Chapter 4/5 Flashcards
What did human’s attribute epileptic seizures to in the past?
mystical or demonic causes
What did Galviani discover about electrical stimulation
Hypothesized that there was some type of electrical impulse that moved muscles. proven through electrical stimulation moving legs of dead frogs
what is a synapse
The connection between the axon terminal of a presynaptic neuron and the dendrite of a postsynaptic neuron
Cations
positively charged ions
anions
negatively charged ions
what are the two gradients present which create electrical charge in neurons?
concentration gradient and voltage gradient
concentration gradient
movement from high to low concentration of an ion
voltage gradient
movement from high concentration of cations to low, in order to balance charge
why is the gradient highest on the membrane?
because only one ion can pass through and will diffuse down gradient, but is still attracted to opposite voltage so it was stick near membrane where it is close to opposite charged ion
where is the voltage gradient the greatest?
close to the membrane
which ion passes through an ungated channel into the cell
potassium
which ion is controlled by a gated channel to enter cell
sodium
what is the resting potential of a cell
-70 mV relative to the outside
at rest, is sodium or potassium concentration higher inside the cell?
potassium
what pump helps maintain the resting potential of a cell? how?
the sodium-potassium pump, by pumping 3 sodium out for every 2 potassium in, creating a net negative exchange
inhibitory signals
reduce the chance of an action potential
excitatory signal
increases the chance of an action potential
hyperpolarization
increasingly negative charge inside the cell via K+ exit and Cl- entrance
which makes a cell more stable: hyperpolarization or depolarization
hyperpolarization
depolarization
more positively charged due to influx of Na+
which gated channels open to cause an action potential?
Na+ voltage gated channels (floods into cell)
which gated channels open to end the action potential?
K+ gated channels (floods out of cell)
refractory period
transitory hyperpolarization which prevents the AP from going backwards or repeated AP’s
what part of the neuron does the AP begin at?
axon hillock
T/F the size of the action potential is maintained throughout the entire length of the axon
true
T/F the size of the action potential is dependent on the number of excitatory signals received
F - all or none at same size every time
saltatory conduction
for neurons with myelin - electrical signal jumps from gap to gap
EPSP
excitatory postsynaptic potential - encourages response
IPSP
inhibitory postsynaptic potential - decreases chance of response
temporal summation
sum of signals close together - ex: two EPSP signal at same time produce greater effect
spatial summation
sum of signals close to each other on the membrane - ex: two EPSPs beside each other will produce greater effect than two on opposite sides, which would not add together
what area of the neuron to IPSPs and EPSPs have the greatest influence on
near the axon hillock
where is the origin point of the action potential
axon hillock
deep brain stimulation
electrodes implanted in the brain to facilitate behaviour - used for parkinsons and brain disorders
who discovered the first NT
Otto Loewi
how was it proven that chemical signaling was also involved
through stimulation of the vagus nerve on frog hearts, then transfer of the liquid alone causing similar effects
Which of the following is not a criteria for being a NT
1. chemical is created/present inside neuron
2. chemical produces response on target cell
3. chemical removal mechanism is present
4. can be artificially reproduce, with varied effects
4 - effect must be the same every time
what triggers the release of synaptic vesicles
electrical signals
where are NT produced in the cell?
in the cell body and transported or in the axon terminal
storage granule
holds multiple synaptic vesicles
synaptic vesicles
hold NT
what helps transport vesicles throughout the cell
microtubules
what are the 4 steps of neurotransmission
- synthesis of NT
- release of NT into synapse
- receptor action via binding on postsynaptic membrane
- inactivation of NT
what ion triggers the release of NT into the synapse
Ca+
autoreceptors
receptors of the axon terminal of presynaptic neuron that monitor NT levels to stop release
what are the 2 ways to inactivate NT effect
reuptake into presynaptic neuron via channels or break down in synapse via enzymes
agonist drug
enhances the effect of the NT
antagonist drug
restricts/prevents the effect of the NT
what are the various ways that agonist drugs work?
increasing NT production or release, stimulating receptors or blocking inactivation
what are the various ways antagonist drugs work?
blocking NT release or receptors
Ionotropic receptors
receptors on postsynaptic cell that cause an immediate change in electrical charge of receiving cell
how do ionotropic receptors work?
NT binds to receptor, which causes pore to open and ions to enter/leave the cell
metabotropic receptors
receptors on the postsynaptic cell which have a slower, longer lasting effect on cell
T/F Ionotropic, but not metabotropic receptors, have pores
T
how do metabotropic receptors elicit a response
NT binds to receptor, which activates a G-protein. the G protein either elicits response directly on a channel or acts as a second messenger by attaching to an enzyme and activating other pathways
What unit of the G-protein detaches?
alpha subunit
If the G-protein enzyme are the second messengers, what is the first?
NT
which type of receptors can travel deep into the nucleus of a cell and activate transcription/ translation?
metabotropic through secondary messengers
what are the plastic changes that can occur from secondary messengers
structural changes from transcription and translation which strengthen the signals between the two neurons
what are some examples of structural changes in neurons?
increased axonal transport, vesicles, terminal area
change in cleft size and density of vesicle contact zones
neurotransmitter activating systems
a series of connected neural pathways where one specific NT dominates
where are NTAS located?
cell bodies originate in brainstem or midbrain, axons extend throughout brain
what are the four NTAS
Cholinergic (ACh)
dopaminergic
noradrenergic
serotonergic
What NT is involved in memory and learning through mediation of attention
cholinergic NTAS
what area of the brain is cholinergic
midbrain and basal forebrain
which NT synapses directly against mucle
ACh
what system slows the HR
cholinergic
what are the two dopaminergic pathways
mesolimbic and nigrostriatal
Where the the “reward center of the brain”
nucleus accumbens (forebrain), the mesolimbic pathway of the dopaminergic system
dysregulation of what pathway leads to addictive behaviour
mesolimbic
what dopaminergic pathway is involved in mediating moods and intentional actions
nigrostriatal pathway in the substantia nigra
which system is damaged in parkinson’s
nigrostriatal pathway of the dopaminergic system
which NTAS increases energy and heart rate (arousal)
noradrenergic
what NTAS control moods/emotions and appetite/digestion
Serotonergic
what happens if levels of serotonin are too high
hallucinations
what are the two amino acid NTs
GABA and glutamate
GABA
An inhibitory AANT the decreases the response of receiving cell and slow the system
Glutamate
and excitatory AANT that increases the response of the receiving cell and is involved in almost every system in the body
what is the most numerous NT in the body?
Glutamate
endorphins
Peptide NT which relieves pain and increases pleasure
what happens when you go into withdrawal from drugs that engage endorphins?
increased pain and negative feelings
