physio cns 2006

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    VI. CNS

    Metabolic and circulatory features of the brain and CNS

    Electrophysiological properties of CNS neurons

    Neurotransmitters I: localization, synthesis, storage and transport

    Neurotransmitters II: release and neurotransmitter receptorsNeurotransmitters III: transduction of neurotransmitter signals in the CNS

    The chemical senses: taste and smell

    Auditory physiology

    The vestibular system and somatosensory physiology

    Somatosensory physiology: pain and temperature

    Signal transduction and processing in the retinaSignal processing and perception in the visual system

    Spinal reflexes

    Descending control of movement and posture

    Basal ganglia

    Cerebellum and cerebral cortex

    The reticular formation, reinforcement pathways, cortex, and EEGSleep-wakefulness

    DOP: Higher cortical functions and imaging

    Learning and memory

    Lateralization of function, language and emotion

    Hypothalamic function I and II

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    CNS Physio

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    Brain Metabolism and Circulation

    5. Cerebral blood flow increases in cases of

    a. influenza.

    b. hypoxia (Arterial P02= 75 mmHg).

    c. hypertension (Arterjal pressure= 140 mm Hg).

    d. coma.

    e. hypercapnia (Arterial PCO2 = 75 mmHg).

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    Regulation of Cerebral Blood

    Flow

    60

    120

    60 120 180

    Mean Arterial Blood Pressure (mmHg)

    Cereb

    ralBloodFlow

    (ml/min/100g)

    Autoregulation

    of cerebral

    blood flow

    Hypercapnia

    Sympathetic

    nerve stimulation

    Remember

    Metabolic

    Hyperemia!

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    Electrophysiology of CNS Neurons

    The resting membrane potential for all brain neurons is:

    a. at an equilibrium state for potassium ions.

    b. at an equilibrium state for sodium ions.

    c. at an equilibrium state for chloride ions.

    d. a steady- state level between the equilibrium potentials of the ionsinvolved, weighted by their relative permeabilities/conductances.

    e. is the same as the resting membrane potential for brain glial cells.

    Which of the following changes would increase the driving force for

    sodium entry into a neuron?

    a. depolarization of the membrane potential

    b. hyperpolarization of the membrane potential

    c. an increase in the extracellular sodium concentration

    d. The sodium equilibrium potential ENabecomes more positive.

    e. b, c and d are correct.

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    Membrane Potential

    Excitation is caused by:

    Depolarization or Hyperpolarization

    Increase in gK+or gNa+

    Increase in ENa or EK

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    Major Neurotransmitters

    Name Effect Synthesis Degradation Location

    GABA Inhibitory GAD from

    Glutamate

    Transported,

    GABA-T

    Ubiquitous

    Glutamate Excitatory Gluatminase,

    other

    Transported Ubiquitous

    Acetylcholine Excitatory Choline,acCoA, CAT

    AchE Basal Foreb.

    Hippocampus

    Epi, NE, DA Excitatory

    (except a1)

    Tyrosine, TH Trans, MAO,

    COMT

    NE- LC,Teg.

    DA- SN, Stri.

    Serotonin(5-HT)

    Excitatory Tryptophan,TH

    Trans, MAO Pons Raphe

    Histamine Excitatory Histidine,

    (Decarboxyl)

    Transferase,

    MAO

    Hypothalamus

    Peptides Both Precursors Proteases Ubiquitous

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    Catecholamine Synthesis

    Tyr L-Dopa DA NE Epi

    Tyr Hydroxylase AAAD DbH PNMH

    MAO or COMT

    MHPG, VMA, HVA

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    Neurotransmitter Receptors

    GABA GABAA

    Postsynaptic Cl-channel

    Agonists- Muscimol, Barbs, (Benzos)

    GABAB G-protein-coupled, activates Adenylate Cyclase

    Axoaxonal inhibition. Prevents NT release

    GABAB

    -

    Pre

    Post GABAA

    GABA

    GABA

    GABA

    -

    GABA

    GABA

    NE

    (-)

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    Neurotransmitter Receptors

    Ach Nicotinic

    Cation Channel (Ca++in CNS)

    Spinal Cord, Sup. Colliculus

    Muscarinic G-protein-coupled, Giinactivates Adenylate

    Cyclase, Gqactivates PLC- Ca++ influx

    M1- striatum, hippocampus, cerebrum M2- cerebellum

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    Somatosensory

    Mechanoreceptors (Abafferents) Touch and Pressure (Slow Adapting)

    Merkels Disk

    Ruffini Corpuscles

    Touch (Fast Adapting) Meissners (low-freq.)

    Hair Follicle

    Pacinian Corp. (high-freq.)- wide receptive field

    Proprioception

    Joint Receptors

    Dorsal Column-Medial Lemniscus

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    Pain Modulation

    Nociceptive Fibers

    (Ador C)synapse on

    SC neurons in the

    anterior horn (A). Descending 5-HT or

    NE neurons can

    modulate these

    synapses to preventpain transmission.

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    Temperature Sense

    Cold (Ad) and Warm (C) fibers:

    Enter the Spinal Cord at:

    Dorsolateral Lissauer fasciculus

    Ascend and Descend

    Cross SC through ventral w.c. to:

    contralateral ALS

    Ascend through ALS to reticular formation,thalamus

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    Axonal Pain Reflex

    P

    P

    P

    P Rubor- Red from enlarged

    arterioles (oxygenated

    blood)

    DolorNociceptionTumorSwelling from

    extravasated fluid

    Type C

    (Also bradykinin)

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    Basal Ganglia Disturbances Parkinsonism

    Degradation of DAergic neurons in SN Tremor, akinesia, bradykinesia,

    cogwheel rigidity

    Huntingtons Chorea

    Loss of intrastriatal med. SpinyGABAergics (caudate atrophy)

    Chorea, dementia, deceased tone

    Ballism Damage to STN (corpus luysii) -

    unilateral- hemiballismus

    Flailing movements

    Athetosis

    Damage to GP and Putamen

    Wormlike, writhing movements,

    dystonia (posture issues) Tardive Dyskinesia

    Iatrogenic side effect of neuroleptics(thorazine)

    Involuntary mouth movements due tosupersensitivity of DA receptors

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    Cerebellum

    Architecture (covered before) Remember that climbing fibers

    from inferior olivary nucleicause complex purkinje spikes,

    Mossy fibers from other nucleicause simple spikes in purkinje

    cells. Divisions

    Cerebrocerebellum

    Spinocerebellum

    Vestibulocerebellum

    Deep nuclei (send out

    transmissions) Fastigial, Interposed

    (globose,emboliform), Dentate,Lateral Vestibular Nucleus

    Granule Cells are the onlyexcitatory ones!Parallel fibers

    Cerebellar Lesions May Cause:

    1. Motor Delay

    2. Dysmetria (inaccuracy)

    3. Dysdiadochokinesia

    (alternating movement

    disorders)

    4. Intention Tremor, Ataxia, andApraxia

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    Decorticate and Decerebrate

    Postures

    Decorticate: CNS Damage above level of

    Red Nucleus

    Rubrospinal Tract active- activates arm

    flexors with response to pain or head turn incontralateral direction

    Decerebrate: CNS Damage at or below

    level of Red Nucleus Everything extended except fingers.

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    The Human Retina

    Light changes 11-cisretinal to: All-transretinal

    This activates:

    Transducin This activates

    Phosphodiesterase

    This changes:

    cGMP to GMP

    This causes: Cation channels to close - hyperpolarization

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    Sleep Stages

    REM-

    Sawtooth waves, mixed frequency EEG

    Dreaming, Paralysis

    NREM-

    Stage 1Low voltage, mixed freq

    Stage 2Sleep spindles, K complexes

    Stage 3Delta waves

    Stage 4More Delta waves

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    Reticular Formation

    Raphe Nuclei Serotonin

    SN, Ventral Tegmental Area

    Dopamine

    Nigrostriatal pathwayMotor Control

    VTA-frontal cortex and VTA-nucleus accumbens

    Dopaminergic neurons overactive in schizophrenia

    Also important in reward effects of food, water, and drug

    abuse

    Locus Ceruleus:

    Noradrenergic neurons control arousal and sleep-

    wake cycle

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    Learning and Memory

    AMPA vs. NMDA

    AMPA Glu receptors

    are active during low-

    frequency stimulation

    Na+ channels

    NMDA channels

    require previous

    depolarization through

    AMPA channels, allow

    Ca++ in.

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