Lecture 7 and 8 Flashcards
(31 cards)
blood brain barrier
a physical barrier between capillaries and extracellular brain fluid that is formed by endothelial cells. Allows oxygen, glucose, amino acids, and lipid soluble molecules to pass
curare
big molecule that is an Ach-R antagonist, can’t get into blood brain barrier so acts on nerves, muscles, and causes paralysis
effects on transmitter production
inhibition of transmitter synthesis
blockade of axonal transport
interference with storage of transmitters
effects on transmitter release
prevention of synaptic transmission
alteration of synaptic transmitter release
alteration of transmitter release through modulation of presynaptic activity
effects on transmitter clearance
inactivity of transmitter reuptake
blockade of transmitter degradation
effects on transmitter receptor
blockade of receptors
activation of receptors
effects on cellular processes
regulation of the number of post synaptic receptors
modulation of intracellular signals
DREADDs
designer receptors exclusively activated by designer drugs
antidepressant examples
monoamine oxidase inhibitors
buropion
monoamine oxidase inhibitors
and why is it seldom used
MAOs breakdown monoamines (DA, NE, serotonin) so MAOIs increase monoamine activity at synapse
effective but seldom used because fatal increase in blood pressure can occur if people eat food with tyramine like cheese or alcohol
buropion (wellbutrin)
thought to increase the activity of serotonin, DA, and NE (reuptake inhibitor) alleviation of depression takes a couple of weeks.
what does delayed action of helping depression suggest
depression is not a simple matter of too little or too much serotonin, have affects on mood too
antipsychotics first gen
D2-R antagonists, relieve positive symptoms of schizophrenia (hallucinations, delusions, rapid speech)
atypical antipsychotics
more specific antagonists of D2-R and serotonin receptor
early evidence of negative schizophrenia relief
anxiolytics examples and act primarily by…
effective drugs are alcohol, opiates, barbiturates, benzodiazepine agonists
drug actions primarily by increasing neural inhibition via enhancing actions of GABA neurotransmitter
opiates examples and effects
morphine, cocaine, heroine
analgesics, sleep inducing, high abuse potential
pain control gate theory
pain signals are sent to the periaqueductalgrey (PAG)
descending information from the brain can gate incoming pain signals in the spinal cord
electrical stimulation of periaqueductalgrey produces analgesia
enkephalins and endorphins are
endogenous substances that are anagesic and addictive
opiate tolerance
opiate receptors become less sensitive
the DA reward hypothesis
anything that causes the release of DA especially in nucleus accumbens produces a pleasurable sensation
evidence of DA reward hypothesis
intracranial self stimulation
drug self administration
drugs of abuse
how do opioids activate DA pathway
GABA neurons typically inhibit DA neurons in VTA, Mu opioid receptors (MOR) on GABA neurons are inhibitory,
activation of MOR inhibits GABA, which causes a disinhibition of DA
therefore endorphins of opioids activate DA reward pathway
(sexual activity activates MOR)
stimulants examples are
nicotine, alcohol, cocaine
nicotine acts on what receptors
nicotinic ach receptors