Basic Neurotransmission & Neuroendocrinology Flashcards
senescence
inorganisms: gradual deterioration of function
in cells: cessation of cell division
inhibitory interneurons
release GABA
absence increases risk for seizure
are more vulnerable to cell death
lost in AD
glutamate
excitatory
amino-acid derived
synthesised from glutamine
in glial cells
abundant in brain
neuromodulatory
iono- and metabotropic
doesn’t cross BBB
GABA
inhibitory
amino-acid derived
made from glutamate
only expressed in interneurons
iono- and metabotropic
systems affected by GABA
noradrenalin
dopamine
serotonin
anticonvulsant
what makes a neuron?
speed
-> giving the ability to react, not only adapt
defining properties of neurotransmitters
- synthesised in neuron
- released in synaptic cleft
- binds to post-synaptic membrane
- removed / degraded from synaptic cleft
ways of intracellular messaging
- ligand
- G protein
- kinase
- nuclear receptors
-> only ligand and G protein are high speed
kinase-linked receptors
kinase = enzyme transferring phosphate donating molecules to substrate
-> phosphorylating
affect gene transcription
nuclear receptors
within nucleus
bind to DNA
act as transcription factor
e. g. steroids, thryroid hormones, cholesterol, vitamins
co-packing
co-release of two neurotransmitters
could even be excitatory + inhibitory
glutamate transporters
VGLUT 1, 2 and 3
in neurons
EAAT 1 & 2 = excitatory amino acid transporter
in dendrites and axon terminals
glutamate receptors
all ionotropic
AMPA
NMDA
kainite
AMPA
glutamate receptor
the fastest
only ligand activated
NMDA
glutamate receptor
slower
ligand activated
voltage + ligand activated
pentameric structure
five proteins
lipophilic loops inside
another loop forms channel
subunits denoted by Greek letters
negatively charged to attract positive ions
receptor sides
receptor side, where ligand attaches
modulatory side
artificial GABA ligands
ethanol
benzodiazepines
GABA receptor pentamer
two alpa
two beta
one gamma subunit
each subunit has variations
thereby hundreds possible combinations
modes of modulation
phasic: acute, by neurotransmitter release
tonic: chronic, background threshold neurotransmitter
caused by spillover / incomplete cleanup
GABA’s main purpose
increasing membrane permeability to chloride and ions
tonic activation function
increasing cells’ conductance
reducing probability of ESPS
receptors for phasic inhibition
gamma 2
alpha 1, 2 and 3
receptors for tonic inhibition
alpha 4, 5 and 6
LTP cascade
glutamate binds to AMPA and NMDA
consolidation
morphogenesis of spines
by actin polymerisation
-> number of AMPA receptors increases
LTP maintenance stabilises spines
by stabilising actin filaments
trisynaptic circuit
- dentate gyrus
- CA3
- CA1
dentate gyrus cells
granule cells
mossy fibers
CA3 cells
pyramidal cells
CA1 cells
pyramidal cells
Schaffer collateral pathway
connecting CA3 and CA1
window of plasticity in neurons
around four days
until then everything is excitable
immature cells
GABA is excitatory in these neurons
have lower resting potential
large NKCC1
small KCC2
mature cells
GABA is inhibitory
small NKCC1
large KCC2