Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
72 Cards in this Set
- Front
- Back
|
What are the two major components of the BBB?
|
tight junctions
glial endfeet |
|
|
What 4 molecules (or types of) may pass the BBB via passive diffusion?
|
H2O
CO2 O2 FREE steriod hormones |
|
|
How does glucose cross the BBB?
|
GLUT-1 transporters on capillaries (and astrocytes)
|
|
|
Which direction do Na, K, & Cl move via their collective transporter?
|
from CSF to blood
expression of this transporter is tied to endothelin 1 and 3 |
|
|
If many drugs can readily cross the BBB, what stops them?
|
P-glycoprotein moves them back to the blood
|
|
|
These areas are neural tissue that is "outside" or not quite as protected by the BBB as other neural tissue.
|
What are the circumventricular organs?
|
|
|
What are the 4 "exceptions" to the BBB?
|
1. Post pituitary
2. area postrema: vomiting 3/4> OVLT (organum vasculosum of lamina terminals) & subfornical organ: control body water/thirst/BV |
|
|
What three molecules are found in relatively equal concentrations in the plasma and CSF?
|
Na
Cl HCO3 |
|
|
What three molecules are found in GREATER concentration in the CSF compared to plasma?
|
Mg
CO2 creatinine |
|
|
What four molecules are found in LESSER concentration in the CSF compared to plasma?
|
K
Ca++ protein inorganic PO4 |
|
|
What are the 3 central locations of Ach in the brain?
|
cortex
thalamus striatum |
|
|
How is Ach transported into viscles?
|
via VAchT
|
|
|
How is Ach catabolized?
|
via acetylchoniesterase
|
|
|
What muscarinic receptor type is found in the CNS?
What is the effect? |
M1: inc IP3/DAG --> Inc Ca++
serpentine, g-prot receptor |
|
|
What are the characterstics/locations of nicotinic receptors?
|
1. ionotropic --> allow Na+ entrance
2. NMJ, autonomic ganglia, other parts of CNS |
|
|
What are the 5 monoamines?
|
E
NE dopamine serotonin histamine |
|
|
Where can you find E & NE in the CNS?
|
E: medulla
NE: locus ceruleus, other pontine/medullary areas |
|
|
How does E/NE get into transport vesicles?
What inhibits uptake? |
VMAT1
VMAT2 Reserpine inhibits |
|
|
What two enzymes can degrade E/NE?
|
monamine oxdase
COMT (in glial cells/post-syn membrane) |
|
|
What is the molecular effect of binding to beta-ad receptors?
|
all inc. cAMP
|
|
|
What is the effect of binding to the following alpha-ad receptor types?
1. 1a, b, and d 2. 2a, b, and c |
1. inc IP3/DAG --> dec gK+
2. dec cAMP --> dec Ca++ & inc. K+ |
|
|
What 4 areas of the brain can you find dopamine?
|
basal ganglia
hypothalamus limbic system cortex |
|
|
What kind of receptors bind dopamine? What are the subtype groupings based on effect?
|
1. serpentine receptors --> G proteins
2. D1/D5 --> inc cAMP D2: dec cAMP --> dec gCa and Inc. gK+ D3/D4: dec cAMP |
|
|
Where can you find serotonin in the CNS (5 places)?
|
hypothalamus
limbic system cerebellum brainstem raphe nuclei spinal cord |
|
|
What serotonin receptor subtype is ionotropic?
|
5HT3 --> Na+
|
|
|
What serotonin receptor subtype is a target for selective anti-depressants?
|
5HT6
|
|
|
What serotonin receptor subtype is found in the limbic system?
|
5HT7
|
|
|
Where can you find histamine in the CNS?
|
hypothalamus (wakey wakey)
|
|
|
How is histamine catabolized?
|
DIAMINE oxidase and COMT
|
|
|
Which histamine receptor subtype is found in the presynaptic membrane.... and decreases its release?
|
H3
|
|
|
Which histamine receptor subtype is involved in wakefulness?
|
H1
|
|
|
What are the 5 important NT's in the amino acid class?
|
excitatory: glutamate, aspartate, taurine
Inhibitory: GABA, glycine |
|
|
What 3 places can you find GABA?
|
cerebellum
cortex retina |
|
|
What enzyme makes GABA?
What is its precursor? |
1. GAD (glutamate decarboxylase)
2. derived from glutamate |
|
|
What are the characteristics of GABA-A receptors?
|
ionotropic
5 subunits inc. Cl- conductance benzodiazepine potentiates! |
|
|
What are the characteristics of GABA-B receptors?
|
serpentine
herterodimer G protein effects :dec andylyl cyclase inc IP3/DAG inc. gK+ |
|
|
What is the major inhibitory NT of the brian?
Spinal cord? |
brain: GABA
spinal cord: glycine |
|
|
Where can you find glycine in the CNS?
|
SPINAL CORD
brainstem forebrain |
|
|
What are the characteristics of glycine receptors?
|
ionotropic
pentamer alpha sub binds the NT Cl- channel strychnine BLOCKS! |
|
|
What NT class do opiods belong to?
|
peptides
|
|
|
In what 4 parts of the CNS can you find opiods?
|
basal ganglia
hypothalamus parabrachial nuclei raphe nuclei |
|
|
What are 4 key precursor molecules of opiods?
|
proenkaphalin
pro-opiomelanocortinin (for endorphins) prodynorphin endomorphin |
|
|
What enzymes can degrade opiods?
|
enkephalinase A/B
aminopeptidase |
|
|
What are 3 important effects of opiods binding to their serpentine u (mu) receptors?
|
analgesia
respiratory depression euphoria |
|
|
What are 2 important effects of opiods binding to their serpentine kappa receptors?
|
analgesia, dysphoria
|
|
|
What is the main effect of opiod-binding to delta receptors?
|
analgesia
|
|
|
What are two vital components to brain functioning (molecules)?
|
calcium
oxygen |
|
|
What EAA is found in the visual cortex & pyramidal cells?
|
aspartate (from OAA)
|
|
|
What is the ionotropic receptor of EAA's?
What is the effect of receptor binding? |
NMDA receptors --> allow Ca++ influx (and a little Na+)
|
|
|
What other molecule must be present in order for EAA to have its effect on NMDA receptors?
|
glycine (it is a co-agonist)
|
|
|
What ion sits in the NMDA receptor channel, blocking Ca++ influx?
What must happen to remove it and open the channel? |
1. Mg++
2. membrane depolarization causes it to leave |
|
|
What drug can bind the NMDA receptor internally and block it?
|
PCP
|
|
|
Activation (and Ca++ influx) of NMDA receptors leads to what overall outcome?
|
EPSP (slow onset but prolonged duration)
|
|
|
Activation of non-NMDA receptors causes influx of what?
|
Na+ ( and a little Ca++)
|
|
|
What are the two (pharmacological) subtypes of non-NMDA receptors?
|
AMPA
kainate |
|
|
What drug can bind to AMPA receptors and inhibit response to EAA's?
|
benzodiazepine
|
|
|
What important relationship accounts for interplay b/w AMPA/kainate receptors w/ NMDA receptors?
|
they are often co-localized soo.......
activate non-NMDA --> Na+ influx --> membrane depol --> Mg++ release from NMDA --> Ca ++ influx can now occur |
|
|
Are EAA metabotropic receptors located pre or post-synaptically?
|
trick! both locations
|
|
|
This type of EAA receptor is found in primary afferent neurons and premotor (upper mn) neurons.
|
What are non-NMDA receptors
|
|
|
These EAA receptors are associated with long-term changes in synaptic strength, learning, and memory.
|
What are NMDA receptors
|
|
|
These EAA receptors are associated with learning, memory, and motor systems.
|
What are metabotropic receptors?
|
|
|
How can glia catabolize EAA's?
|
convert it to glutamine and relase it into the ECF --> neurons can convert back to glutamate
|
|
|
How is EAA function connected with NO?
|
influx of Ca++ --> bind calcineurin --> activate NOS -->arginine converts to NO --> long-term potentiation and memory (and CV/resp. control)
|
|
|
Why can NO be very toxic?
|
leads to production of free radicals
|
|
|
What are 5 pathological/clinical situations in which excitotoxicity is implicated?
|
cerebral ischemia/stroke
hypoxia/anoxia trauma to CNS hypoglycemia possibly epilepsy |
|
|
What happens to the cell membrane when cells can't meet metabolic demands?
|
depolarization
(trigger for EAA release?) --> NMDA activation --> Ca++ influx in cells --> baaaad |
|
|
increased intracellular Ca++ leads to activation of what 4 intracelllular paths?
|
activates:
PLA2 calcineurin u-calpain (a protease) apoptosis |
|
|
Activation of PLA2 via Ca++ causes release of what in the cell?
|
arachidonate (physical damage to the membrane)
|
|
|
What is the effect of calcineurin in the cell?
|
increases NO synthesis
|
|
|
mitochondrial membrane disruption leads to activation of what 2 apoptotic molecules?
|
cytochrome C
caspase 9 .... this activates caspase 3 --> proteolysis/apoptosis |
|
|
Why is introducing oxygen to a ischemic (damaged) cell problematic?
|
oxygen often ends up as free radicals
|
|
|
In reperfusion injury, kinsases convert ATP to what?
|
ADP + PO4 --> phosphorylation and further mod of proteins
|
