Chapter 9 Study Questions (Part 2) Flashcards
what is a current hypothesis to explain why treating post traumatic stress disorders is so difficult?
basically: harder to forget and easier to recall.
trauma often involves stimuli
increased strength and increased variety of stimuli lead to increased burned in memory
any one of the stimuli can bring back traumatic memories, you don’t need all of them
how does the limbic system figure into the difficulty in treating PTSD?
hippocampus: memories
amygdala: fear
olfactory: smell
what is the difference between reflexive and declarative memory? can you give an example of each please?
R:
doesn’t require conscious process, can’t describe the steps
ex. muscle memory
D:
facts, events, inference, comparisons, evaluation. requires conscious process and can be reported verbally (describe the steps)
ex. how you arrive to class today
explain the knee jerk reflex
hitting the tendon activates mechanoreceptors
when mechanoreceptors in the quad muscle are activated, sodium rushes in
when sodium rushes in, the afferent neuron is depolarized
afferent neuron splits three ways: extensor motor neuron to signal to muscle, neurons that communicate with the brain, and inhibitory interneuron to inhibit flexing in the hamstring
quad is told to contract, hamstring is inhibited from flexing
the knee jerk reflex is an example of what type of reaction?
spontaneous/subconscious
in physiological terms, explain the difference between a “knee jerk reflex” and the expression a “knee jerk response”
knee jerk reflex: rapid physical response to a physical stimulus: we don’t think about it
knee jerk response: an automatic response that one gives without thinking
what is synaptic plasticity?
how easy it is for a presynaptic neuron to cause a change in a postsynaptic neuron.
change in the strength (ability to trigger an AP) of a synapse
what is a primary cause of temporary synaptic depression ?
enough time between APs for:
calcium from 1st AP to be removed from presynaptic neuron
not enough time between APs for:
restocking of vesicles we lost through exocytosis @ axon terminal, so the number to be released is less, and therefore the physical response is less
explain how the glutamate receptors AMPA and NMDA are involved in a long term potentiation
due to an actual stimulus occuring, presynaptic neuron releases glutamate to AMPA and NMDA
AMPA lets sodium in
NMDA lets Mg, Na, Ca
NMDA undergoes a conformational change, and closes
increased glutamate = increased sodium released = increased membrane potential strength
increased Na inside keeps NMDA open by repelling Mg and Ca
increased calcium –> kinase phosphorylates AMPA
phosphorylated AMPA allows more Na to enter, and activates gene transcription for AMPA receptor
more receptors means it’s easier to get in
when it’s easier to get in, it’s easier to stimulate and respond to different stimuli
how does the involvement of glutamate receptors AMPA and NMDA in long term potentiation contribute to the formation of long term memories?
due to an actual stimulus occuring, presynaptic neuron releases glutamate to AMPA and NMDA
AMPA lets sodium in
NMDA lets Mg, Na, Ca
NMDA undergoes a conformational change, and closes
increased glutamate = increased sodium released = increased membrane potential strength
increased Na inside keeps NMDA open by repelling Mg and Ca
increased calcium –> kinase phosphorylates AMPA
phosphorylated AMPA allows more Na to enter, and activates gene transcription for AMPA receptor
more receptors means it’s easier to get in
when it’s easier to get in, it’s easier to stimulate and respond to different stimuli
what is a primary cause of temporary synaptic facilitation ?
not enough time between APs to restock vesicles, or remove calcium. so, calcium sums with calcium from previous action potentials.
increased calcium = increased calmodulin –> increased PKA = increased vesicle release, larger % of the vesicles are released.
in other words, the activity of the calcium pathway is increased.
what is synaptic depression?
decrease in synaptic plasticity
what is synaptic facilitation?
increase in synaptic plasticity
what is the definition of long term potentiation?
membrane potential changing on the long term
