physio cns 2006
TRANSCRIPT
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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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