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Ependymal Cells

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Ciliated cells that line the cavities of CNS and spinal cord Secrete CSF, act as shock absorber, pluripotent stem cells

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Multiple Sclerosis

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Demyleinating disease, both phospholipid and sphingolipi levels decreased from brain and spinal cord Nystagmus, intention tremor, scanning speech. Oligodendrocyte damage, which has limited ability for mitosis

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Guillain-Barre Syndrome

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Injury to schwann cells of PNS

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Proteolpid Protein(PLP)

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Hydrophobic, highly conserved, crosslinks layers of CNS myelin by compacting the layers, Po is the version of PLP in the PNS

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Myelin Basic Protein(MBP)

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Stabilize the structure from within the membrane, in CNS and PNS

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Blood-Brain Barrier Structures

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Formed from: Tight junctions between nonfenestrated capillary endothelial cells Basement membrane Astrocyte foot processes

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Things That Can Cross BBB

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Nonpolar/lipid-soluble substances diffuse rapidly Glucose and amino acids cross slowly via carrier-mediated transport

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Areas of Brain with Fenestrated Capillaries and No BBB

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Area postrema, reached by Chemo drugs, causes vomiting

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Vasogenic Edema

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Destruction of cell tight junctions in BBB, caused by infarction or neoplasm

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Glucose Transporters

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GLUT-3- on neurons, transport glucose from ECF GLUT-1- transports glucose

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Transport of Other Fuels in Brain

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Lactate, acetate, pyruvate, ketone bodies, acetoacetate and beta-hydroxybutyrate transported by slower transporter than Glut, upregulated when ketone bodies elevated

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Glut-1 Deficiency Syndrome

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Low glucose levels in CSF Clincial features variable- seizures, developmental delay Treated with ketogenic diet(high fat, low carbs)

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Large Amino Acid Transport

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For large, neutral amino acids single transporter(Phe,Leu,Tyr,Iso,Val,Try,Met,His) if one of these in excess can result in lower transport of the other amino acids, e.g. PKU Phe

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Small Neutral Amino Acid Transport in BBB

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Restricted transport Glycine, glutamate(GABA)

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Receptor-Mediated Transcytosis

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Insulin, transferrin, insulin-like growth factors Endocytosis Absorptive-mediated transcytosis- protein binds nonspecifically to membrane and not to a specific receptor

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Neurotransmitter Categories

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Small nitrogen-containing molecules- Glutamate GABA, glycine, Ach, dopamine, norepi, serotonin, histamine, Epi, aspartate, NO Neuropeptides- Opioid peptides, GH and TSH

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Catecholamine Storage

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Dopamine taken up into storage vesicles by protein VMAT2, which is driven by the proton gradient Catecholamines exist in complex with ATP and acidic proteins(chromogranins) AP causes depolarization and influx of calcium, promotes release of catecholamines

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Catecholamine DEgradation

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Catalyzed by monoamine oxidase(MAO) and catechol-O-methyl-transferase(COMT)

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MAO

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Inactivates catecholamines not protected in storage vesicals MAO-A and MAO-B

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MAO-A

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NE, serotonin and dopamine Converts serotonin to 5-hydroxyindoleacetaldehyder, which is proken down to 5-hydroxyindole acetic acid

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MAO-B

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Phenyetyhlamine, dopamine

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COMT

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Works on broad spectrum of extraneuronal catechols and those that have diffused away from the synpase. Transfers metyhl group from SAM, depends on B12 and folate

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Catecholamine End Degradation Prodcut

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3-Methoxy-4-hydroxymandelic acid (Vanillylmandelic acid, VMA)

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PKU

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Decreased phenyalanine hydroxylase or decreases BH4 cofactor Increaed Phe, decreased tyrosine Screening 2-3 days after birth Avoid sweetener aspartame

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Maternal PKU

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When woman with PKU pregnant, lack of proper dietary therapy during pregnancy. Causes microcephaly, intellectual disability, growth retardation, congenital heart defects

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Isoniazid

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Induces neuroligic side effects due to VitB6 deficiency, chemicall similar to B6, competes with it, leading to defective synthesis of GABA, can be prevented with B6 supplementation

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BH4 Neurotransmitter

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Serotonin synthesis via tryptophan hydroxylase

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Vit B6 Neurotransmitter

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Pyridoxal phosphate used in reactions for serotonin, epinephrine, NE, dopamine and GABA production

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Dopamine

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D1- relaxes renal vascular smooth muscle D2- modulates transmitter release, esp in brain Increased in schizo and Huntington Decreased in Alzheimer's and Parkinson's

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L-Dopa

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Increased level of dopamine in brain, used for parkinson disease treatment, capable of crossing BBB where it can be converted to dopamine in CNS via dopa decarboxylase. Dopamine cannot cross BBB

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Norepinpehrine

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Increase in anxiety, decreased in depression

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Serotonin

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Tryptophan can form serotonin and niacin, tryptophan hydroxylase requires BH4. Serotonin can be inactivated by MAO Decreased in anxiety and depression, increased in parkinson's

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Serotonin Syndrome

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Can occur with any drug that increases 5-HT(MAO inhibitors) 3 A's Activity(tremor, seizure) Autonomic stimulation(hyperthermia) Agitation

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Dopa Decarboxylase Serotonin Production

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Converts 5-HT to serotonin

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Melatonin

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Produced in pineal gland in response to light-dark cycle. Produced from N-acetyl serotonin with methyl donation by SAm

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Tyramine

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Degradation product of tyrosine, normally degraded by MAO. Increased in patients on MAO inhibitors who ingest tyramine-rich foods(aged cheese and wine) Mimics norpepinephrine, causes hypertensive crisis

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Selective Serotonin Reuptake Inhibitors(SSRIs)

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5-HT specific reuptake inhibitors, normally takes 4-8 weeks for antidepressenats to have effect Used for: Depression, generalized anxiety disorder, panic disorder, OCD

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Monoamine Oxidase Inhibitors

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Nonselective inhibition can increase level of amine neurotransmitters(Norepi, 5-HT,. Dopamine) Used for: atypical depression, anxiety Hypertensive crisis with ingestion of tyramine rich foods Contraindicated with SSRIs(prevents serotonin syndrome) 2 week wait after stopping these before starting serotnergic drugs or stopping dietary restrictions

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Histamine

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Produced by mast cells and neuronal fibers Histidine decarboxylase requires PLP(converts histidine to histamine) Not recycled, astrocytes main site of inactivation and defradation

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Histamine Inactivation

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In brain Methylated or oxidized by MAO-B In peripheral tissues deamination by diamine oxidase

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Deamine Oxidase

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Converts histamine to imidazole acetaldehyde, and then to imidazole acetic acid through reduction of NAD+

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MAO-B Breakdown of Histamine

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Histamine first metyhlated by SAM and histamine metyhl transferase Metyhlhistamine then broken down by MAO, intermediate reduces NAD and produces metyhlimidazole acetic acid

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Acetylcholine

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Synthesis from acetyl CoA and choline, catalyzed by choline acetyltransferase Inactivated by acetyhlcholinesterase(AChe) Decreases in Huntington's and Alzheimer's Increased in Parkinson's

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Acetylcholinesterase Products

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Produces acetic acid and choline, choline is then taken up by presynpatic terminal from blood(low affinity) and from synpatic cleft(high affinity) or choline produced from phosphatidylcholine

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Neurotoxin(Sarin) Effects

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Nerve gas that inhibits AchE, causes paralysis

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Botulinum Toxin

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Prevents release of acetylcholine at cholinergic terminals

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Glutamate

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Excitatory neurotransmitter in CNS Three synthesized routes Ca2+ dependent release Glutamate and aspartate are endogenous ligands for NMDA receptor

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GABA

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Major inhibitory neurotransmiter Synthesized by decarboxuylation of glutamate Upatke in glial cells, recycled in GABA shunt Requres B6 Decreased in anxiety and Huntington's

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Clostridium Tetani

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Decreases GABA and glycine, causes spastic paralysis

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Tiagabine

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Inhibits reuptake of GABA, increased GABA is used to treat epilepsy

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GABA Shunt

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GABA converted to glutamate via Carboxylation reaction, via PLP and Carboxyl donation from alpha-ketoglutarate, produces succinate which can be used in TCA cycle, or receives another AcCoA to reform alpha-KG

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Aspartate

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Excitatory, synthesized from TCA cycle intermediate oxaloacetate Cannot pass through BBB

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Glycine

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Inhibitory in spinal cord From serine Glycine content best reflects collagen synthesis- collagen is 1/3 glycine

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Amino Acids Required for Purine Synthesis

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GAG Glycine Aspartate Glutamine

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Sildenafil

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Inhibits cGMP phosphodiesterase-5 Also known as viagra

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Hypoglycemic Encephalopathy

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Early- sweating, palipiations, anxiety and hunger Later- confusion, seizures and coma

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Blood Glucose <2.5 mM

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Brain attempts to use internal substrates, glutamate and TCA cycle intermediates as fules

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Blood Glucose 2.0-2.5 mM

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Decreased synthesis of neuron transmitters in particular regions

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Blood Glucose <1 mM

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Neuronal cell death, hippocampal and cortical structures selectively vulnerable Mechanisms: Glutamate excitotoxicity- prolonged glutamate receptor activation leads to influx of lethal Ca2+

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Hypoxi Encephalopathy

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High altitudes, anemia, cyanide poisoning Results in diminished neurotransmitter synthesis

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PaO2 25-40 mmHg

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Severe cognitive dysfunction resulted from impaired neurotransmitter snythesis Anaerboic glycolysis maintenance of ATP levels-> lactate and decrease in pH

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Acute Hypoxia(PaO2 <20mmHg)

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Coma

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