendoglia, ependymal cells, radial glia  Peripheral Nervous System – satellite cells, Schwann cells 1 PSYCH 2NF3 2013  Microglia – rid of bacteria and toxins; concentrate around blood vessels (anything coming out of blood to brain is destroyed); “local police” o Breaks down polymorphonuclear cells and other blood cells that infiltrate brain (toxic; from trauma or hemorrhage) – by phagocytosis (process of microglia engulfing substances – offers neuroprotection)  Time-lapse video imaging of microglia engulfing polymorphonuclear leucocyte (PMN) – 19 mins PMN engulfed o Release neurotrophic factors that are important in nerve cell repair  Astrocyte – most common glia; star shaped o Major contributor to the blood-brain barrier (BBB) system (Tight Junctions) – barrier that prevents anything in blood from readily going into nervous system; chemical signals of astrocytes lead to tight junctions o Neurovascular network for microregulation of blood flow – if neurons need more blood flow (more nutrients); astrocyte dilates blood vessel and regulates microcirculation around neuron  astrocyte foot-processes tightly wrap around blood vessels o Astrocytes in visual cortex show robust calcium currents and orientation sensitivity o Release neurotrophic factors o Extensive branches extending between ependymal of ventricle, neuron and blood vessels o Major role in clearing neurotransmitters from synapse – returns glutamate (excit) and GABA (inhib) to presynaptic terminal of the neuron  Regulation process – removes excess neurotransmitter to avoid too much excitation o Symbiosis (glial-neuron) – strengthens synapse and adds plasticity  Neurotransmitter released from neuron  astrocyte receptor activated  Ca+ entry into astrocyte  astrocyte releases neurotrophic factor  synapse o K+ Homeostasis – increased firing in a neuron causes accumulation of K+ ions inside synapse; excess K+ is buffered by astroglia  cell and nerve death if astrocytes does not buffer K+ o Head trauma  too many abnormal glia causes reactive gliosis (scar)  poor K+ buffering  severe epilepsy o Tripartite Synapse – presynaptic nerve and postsynaptic nerve terminals and astrocytes as one unit  Gliotransmitters – glial chemical messengers  Use calcium signals to show electrical signals like a neuron o Disturbance in astrocyte – associated with epilepsy and schizophrenia  Ependymal Cells o Lines ventricles (cavities in brain) o Clilliary processes facilitate CSF (cerebral spinal fluid) flow o Some continuously differentiate into neurons (especially in early brain development)  Radial Glia Cells o Path for neuronal migration – neurons migrate along radial processes; signals tell neurons to stop at certain locations; radial processes extend to developingcortical mantle o Cell body remains in developing ventricle – lines the ventricle and can tract across the brain o Radial processes generally disappear in developed brain o Development of corpus callosum o May have differentiated from ependymal cells o Defective radial glia – agenesis or hypogenesis of corpus callosum  Neurons may go to wrong regions and make abnormal connections; causes problems and cognitive malfunctions o Bergman Glia – persists into adulthood; located in cerebellum; cell body close to granule cell layer; radial processes extend until pia matter; important for neuronal migration maintains glutamate homeostasis  Satellite Glia o Line cell bodies of peripheral nerves – damage can be fixed easier if near cell bodies o Nerve repair following trauma to the peripheral nerve  work with macrophage system to offer protection and facilitate repair near the dorsal root ganglion (cell body) o Neuroprotection and neurotrophic factors to sensory neuron  Oligodendroglia/Oligodendrocytes and Schwann Cell o Oligodendrocytes – myelinogenesis in CNS (~50 segments) o Schwann Cell – myelinogenesis in PNS  work with macrophage system to lay re-growth for new axons  Neurotrophic Factors – produced by most glial cells; for nerve development, nerve maintenance, nerve sprouting, synaptic plasticity, synaptic/nerve repair Synapses  Synapses – specialized zone of contact between nerves or between nerve and muscle  Types – can be nerve-nerve or nerve-muscle o Based on Structure  Axosomatic – synapse formed from axon to cell body  Axodendritic - synapse formed from axon to dendrite  Axo-axonic synapse formed from axon to axon o Based on Difference in Transmission Mechanisms  Electrical Synapse – bidirectional flow of charges (pre post); no synaptic delay (extremely fast); passive flow of ions across gap-junctions; contains connexon proteins; synchronized pre and post synaptic activity (stimulate neuron 1, neuron 2 mirrors same response with no delay)  Eg/ interneurons, glia  Chemical Synapse – unidirectional; synaptic delay (slow); neurotransmitter and receptor required; allows for differentiation between neurons in close proximity; balances excitatory and inhibitory responses 2 PSYCH 2NF3 2013  Eg/ most vertebrate neurons Neurotransmitter Release  Neurotransmitter Criteria o Chemicals stored in presynaptic terminal in vesicles o Release of chemical associate with AP o Chemicals bind to postsynaptic receptor  Dales Hypothesis – metabolic unity of a neuron requires that the same neurotransmitter is released at all its synapses (given neuron produces only one neurotransmitter), but one neurotransmitter can have different actions  modified; neurons can produce more than one neurotransmitter; several neurons have a neuropeptide along with a neurotransmitter  Ionic movement determines electrical state of membrane; neurotransmitter binds to receptor and induces excitatory or inhibitory response o EPSP  Na+ entry (depolarization) or Ca++ entry (activates enzyme) o IPSP  K+ exits or Cl- entry (hyperpolarization)  Differential release of neurotransmitters (small chemical messengers) and neuropeptides (large chemical messengers) o Large chemical messengers  neuromodulators; may not bring about effect, but modulates other neurotransmitter effects  Neuropeptides – 3-10 amino acids  Eg/ neurotrophic factors, endorphins  Large vesicles o Small chemical messengers  neurotransmitters  Small vesicles o Low frequency stimulation  releases neurotransmitters; localized increase in Ca++ concentration o High frequency stimulation  releases both neuropeptides and neurotransmitters; maximum Ca++ activation  Resting Neuron (no AP)  Vesicle Docking; Ca++ levels are low o Vesicles free floating, contain SNARE proteins (Syntaxin, SNAP-25); target SNARE proteins (synaptobrevin, synaptotagmin) docked on presynaptic neuron determine where vesicle will bind o SNARE complex formed by vesicular and target SNARE protein association – docks vesicle on presynaptic neuron  Activated Neuron  Vesicle Fusion and Exocytosis o Stimulation of neuron increases Ca++ levels in nerve terminal – activates synaptotagmin; changes state and gets entangled with target SNARE proteins  leads to vesicle fusion and neurotransmitter release Botulism  Paralysis of face muscles then respiratory muscles (unable to breath) – becomes lethargic because no oxygen can reach brain; flabby  Paralysis of muscles due to prevention of Ach vesicle docking and Ach release by inactivating SNARE proteins through proteolytic cleavage by clostridium botulinum toxins  Prevention – proper cooking and canning process  Small doses; harmless and therapeutic – strabismus (squint; due to muscle spasms); hemifacial spasm; dystonia (muscles fail to relax) in jaw, larynx; writers cramp; cosmetics (eliminates facial wrinkles)  Treatment – wash toxins with lots of fluids; start on antitoxin Tetanus  Muscle stiffness due to prevention of release of inhibitory neurotransmitters GABA and glycine in spinal cord by activating SNARE; only excitation, neurons continuously sending impulses to nerves that now cannot contract muscles  Caused by clostridium tetani Neuromuscular Junction  Stimulate motor neuron  AP in neuron  Ca++
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