Neurophys 3 Ex 1

Front 1

Electrical synapse occur at

Back 1

gap junctions for instance

Front 2

Type of synapses Chemical synapses

Back 2

Axo-axonic
Axo-dendritic
Axo-somatic

Front 3

Glia communicates
through

Back 3

gap junctions

Front 4

Neurotransmitter transport is bidirectional, but faster in the

Back 4

orthograde direction
(away from the cell body)

Front 5

Actions of Neurotransmitters

Back 5

Rapid activation of ion channels
• Slow, sustained activation or inhibition
of ion channels
• Modulation of ion channels (2nd
messengers)
• Activation or inhibition of gene
transcription
• Modification of morphology or synapse
(These are order from fastest to slowest)

Front 6

What makes a nt? Not only the fact of being present in
the neuron..for instance glutamate and GABA are in
neurons but also throughout the body..so how to prove
that they are released on cue from neuron

Back 6

Dye,
antibody etc..but it is no easy to show that they are
there..but it is easier to screen for enzymes that make
the neurotransmitters, usually antibodies use to screen
for these enzymes but there's also protein synthesis on
dendrites..for what? Receptors. These can be detected
by pet

Front 7

Estrogen has estrogen membrane bound receptors
allowing rapid enter and action through

Back 7

a gprotein

Front 8

Endocannabanoids ( resemble marihuana receptors)
A knock out of cb1 receptor can't sense

Back 8

marihuana like
substance..mouse become more sensitive to pain

Front 9

A knockout of FAAH which breaks anandamide the
mouse becomes more resistant to

Back 9

pain

Front 10

Endocannabanoids

Back 10

cb1
FAAH
Rimonabant

Front 11

Rimonabant is a drug that reduce appetite and
smoking..but many people became suicidal or
depressed..so this led to the conclusion that perhaps

Back 11

our natural endocannabanoids have an influence on our
mood

Front 12

90% of our neurotransmission via

Back 12

glutamate (
excitatory) and GABA (INHIBITORY)

Front 13

Ach about 10%function can be inhibitory of excitatory
depending on

Back 13

the receptor that binds...ach is
concentrated on basal forebrain

Front 14

Neroepinephrine is about 1% or less...this is located in
brain stem..related to

Back 14

attention, mood and reward
system.

Front 15

Dopamine on caudate. Important for

Back 15

movement and
reward system

Front 16

Serotonoin in brain stem..involved in

Back 16

mood and appetite

Front 17

circadian rhythm

Back 17

Melatonin

Front 18

Certain receptors of Adenosine involved in

Back 18

adenosine
involved in migration and growth of dendritic spines

Front 19

Nitric oxide lots in cerebellum and hyppocampus and
Cortex and is

Back 19

diffusable which is not common

Front 20

There is coexistence of peptides and small NTS in a
neuron, they can be differentiated by

Back 20

the train of stimuli
for which they released..under slow stimulus only one
NTS may be released after increasing the stimulus
more than one type of NTS may be released

Front 21

Glutamate synthesis

Back 21

Glutamate is released, glutamate is up taken up.
Glutamate is broken down into glutamine and then
transported itno the glutamate containing cell.
Glutamase acts on glutamine and glutamate is made
again. Limiting factor is the uptake of glutamate which
will determine its availability in the cleft as well as the
amount that is in the terminal

Front 22

GABA synthesis

Back 22

Glutamate is being taken up which is acted
on by glutamine synthetase and makes
glutamine..which in turn is acted on glutamate
decarboxylase go give GABA and then GABA is
released from cell. It is interesting that GABA and
glutamate which antagonize each other use the same
building blocks..this is so because when one gets high in concentration the other one gets regulated

Front 23

Ach comes through pyruvate system..ach is limited by

Back 23

the availability of choline which is low

Front 24

Ach synthesis

Back 24

There choline
receptors on the cholinergic neurons which bring
choline into the neuron when ach is broken down which
is the main source. Also there is dietary choline from
phosphotyl choline (lecitine)

Front 25

Alzheimer's patient
seemed to lack ach..so why not give a supplement?

Back 25

plement..this
wouldnt work because as concentration of acetylcholine
in the cholinergic neuron becomes adequate it inhibits
the choline transport.

Front 26

is cathecholamine substrate depedent?

Back 26

NO. Tyrosine and
phenylalanine is substrate for Catecholamine

Front 27

Dopamine synthesis

Back 27

transporter. Tyrosine hydroxylase gives
dihydroxyne phenylalanine or dopa and they are acted
on dopadecarboxylase to give dopam

Front 28

dopamine. If a neuron is
a dopanergic it won't have dopamine betahydroxylase
because

Back 28

dopamine is converted to neuroepinephrine is
made. If it is an epinephrine containing cell is going to
have phenyl ethylonamine and phenyl ethyl transferase
which converts norepinephrine into epinephrine

Front 29

In Catecholamine synthesis tyrosine is not limited but

Back 29

the Pterin cofactor is limiting

Front 30

limiting. Lots of Catecholamine is
gonna compete for

Back 30

compete for the Pterin cofactor site on tyrosine
hydroxylase and inhibits it...tyrosine hydroxylase is the
enzyme limiting and all Catecholamine synthesis
require tyrosine hyd

Front 31

hydroxylase. As we get more Nerve
activity more cyclic camp and calcium which
phosphorylase tyrosine hydroxylase to inhibit the
enzyme. So negative

Back 31

feedback inhibition by product and
activity of the nerve. Constant nerve activity increases
synthesis of enzymes involved in Catecholamine

Front 32

Serotonin synthesis, tryptophan is the limiting substrate because i

Back 32

is not abundant in our diets

Front 33

is the limiting factor because is
not abundant

Back 33

on our diet. What happens when
tryptophan intake is high? An increase in insulin during
a meal which activates amino acid carriers in the liver,
and many of these carriers take up preferentially
tyrosine and phenylalanine leading to an increase of
tryptophan in our blood stream. Once the blood reaches
the brain it is absorbedati by the amino carriers in the
brain. So more tryptophan gets into

Front 34

Melatonin synthesis requires

Back 34

serotonin. Light regulates its pathway by decreasing the amount of melatonin

Front 35

In nonhuman mammal in the pineal gland melatonin has

Back 35

a tropic effect negative by having less fsh and lsh when dark. When photoperiod grows longer bird testes grow 40 folds because LSH and FSH increase

Front 36

Peptide NTs are regulated at the level of

Back 36

cleavage

Front 37

On glutanergic neurons what kind of transporters present?

Back 37

excitatory AA

Front 38

GABA transaminase and glutamate decarboxylase both
have

Back 38

a pyridoxal cofactor (folate is increased when
there is a lack of this cofactor)

Front 39

if there's hydroxine
overdose, there's convulsion because

Back 39

convulsion because the amount of
GABA is inhibited. Similarly lesser toxic amounts of
hydroxine which inhibit GABA transaminase which
increases GABA leading to neuropathy

Front 40

where does Acetylcholinestarse break down acetylcholine

Back 40

extracellulary