Pharm-Exam4-Goz_Lecture1-Cvo

Front 1

brain stem

Back 1

CV
electrolyte
respiratory REGULATIONS

Front 2

cerebrum

Back 2

sight, sound, thinking

Front 3

limbic system

Back 3

thalamus...communication relay center

Front 4

cerebellum

Back 4

stand up/ walk

Front 5

3 kinds of ion channels important in the brain and their relative speeds

Back 5

voltage gated channels are fast (milliseconds

metabotropic channes are slower (minutes)

ligand gated ion channels are fast (milliseconds)

Front 6

how do ligand gated ion channels work?

Back 6

drug or Nt binds and opens channel

Front 7

tell me about metabotropic ion channels

Back 7

G-protein binds to channel and opens or G-protein 2nd messenger cAMP interacts w/ ion channel

Front 8

2 classes of arrangement in the brain

Back 8

1. heirachial system (long, projecting, excitatory neurons AND feed forward/backward inhibitory neurons)

2. non-specific/diffuse where the Nts like NE, E, Dop, Sera have a "diffuse" effect

Front 9

tell me about the hierachical system. what kind of neurons?

Back 9

2 kinds: long projecting excitatory and short interneurons that feed for/backward causing inhibition

Front 10

tell me about the hierachical system. part 2

Back 10

projects over long distances
involves sensory, pain, motor control

Front 11

what are the Nts in the hierachical system?

Back 11

glycine, GABA, glutamate

Front 12

non-specific/diffuse system.....what Nts? and what does it involve?

Back 12

NE, E, Dopa, Sera

INVOLVES "global funcitons" like wakefulness, attention, appetite, emtional state

Front 13

signal strength is important in what?

Back 13

memory

Front 14

emotionally, what can happen if you deplete NE in vesicles

Back 14

lead to depression (ppl w/ reserpine)

Front 15

regarding signal strength, you can impact it pre and post synaptically...tell me about it

Back 15

pre - alter [ ] of NE in vesicles
post - depends on nerve density and ion channels....if you incre K efflux and influx of Cl you can make the neuron harder to stimulate

Front 16

how do you make a nerve harder to stimulate post synaptically?

Back 16

increase efflux of K
increase influx of Cl

Front 17

tell me about amino acid Nts and their respective receptors

Back 17

Nts = glycine and GABA and glutamate and aspartate

receptors are GABA A and GABA B (for glycine and GABA) dont know names for glu and asp

Front 18

tell me about GABA A

Back 18

first off, GABA is an inhibitor Nt
this receptor is located in the Cl- ion channel....when occupied it opens up the channel allowing for Cl- influx....making it harder for nerve stimulation

Front 19

tell me about GABA B

Back 19

presynaptically decreases calcium influx (decrease Nt release) and increase K efflux postsynaptically (inhibiting impulse conduction)

Front 20

two excitatory amino acid Nts

Back 20

glutamate and aspartate (receptors not important)

Front 21

M1 and M2 receptors

Back 21

for AcH in brain....M1 is excitatory (decr. K efflux) M2 is inhibitory (incr K efflux)

Front 22

Seratonin Nt involved in what

Back 22

global functions
12 receptors, dont know them
sometimes excitatory sometimes inh

Front 23

dopamine Nt

Back 23

involved in mood
receptors = D1 and D2

Front 24

NE nt

Back 24

involved in global functions
alpha1, beta 1 and 2 all decrease K efflux

alpha 2 increases K efflux

Front 25

what receptor when occoupied by NE increases K efflux

Back 25

alpha 2

Front 26

monoamine Nt in brain

Back 26

dopamine, NE, seratonin

Front 27

enkephalins, endorphins, substance P, CCK

what are the receptors?

Back 27

peptide Nts

mu, kappa, delta receptors

Front 28

list some neuromodulators

Back 28

NO, prostaglandins, corticoid hormones

Front 29

tell me about neuromodulators

Back 29

not really NT (released at non-synaptic sites) but can function as Nt....released by glial cells...involved in pain

Front 30

tell me about cannabinoid receptors

Back 30

CB1 and CB2
play a role in pain releif

Front 31

what is sad news for high times?

Back 31

some drugs are CB2 selective