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53 Cards in this Set
- Front
- Back
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Describe the two components capillaries in the brain have to limit exchange
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1. tight junctions between endothelial cells.
2. Glial endfeet come in close contact with blood vessel- make things not lipid soluble not get through as well |
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What passively diffuses across BBB?
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1. H20
2. CO2 3. O2 4. free steroid hormones |
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Why is K so important to maintain levels at rest?
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it is permeable through the leak channels at rest so throwing off concentration changes the resting membrane potential
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What is the major energy source for neuron and how does that source cross the BBB?
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1. Glut1 transporter, not insulin dependent and has two forms
a. 55k on capillaries b. 45k on astroglia |
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What occurs if you have a problem or deficeincy with GLUT1 transporter at the BBB?
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could cause seizures and brain damage because because the neurons will depolarize spontaneously due to reduced levels of ATP
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What is the most important reason the Na/K/2CL transport protein must be functioning at the BBB?
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Maintaining extracellular K concentration of the CSF
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Drugs that cross the BBB are moved back into the blood by what?
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P-glycoprotein
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What areas of the brain are "outside" or not as well protected by the BBB?
Name the four "regions" |
Circumventricular organs (neural tissues)
Which includes 4 regions 1. Posterior pituitary 2. Area Postrema 3. OVLT- (organum vasculosum of the lamina terminalis 4. Subfornical organ |
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Describe the reason the 4 regions without the BBB are different from the other areas...
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they are missing the tight junctions
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What is the role of the posterior pituitary as a circumventricular organ?
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releases hormones into the blood that are not steroids
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What is the role of the Area Postrema as a circumventricular organ?
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located in the brain stem focus is on vomiting
- detects chemical signals in the blood from GI |
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What is the role of the 3. OVLT- (organum vasculosum of the lamina terminalis
4. Subfornical organ as a circumventricular organ? |
involved in control of body water/thirst/blood volume control (angiotensin)
- around the ventricles |
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Benefits and costs of the circumventricular organs?
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Benefits
1. Easy access to blood brain chemicals required for region to function 2. Responds to composition of the blood Negative 1. toxins can cross the BBB and effect circumventricular (postrema causing vomiting) |
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How much CSF is made per day and how much is usually circulating?
Where is it made? |
150ml circulating and 550ml/day made
- choroid plexus makes 50-70% of CSF, remaining made by tissue that lines ventricles and blood vessels |
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Does production of CSF change with increased intracranial pressures?
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No constant production
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What ions are nearly equal in concentration in plasma and CSF?
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Na, Cl, HCO3
HCO3 swings the most |
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What ions are greater in concentration in the CSF than in the blood?
Which are less in concentration? |
Mg, CO2, and creatinine
- K, Ca, protein, and inorganic PO4 |
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Describe the flow of CSF
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One way path from ventricle through foramens of Magendie & Luschka and eventually to outside surface of brain to the subarachnoid space
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Describe how CSF is absorbed into the blood
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From the arachnoid villi, the CSF enters the venous sinuses by bulk flow.
- Usually through the cerebral venous sinuses |
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Describe where the presynaptic inhibition occurs and how it occurs
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a. occurs at axo-axonal synapse
1. it is the axon terminal that delivers the inhibition to a presynaptic termonal of another axon Axon terminal releases GABA into synaptic cleft and it diffuses to post-synaptic side (presynaptic of second axon) and causes hyperpolarization by allowing Cl- to flood into cell |
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After GABA causes cell hyperpolarization in the process of presynaptic inhibition... What does it to do to Ca?
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Hyperpolarization does not allow as much Ca to enter the pre-synaptic terminal of neuron A --> leads to less neurotransmitter release
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Where is Ach centrally located in the CNS?
How is it moved into vesicles? |
Thalamus
Cortex Striatum - moved into vesicles by VAchT (vesicular achetylcholine transport) |
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What type of receptors is Ach bind to?
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1. Muscarinic receptors
4-5 different types - serpentine receptor - G-protein coupled (M1-5) *M1 (neuronal): increase IP3/DAG==> increases Ca 2. Nicotinic Receptors- located at NMJ, autonomic ganglia, and other parts of CNS - made of 16 genes- which change the affinity for Ach, which changes influx of Ca a (1-9), B (2-5), gamma (1), delta (1), Epsilon (1) |
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Describe and give some examples of the neurotransmitters known as the monoamines...
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This class of neurotransmitters includes all of those that are created by modifying single amino acids
1. Catecholamines a. epinephrine (=adrenaline) b. norepinephrine (=noradrenaline) c. dopamine -serotonin -histamine |
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Where is norepinephrine found in CNS?
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locus ceruleus
- other pontine medullary areas which are specific for sleep cycles |
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Where is epinephrine found in CNS?
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medulla
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How are epinephrine and norepinephrine made?
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derived from tyrosine
tyrosine dopamine norepi epi tyrosine hydroxylase conversion of tyrosine to DOPA is rate-limiting step. PNMT converts NE to epi |
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What moves epi and norepi into the vesicles?
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VMAT1 and VMAT2
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How are the actions of epi and norepi limited?
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Reuptake
Enzyme degradation (monoamine oxidase) COMT- catechol-O-Methyl-transferase (glial cells/ post synaptic membrane) |
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what does norepi and epi bind to?
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a-adrenergic and b-adrenergic receptors (bothe are serpentine)
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What do the B-adrenergic receptors do?
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all increase cAMP
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What do the a-adrenergic and b-adrenergic receptors do when they bind epi and norepi
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1a, 1b, and 1d: increase IP3 and DAG leading to decreased gK+
2a, 2b, 2c: decrease cAMP leading to decreased Ca++ and increased K+ |
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Describe the imidazoline receptors for epi and norepi
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Imidazoline receptors
clonidine – agonist @ 2 receptors Now recognized to have its own receptor Not sure of relationship to epi/norepi receptors |
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Where is dopamine found in CNS?
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it is monoamine found in basal ganglia, hypothalamus and limbic system in cortex
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How do you limit action of dopamine?
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Catabolism by MAO and COMT
and Reuptake |
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Describe the 5 receptor types for dopamine
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Connected to G proteins
D1 and D5: increase cAMP D2: decrease cAMP leads to decrease gCa and increase gK D3 & D4: decrease cAMP |
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Where do you find serotonin (5HT) in CNS?
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hypothalamus and limbic system
- brainstem raphe nuclei and spinal cord - cerebellum |
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How do you make it serotonin
How do you limit actions? |
1. Derived from tryptophan
2. Reuptake Catabolism by MAO and COMT |
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Describe the 5HT (serotonin) receptors...
What is the postrema receptor? Which 5HT receptor has anti-depressent? |
5HT have multiple subtypes
- Key to remember 5HT3= area postrema vomiting 5HT6- anti depressant |
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Describe where histamine is made in CNS...
How do you make histamine |
hypothalamus ya dig
- derived from histidine |
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How do you limit its action?
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Reuptake
Catabolism by diamine oxidase (peripheral), histidine methyl transferase (central) and MAO-B |
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Describe the histamine receptors and which are more important in the brain?
Which H receptor is blocked hardcore by Benadryl's bitch ass |
H1: PLC activation
H2: cAMP H3: presynaptic, decrease histamine release More H1 and H3 in brain than H2 H1 involved in wakefulness and thus H1 is blocked by Benadryl's bitch ass |
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Describe the class of neurotransmitters known as the Amino Acids from Asstown
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Excitatory AA's ((glutamate, aspartate, taurine)
Inhibitory AA'sGABA (gamma -amino-butyric acid) Glycine |
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Where is GABA located in CNS and how is it made?
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1. Located: cerebellum
cortex retina 2. Made: Glutamate decarboxylase (GAD) derived from glutamate |
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How is GABA action limited?
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Reuptake
Catabolism by GABA-transaminase |
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Where does GABA bind to?
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GABA a receptors- these are ionotropic 5 subunits, conduct Cl, and is potentiated by benzodiazepine
GABA b - serpentine heterodimer g protein that decreases: adenylyl cyclase, increase: IP3/DAG and gK+ |
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Where would a dumbass find Glycine squirting out in the CNS?
Anything a bitch needs to know about glycine? |
spinal cord, brainstem, and a little bit in the forebrain
- Also a non dumbass would know it is the most prevalent inhibitory NT in the spinal cord |
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Describe the receptors for glycine and what blocks glycine's actions...
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ionotropic
pentamer alpha subunit: glycine binding beta subunit is structural Chloride channel Block by strychnine |
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Describe the neurotransmitters known as the peptides
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These neurotransmitters are (as the name implies) peptides coded for by genes. Many were originally thought to be neuromodulators, but are now recognized as neurotransmitters. This group includes (but is not limited to):
Tachykinins (includes Substance P) Opioids – only one I’ll discuss further… Somatostatin CCK CGRP |
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Where are the opioids NT's located in the CNS?
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basal ganglia, hypothalamus, parabrachial nuclei and raphe nuclei
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Describe the class we know as mother f-ing opioids...
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1. Proenkephalin (tyr-gly-gly-phe-x)
a. met-enkephalin b. leu-enkephalin 2. Pro-opiomelanocortinin- also precurser for ACTH a. Beta-endorphins 3. Prodynorphin a. 3 molecules of leu-enkephalin b. dynorphins (1-8 and 1-17) 4. Endomorphin |
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How are opioids made?
How does a stooge limit the actions of the all powerful opioids |
since peptide, coded and created via DNA/RNA/Protein synthetic machinery
Enzymatic, possibly after reuptake Enkephalinase A and B Aminopeptidase |
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What are the binding shits of opioids?
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m (mu) receptors- are serpentine receptors causes for analgesia, respiratory depression, euphoria, sedation, and constipation
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