Exam 4 | Nervous system pt. 2 Flashcards

1
Q

What happens at the synaptic cleft?

A

The depolarization at the synaptic terminal opens voltage-gated Calcium (Ca2+) ion channels.

This Calcium influx triggers the relocation and fusion of vesicles with the cell membrane at the synaptic terminal.

Once these vesicles fuse with the cell membrane, they release their contents (neurotransmitters) into the synaptic cleft. The neurotransmitters will diffuse across the synaptic cleft to eventually bind to their corresponding receptors on the postsynaptic cell, triggering the opening of ligand-gated ion channels to cause an electrical change in the postsynaptic cell.

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2
Q

What type of cells are the presynaptic and postsynaptic cells?

A

The presynaptic cell is always a neuron, the postsynaptic cell could be a neuron or another electrically-excitable cell (most often a muscle cell).

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3
Q

What’s a presynaptic cell?

A

The presynaptic cell/ neuron is the cell that releases neurotransmitters into a synapse, essentially “initiating” the line of communication in the circuit.

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4
Q

What’s a postsynaptic cell?

A

The postsynaptic cell/ neuron is the cell that binds neurotransmitters once they’ve diffused across the synaptic cleft, essentially “receiving” the line of communication in the circuit.

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5
Q

What’s the role of synaptic vesicles?

A

When enough Calcium (Ca2+) enters the synaptic terminal, it binds to special vesicle docking proteins which trigger the movement of vesicles to the edge of the synaptic terminal. At this point, the proteins undergo a conformational (shape) change to essentially “force” the vesicles to fuse with the cell membrane, which causes them to release their contents (neurotransmitters) into the synaptic cleft.

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6
Q

What’s Dale’s principle/law?

A

It’s a set of “rules” that one can use to determine whether a chemical is potentially a neurotransmitter

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7
Q

What are the rules for Dale’s Principle/law?

A

1) Be produced/ be present in the presynaptic cell

2) Must be released upon depolarization of the presynaptic cell (and this release must be Calcium-dependent)

3) Specific receptors for the chemical must be present on the postsynaptic cell

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8
Q

What are neuromodulators?

A

These are chemicals that signal more slowly and diffuse across further distances

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9
Q

What are the 2 most common neurotransmitters?

A

Excitatory and Inhibitory

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10
Q

What are excitatory neurotransmitters?

A

Those that promote signal transmission between neurons; typically cause depolarization in the postsynaptic cell

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11
Q

What’s an example of an excitatory neurotransmitter?

A

Glutamate which is found in the entire CNS

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12
Q

What are inhibitory neurotransmitters?

A

Those that prevent signal transmission between neurons; typically cause hyperpolarization in the postsynaptic cell

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13
Q

What are some examples of inhibitory neurotransmitters?

A

GABA (found in the brain) and Glycine (found in the spinal cord)

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14
Q

What’s synaptic plasticity?

A

It describes the importance of practicing skills and continuing to challenge yourself cognitively; Professor Marian Diamond at USC coined the term “use it or lose it”

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15
Q

What’s Hebbian plasticity?

A

It is the theoretical means by which individual synapses can be strengthened after prolonged stimulation (LTP, long-term potentiation), and the opposite phenomenon would occur as a result of prolonged lack of stimulation (LTD, long-term depression). This takes place over several hours.

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16
Q

Why is long-term potentiation so important?

A

LTP is considered to be one of the primary mechanisms for learning across the cerebral cortex in humans and other animals.

17
Q

What 2 receptors are important for LTP?

A

AMPA receptors and NMDA receptors

18
Q

Which receptor is the most important for LTP to occur?

A

NMDA

19
Q

What are AMPA receptors?

A

These receptors are ionotropic ligand-gated glutamate receptors that bind glutamate and allow cations (specifically, Sodium and Calcium) to flow into the postsynaptic neuron to trigger depolarization.

20
Q

What are NMDA receptors?

A

These receptors are ionotropic ligand-gated glutamate receptors that bind glutamate and also flux cations into the postsynaptic neuron to trigger depolarization. It contains a Magnesium (Mg2+) ion blocking the pore of the channel, and this Magnesium ion is only removed when the postsynaptic membrane potential reaches a specific threshold. Thus, NMDA receptors are not the first glutamate receptors to become activated during synaptic transmission at a glutamatergic synapse, but they are considered necessary for LTP to occur.

21
Q

What’s short-term plasticity?

A

In between occurrences of LTP and LTD, there are refractory periods where in neurons need to take time to refresh their synaptic vesicles in order to allow further synaptic transmission

22
Q

What’s short-term facilitation?

A

Short-term Facilitation occurs when synaptic vesicles are at their greatest concentration; pre-synaptic & strengthens synapses (leads to LTP)

23
Q

What’s short-term depression?

A

Short-term Depression occurs when synaptic vesicles are at their lowest concentration; presynaptic & causes synapse to weaken (leads to LTD)

24
Q

What’s short-term saturation?

A

Occurs when the maximum number of ionotropic glutamate receptors (NMDA and AMPA) are binding glutamate, resulting in the maximum level of depolarization of the postsynaptic neuron; post-synaptic & leads to strengthening of synapse (LTP)

25
Q

What’s short-term desensitization?

A

occurs when there is reduced expression of ionotropic glutamate receptors (NMDA and AMPA), resulting in reduced depolarization of the postsynaptic neuron; post-synaptic & leads to weakening of synapse (LTD)

26
Q

What’s homeostatic plasticity?

A

It’s by definition a negative feedback loop, in that the long-term “goal” of a synapse is to maintain a balance between high firing rates (activity), low firing rates (activity) and the baseline firing rates (basal activity).

27
Q

How does sleep play a role in homeostatic plasticity?

A

Many neurophysiologists hypothesize that homeostatic plasticity might be the “key” to memory consolidation during sleep; during this period, the synapses that were most active while you were studying during the day become less active, allowing for reduced energy consumption on the part of those cells and over time, reduced expression of AMPA (and to some extent, NMDA) receptors on the postsynaptic neurons. This allows the neuron to be “refreshed” and ready for increased activity during the day

28
Q

What are some positive influences of neuroplasticity?

A

Mental stimulation (“use it or lose it”!), Physical activity, Social interaction, and Cognitive remediation (primarily sleep)