Nerve/Synapse - Lecture 6 Flashcards
what type of ion channel not found on dendrites
voltage-gated ion channels
why neurons evolved to have many EPSPs necessary to fire an AP
to be able to process information received from multiple neurons (different inputs)
why fact that many EPSPs necessary for neuron to fire AP is advantageous for sensations/sensory abilities
neurons can unify different perceptions (ex auditory and visual)
Structure of NMDA receptor and what activates them
Same structure as AMPA receptors and activated by glutamate
First key property of NMDA receptors
At resting memb. potential, pore is blocked by Mg2+ and depolarization of memb. expels Mg 2+ , enabling pore to conduct
Second key property of NMDA receptors
Open pore is highly permeable to Ca 2+ as well as monovalent cations
What is necessary for NMDA to release its Mg 2+ and become permeable to calcium
Glutamate must bind when memb. is already depolarized (-50 mV ex.)
Concentration of calcium outside cell vs inside
out : 0.5 mmol/L in : very little
calcium property for cells/what it serves for
signaling molecule/messenger
T/F : if memb not depolarized, glutamate wont bind NMDA
F : will bind it but NMDA wont open
T/F : if memb. depolarized, glutamate only binds NMDA
F : always binds both but will OPEN NMDA if memb. depolarized
NMDA ‘detects’ what 2 things
1) That glutamate is released (synaptic cleft)
2) Cell is already depolarized
2 other a.a that bind NMDA
glycine and D-serine
What is synaptic plasticity
Process involving NMDA receptors by which highly ACTIVE excitatory synapses become stronger (STRONGER = LARGER EPSPs)
What is LTP
long-term potentiation -> model of synaptic plasticity (synaptic plasticity that can be shown experimentally)
3 steps in experiment for LTP
- Control = 1 AP and measure little EPSP
- Induction = Burst of APs and measure higher depolarization
- LTP = 1 AP and measure higher EPSP
Proportion of neurons using glutamate
3/4 of neurons
Phenomenon name for glutamate toxicity and what receptors it involves
Excitotoxicity . Involves calcium flux through NMDA receptors
Steps of excitotoxicity
1) Lots of glutamate released near neuron
2) AMPA and NMDA receptors hugely activated all over neuron
3) High concentration of calcium in neuron
4) In any cell, conc. of calcium stays high and is known to be bad so cell commits suicide.
2 diseases situations that can lead to excitotoxciity
1) Severe epileptic seizure - lot of glutamate released
2) Stroke : neurons die from not getting oxygen and release all their glutamate to nearby regions
During induction step of long-term potentiation, which ions enter cell/why
burst of APs = more and more glutamate released so sodium enters cell (AMPA) and then other glutamate released will bind to NMDA and calcium will enter (because of depolarization)
LTP range of time it could work
Can work for days
what process is related to LTP and how
Memorization because involves synapses getting stronger in a process that ressembles LTP experiment
What is the substance responsible for LTP / that LTP couldn’t happen without
calcium
Why calcium makes synapse stronger
biochemical events in the cell that make it produce more AMPA receptors
excitotoxicity can contribute/cause to what 2 diseases
Stroke and in some neurodegenerative diseases
Main inhibitory neurotransmitter in the brain and abreviation + its receptor’s name
GABA : gamma-aminobutyric acid
Receptor is GABAa receptor
What type of receptor GABAa is and what it is permeable to
ionotropic receptor. becomes permeable to chloride
How many GABA molecules can bind GABAa receptor and consequence
2 (on image) -> hyperpolarization of membrane
Concentration of chloride in/out neurons
Generally, concentration of Cl- higher outside of neuron
What does it mean when a substance ‘potentiates’ a particular receptor. What does it do exactly
when it binds it, increases its effect by making it more receptive to its original neurotransmitter/substance
3 types of drugs that potentiate GABAa receptor + what it means and what it does
benzodiazepines, barbiturates and ethanol : make GABAa more receptive to GABA when they bind it and the IPSP from one GABA receptor is higher
where excitatory inputs (EPSP) are generally located
on dendritic spines
where inhibitory inpus (IPSP) are generally located and why
on or near the cell soma because inhibitory effect is maximal there
What is synaptic integration
Constant decision of firing APs or not by a neuron based on sum of EPSPs and IPSPs reaching the initial segment
What happens to EPSP as it spreads to the initial segment and why
Dissipates because dendrites don’t have voltage-gated ion (sodium) channels
What particularities of the APs are determined by the sum/balance of EPSPs/IPSPs and why
pattern and frequency of APs because they can be different depending on timing and synchronicity of EPSPs/IPSPs
What are metabotropic receptors
Neurotransmitter receptors that are not ionotropic (no ion channel) and that change biochemical activities/properties in the cell
other name for metabotropic receptors
G-protein coupled receptors (GPCRs)
Different receptors found on glutamate synapses (3)
Ionotropic receptors (1.AMPA and 2.NMDA) and metabotropic glutamate receptors (3.mGluR’s)
Name of the chemical signal that mGluRs send in postsynaptic neuron and what region is it sent into
Second messenger. Postsynaptic spine
What happens to mGluRs for them to initiate a sequence of biochemical events in the cell
When are bound by glutamate, they change their shape from an inactive shape to an active shape
What second messengers do (and 3 exemples)
Activate a range of cellular proteins (ex. Ion channels, Protein kinases, Transcription factors)
How second messengers can act on ion channels
Open/activate a closed ion channel
How second messengers can act on protein kinases
Activate them so they can phosphorylate ion channels or other enzymes
How second messengers can act on transcription factors
Activate them so they can regulate (probably enhance) gene expression
2 things synapse does (short-term vs long-term)
- Short-term : Change electrical properties of the membrane/cell
- Long-term : Change biochemical properties inside the cell (which can last from seconds to weeks …)
Ionotropic receptors activated by glutamate and GABA (respectively)
Glutamate : AMPA, NMDA (binds but activates it if cell is depolarized)
GABA : GABA A receptors
Metabotropic receptors activated by glutamate and GABA (respectively)
Glutamate : mGluRs
GABA : GABA B receptors
Neuromodulator what it is and what it’s involved in
Type of neurotransmitter that interact mainly or only with metabotropic receptors.
Involved in modulating global neutral states, influencing alertness, attention and mood. Not involved in fast flow of neuronal information.
Exemples of neuromodulators (4)
Dopamine, Serotonin, Norepinephrine, Neuropeptides such as endorphins
Synapses exist where there are _______ neurotransmitters for metabotropic that are activated.
only
Each neuromodulator has its specific _________
receptor
Where are neurons (where do they originate) that release neuromodulators and where do their axons go
In small brainstem and midbrain nuclei. Their axons spread diffusely throughout the brain
How neurons for neuromodulators (their cell bodies) are organized
In clusters
Dopamine neurons, in what regions of the brain they originate
Substantia nigra (SN) and Ventral tegmental area (VTA) in the midbrain
Norepinephrine neurons how many and where they start
20 000, in brain stem
What neuromodulators (neuromodulator transmission) are affected by antidepressants + ex. of antidepressant
ex. Prozac. Serotonergic transmission (serotonine)
what neuromodulators (neuromodulator transmission) are affected by amphetamines, cocaine and other STIMULANTS
dopamine, norepinephrine (transmission)
good mood has been associated with _____ levels of _________ (which neuromodulator)
high levels of serotonine
addiction has been related to _______ levels of _______ (which neuromodulator)
high levels of dopamine
Exemples of drugs (2) that can cause addiction (affect dopamine transmission)
Nicotine, Cocaine
