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40 Cards in this Set

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Electrical synapse occur at
gap junctions for instance
Type of synapses Chemical synapses
Axo-axonic
Axo-dendritic
Axo-somatic
Glia communicates
through
gap junctions
Neurotransmitter transport is bidirectional, but faster in the
orthograde direction
(away from the cell body)
Actions of Neurotransmitters
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)
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
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
Estrogen has estrogen membrane bound receptors
allowing rapid enter and action through
a gprotein
Endocannabanoids ( resemble marihuana receptors)
A knock out of cb1 receptor can't sense
marihuana like
substance..mouse become more sensitive to pain
A knockout of FAAH which breaks anandamide the
mouse becomes more resistant to
pain
Endocannabanoids
cb1
FAAH
Rimonabant
Rimonabant is a drug that reduce appetite and
smoking..but many people became suicidal or
depressed..so this led to the conclusion that perhaps
our natural endocannabanoids have an influence on our
mood
90% of our neurotransmission via
glutamate (
excitatory) and GABA (INHIBITORY)
Ach about 10%function can be inhibitory of excitatory
depending on
the receptor that binds...ach is
concentrated on basal forebrain
Neroepinephrine is about 1% or less...this is located in
brain stem..related to
attention, mood and reward
system.
Dopamine on caudate. Important for
movement and
reward system
Serotonoin in brain stem..involved in
mood and appetite
circadian rhythm
Melatonin
Certain receptors of Adenosine involved in
adenosine
involved in migration and growth of dendritic spines
Nitric oxide lots in cerebellum and hyppocampus and
Cortex and is
diffusable which is not common
There is coexistence of peptides and small NTS in a
neuron, they can be differentiated by
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
Glutamate synthesis
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
GABA synthesis
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
Ach comes through pyruvate system..ach is limited by
the availability of choline which is low
Ach synthesis
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)
Alzheimer's patient
seemed to lack ach..so why not give a supplement?
plement..this
wouldnt work because as concentration of acetylcholine
in the cholinergic neuron becomes adequate it inhibits
the choline transport.
is cathecholamine substrate depedent?
NO. Tyrosine and
phenylalanine is substrate for Catecholamine
Dopamine synthesis
transporter. Tyrosine hydroxylase gives
dihydroxyne phenylalanine or dopa and they are acted
on dopadecarboxylase to give dopam
dopamine. If a neuron is
a dopanergic it won't have dopamine betahydroxylase
because
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
In Catecholamine synthesis tyrosine is not limited but
the Pterin cofactor is limiting
limiting. Lots of Catecholamine is
gonna compete for
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
hydroxylase. As we get more Nerve
activity more cyclic camp and calcium which
phosphorylase tyrosine hydroxylase to inhibit the
enzyme. So negative
feedback inhibition by product and
activity of the nerve. Constant nerve activity increases
synthesis of enzymes involved in Catecholamine
Serotonin synthesis, tryptophan is the limiting substrate because i
is not abundant in our diets
is the limiting factor because is
not abundant
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
Melatonin synthesis requires
serotonin. Light regulates its pathway by decreasing the amount of melatonin
In nonhuman mammal in the pineal gland melatonin has
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
Peptide NTs are regulated at the level of
cleavage
On glutanergic neurons what kind of transporters present?
excitatory AA
GABA transaminase and glutamate decarboxylase both
have
a pyridoxal cofactor (folate is increased when
there is a lack of this cofactor)
if there's hydroxine
overdose, there's convulsion because
convulsion because the amount of
GABA is inhibited. Similarly lesser toxic amounts of
hydroxine which inhibit GABA transaminase which
increases GABA leading to neuropathy
where does Acetylcholinestarse break down acetylcholine
extracellulary