1. S3/b2 Neuro Nts

Front 1

Where do NT peptides get made?

Back 1

Cell Body

Front 2

Where do low molecular weight NTs get synthesized?

Back 2

Axon terminal

Front 3

What triggers NT release?

Back 3

1. AP causes Ca release
2. Ca causes NT release

Front 4

Speed of
Ionotropic receptors
Metabotropic receptors(G-protein linked)

Back 4

1. Fast Acting
2. Slow Acting

Front 5

3 ways to remove NTs from the synaptic cleft?

Back 5

1. Degradation
2. diffuse out of cleft
3. reuptake (pharmaceutical target)

Front 6

Ionotropic Receptor Signalling Characteristics, speed and channels?

Back 6

1. Fast Acting
2. Downstream effects;
a. Open K or Cl channels = Hyperpolarization
b. Open Na or Ca channels = depolarization

Front 7

Metabotropic Receptor Signalling, speed/effects?

Back 7

1. Slow Acting
2. Down Stream Effects, affect ion channels, NTs or gene transcription

Front 8

What are the major downstream signal transduction pathways?(3)

Back 8

1. cAMP and cGMP
2. Ca
3. IP3 and DAG

Front 9

What does G-protein coupled opening of K channels do?

Back 9

Hyperpolarize the cell and make the neuron less excitable

Front 10

What makes an NT(2)?

Back 10

1. Made, stored and released in the neuron
2. Able to initiate some post synaptic event

Front 11

What do NTs do?
Excitatory and inhibitory?

Back 11

1. They change the membrane potential of the postsynaptic cell
2. Increase Na or Ca permeability
3. Increase Cl or K permeability

Front 12

Ligand gated Ion channels(ionotropic) mediate? and G protein linked(metabotropic) receptors mediate?

Back 12

1. The fast ( nicotinic, GABAa, NMDA, AMPA)
2. The slower catecholamines, adrenergic, dopamine, 5HT, opiate and muscarinic

Front 13

The three types of NTs?

Back 13

1. Low molecular weight; Amino acids, ACh, and biogenic amines
2. High molecular weight peptides.
3. Retrograde NT, NO and cannabinoids

Front 14

Acetylcholine characteristics(4)

Back 14

1. Low weight
2. Synthesis from acetyl CoA and choline
3. Degradation by acetylcholinesterase
4. Choline reupatke into presynaptic cell

Front 15

Nicotinic and muscarinic receptors?

Back 15

1. Ionotropic excitatory, at NMJ and autonomic ganglia(nicotine is fast)
2. Metabotropic, Gprotein forming IP3 or lowering cAMP

Front 16

Myasthenia Gravis(3 + tx)

Back 16

1. Postsynaptic NMJ Disorder
2. ACh receptor antibodies = progressive muscle weakness
3. Gets worse with muscle use
4. ACh Inhibitors to get better

Front 17

Lambert Eaton Syndrome(3)

Back 17

1. Presynaptic NMJ disorder
2. Ca channel antibodies = . No ACh release

Eaton eats Ca channels

Front 18

Anticholinergic drugs do what?(3)

Back 18

1. Control saliva and gastric acid(antacid)
2. Slow gut motility(anti-Diarrhea)
3. Prevent vomitting(anti emetic)
Triple AAA

Front 19

Glutamate characteristics(3)

Back 19

1. Major excitatory NT
2. Low weight
3. Degradation

Front 20

3 types of glutamate receptors

Back 20

1. NMDA and AMPA, and Kalinate

Front 21

Glutamate action on AMPA and NMDA receptors ...LTP

Back 21

1. NMDA intially blocked by Mg
2. AMPA activation depolarizes NMDA
3. Mg removal and pore opens
4. Na and Ca enter the cell

Front 22

Glu and neurotoxicity

Back 22

1. Low O2
2. no ATP
3. Glu increase in cleft
4. Increase in Ca intracellular
5. Phospholipase activation
6. cell death

Front 23

Glu clinical(5)LASSE

Back 23

1. Learning/memory
2. ALS
3. Seizures
4. Schizos
5. Excitotoxicity

LASSE sniffs glue

Front 24

Glu and LTP

Back 24

Glu firing changes the synapse and helps record memories using NMDA and increased AMPA receptors

Front 25

GABA charcteristics(2)

Back 25

1.Major inhibitory NT
2. AA

Front 26

GABA-a
GABA-b

Back 26

a = ionotropic = Cl
b = metaBotropic = K

Front 27

GABA Drugs

Back 27

1. Barbituates
2. Benzos

Front 28

3 GABA general effects

Back 28

1. Enhanced GABA is sedative, hypnotic, anticonvulsant

Front 29

Glycine(2)

Back 29

1. Inhibitory in the spinal cord
2. Ionotropic receptor - opens Cl channels

Front 30

The 3 catecholamines

Back 30

Dopamine, norepi,epi

Front 31

Dopamine receptors(3)

Back 31

1. both Metabodopic
2. D1 = +cAMP
3. D2 = -cAMP

Front 32

Dopamine neurons areas(3)

Back 32

1. Substantia Nigra
2. Ventral Tegmentum
3. Arcuate nucleus of hypothalamus

Front 33

Parkinson's

Back 33

Degeneration of Nirgro-striatal dopamine neurons

Front 34

DA and Schizophrenia

Back 34

Due to elevated dopaminergic transmission. So we block the D2 receptors

Front 35

Norepinephrine(3)

Back 35

1. Biogenic AA
2. alpha and beta receptors

Front 36

Norepi nuclei in the brainstem

Back 36

1. Locus Ceruleus

Front 37

Norepi receptors(3)

Back 37

1. Alpha 1 - vasoC

3. Beta 1 - HR and force
4. Beta 2 - BronchoD

Front 38

Norepi clinical(2)

Back 38

1. Depression
2. Bipolar 2

Front 39

Serotonin Characteristics(3)

Back 39

1. Indolamine
3. Sleep/wake, pain, apetite, mood

Front 40

Serotonin location

Back 40

Raphe nuclei

Front 41

Serotonin Clinical general (2)

Back 41

1. Depression
2. Migraines

now that serotonin's gone I have headaches

Front 42

Histamine Characteristics(3)

Back 42

1. Biogenic Amine
2. Excitatory = Arousal and attention in brain
Sgt Histamine bring the brain to attention!

Front 43

Opiate Peptides(2 types)

Back 43

1. Beta endorphin
2. Enkephalin