Lecture Three; Cell Communication; Brain Anatomy Flashcards

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1
Q

Whats axodentritic?

A

Pertaining to the synaptic relationship of an axon with a dendrite of another neuron.

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2
Q

what isaxosomatic?

A

referring to a synapse between the axon of one neuron and the cell body of another.

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3
Q

axoaxonic

A

referring to a synapse between the axon of one neuron and the axon of another.

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4
Q

Exocytosis

A

When an action potential arrives vesicles with neurotransmitter (synaptic
vesicles) release their content in the synaptic cleft

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5
Q

What triggers exocytosis?

A

Calcium
Depolarisation of the pre-synaptic membrane leads to the opening of “voltagedependent”
Calcium channels Calcium will flow into the cell

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6
Q

What are the three Fate of vesicles after NT release?

A
  1. kiss and run
  2. merge and recycle
  3. bulk endocytis
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7
Q

What is thebinding site?

A

the location on the surface of a cell or a molecule where other cell fragments or molecules attach to initiate a chemical or physiological action.

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8
Q

What is Excitatory Post-Synaptic Potential

(EPSP)?

A

When the neurotransmitter opens Na+ (sodium)
channels a depolarisation of the postsynaptic
neuron will occur

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9
Q

What is depolarisation?

A

Depolarization is the process or the act by which polarity is eliminated.
Depolarization in a nerve cell occurs when the cell undergoes an electrical change. Most cells are negatively charged relative to their surroundings. This negative internal charge of the cell shifts to a positive through the process of depolarization. Depolarization though occurs for only a brief period of time.
Depolarization is essential because it allows the transmission of electrical signals (impulses) within the cell, and in certain instances, from one cell to another. Depolarization therefore is one mechanism employed by cell to carry on certain physiological functions and also to communicate with another cell.

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10
Q

Hyperpolarisation?

A

any increase in the amount of electrical charge separated by the cell membrane and hence in the strength of the membrane potential. In cardiology this is the process by which an electrical fiber, at the end of phase 3 repolarization, becomes more negative than usual.

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11
Q

repolarisation

A

the reestablishment of polarity, especially the return of a cell’s membrane potential to resting potential after depolarization.

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12
Q

Inhibitory Post-Synaptic Potential

IPSP

A

When the neurotransmitter opens Clchannels
a hyperpolarisation of the postsynaptic
neuron will occur:

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13
Q

What are Metabotropic receptors?

A

Ion channel opened in an indirect way

by small protein in membrane (G protein) or second messenger

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14
Q

Second messengers

A
binding neurotransmitter
2 : leads tot activation G protein
\: α subunit activates enzym
that produces a second
messenger
3
\: the second messenger
opens ion channels
4
\: ions flow in/out the cell
(EPSP of IPSP)
5
\: Second messenger can also
influence other components
of the post-synaptic cell.
6
also! they can change cell function; by turning on/off genes
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15
Q

how is the the NT concentration regulated?

A

Neurotransmitter cleared from
synaptic cleft through diffusion,
re-uptake, or degradation

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16
Q

What is Enzymatic

degradation and which neurotransmitter is associated with it?

A

Only known for the neurotransmitter acetylcholine
(ACh)
The enzyme Acetylcholine-esterase (AChE) in the post-synaptic membrane
splits ACh into Choline and Acetate
Acetylcholine is present, in particular, in synapses on muscle fibers
Myasthenia Gravis: muscle weakness resulting from a deficiency in ACh
receptors
-> Treatment with AChE inhibitors: more ACh to activate remaining receptors

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17
Q

What are autorecptors doing?

A

Autoreceptors regulate the reuptake and release of neurotransmitter by
the neuron.
…they are metabotropic
- Reuptake NT: G proteinen/second messengers activate reuptake transporters
- Reduction NT release: G proteinen/second messengers close Ca2+ channels, reduced
Ca2+ inflow results decreased opening of neurotransmitter vesicles
q Autoreceptoren are generally inhibitory (they reduce the concentration
of neurotransmitter in the synaptic cleft)

18
Q

Define Agonist and Antagonist!

A

Agonist: A substance that acts like another substance and therefore stimulates an action. Agonist is the opposite of antagonist, a substance which interferes with or inhibits the physiological action of another.
“LSD is a serotonin antagonist”

19
Q
Functions of neuromodulaters:
Peptides (Hormones/endogenous opioids)
Lipids (Anandamids, THC: Cannabis)
Nucleosides (Adenosine) 
Gasses (Nitric Oxide)
A

peptides: agression and bonding + pain perception
lipids: mood/ pain perception
nucleosides: control of sleep
gasses: learning/ blood vessel dilation

20
Q

Neurotransmitters vs. Neuromodulators

A

Neurotransmitters are directly involved in contact between neurons, neuromodulators are present in large regions of the brain to sensitise or desensitise complete neural networks.

Neuromodulators bind to receptors of neurons to influence the number of opened ion channels in these neurons. Due to this, many neurons in a network can be either slightly depolarised or slightly hyperpolarised, making the network either more sensitive (in case of depolarisation) or less sensitive (in case of hyperpolarisation) to input.
if many neurons in a network are slightly depolarised, their membrane potential is closer to the threshold of excitation, and therefore it is easier to exit them (you might say that alertness of the network increases).
Conversely, if many neurons in a network are slightly hyperpolarised, their membrane potential is further from the threshold of excitation, and therefore it is more difficult to exit them (you might say that alertness of the network decreases).

21
Q

tryptophan is

A

a precursor processed to serotonine

22
Q

which are the most famous monoamines, how are they called

A

catecholamine: serotonin, dopamin, epinephrine norepinephrine
idolamine

23
Q

Fate of vesicles after NT release

A
  1. Kiss and Run
  2. merge and recycle
  3. bulk endocytosis
24
Q

enzygmatic degradation

A

Only known for the neurotransmitter acetylcholine (ACh)

25
Q

Myasthenia Gravis

A

muscle weakness resulting from a deficiency in ACh receptors
The enzyme Acetylcholine-esterase (AChE) in the post-synaptic membrane splits ACh into Choline and Acetate
Acetylcholine is present, in particular, in synapses on muscle fibers
Treatment with AChE inhibitors: more ACh to activate remaining receptors

26
Q

autoreceptors

A

Autoreceptors regulate the production and release of neurotransmitter by the neuron
they are metabotropic: Reuptake NT: G proteins/second messengers activate reuptake transporters
- Reduction NT release: G proteinen/second messengers close Ca2+ channels, reduced Ca2+ inflow results decreased opening of neurotransmitter vesicles

Autoreceptors are generally inhibitory (they reduce the concentration of neurotransmitter in the synaptic cleft)

27
Q

Effect postsynaptic potentials on postsynaptic neuron

A

spatial integration

EPSPs spread across the neuron through passive conduction
New action potential if sum of all EPSPs results in depolarisation above a threshold
Action potential starts at axon hillock (little hill: highest concentration of Na+ channels

28
Q

In case of EPSP andIPSPs, new action potential only if:

A

EPSP-IPSP=Depolarisation

29
Q

Acetylcholine

A

(learning, memory, dreaming)

30
Q

Monoamines

A

Catecholamines

Indolamines

31
Q

Catecholamines

A

Dopamine (reinforcement, motor)
Norepinephrine (alertness, fight-flight sympathetic nervous system)
Epinephrine (fight-flight sympathic nervous system)

32
Q

indolamine

A

serotonin: mood

melatonin, which regulates the sleep-wake cycle (circadian rhythm

33
Q

Amino acids:

A

Glutamate (excitatory, motor, learning)
Glycine (inhibition [spine], motor)
GABA (inhibitory, motor)

34
Q

What are neuromodulators doing?

A

wander through the brain and sensitize/desensitize complete neural networks (through subthreshold depolarisations or hyperpolarisations)

35
Q

Neuromodulators, Peptides

A

Hormones (excreted by glands: kidneys, pituitary, thyroid, etc -> Vasopressine (agression), Oxytocine (bonding)

Endogenous opioids
β-endorphin, enkephalin en dynorphin (analgesics: pain reduction) –> Morphin from poppy seeds mimics the action of opioids

36
Q

Neuromodulators, Lipids (fats: easily cross the BBB)

A

Anandamide (pain, depression, memory)

TetraHydroCannabinol (THC) = marihuana mimics Anandamide

37
Q

Neuromodulators, Nucleosides

A

part of a DNA base pair bound to sugar
Adenosine (opens K+ channels and inhibits CNS to facilitate sleep)
Adenosine accumulates during the day
Caffeine blocks adenosine receptors

38
Q

Gasses

A

produced by enzymes in certain neurons

Nitric Oxide produced from the amino acid arginine, in different cell regions, and diffuses through the cell membrane
NO diffuses to other cells and activates a second messenger (cyclic GMP)
NO is involved in dilation of blood vessels and learning
Viagra suppresses the destruction of cyclic GMP

39
Q

drug functions as precursor

A

AGO e.g.L-dopa, by enzymes in theneuron it is transformed easily to dopamine

40
Q

differnce of neuromodulators to eurotransmitters:

A

A neuromodulator can be conceptualized as a neurotransmitter that is not reabsorbed by the pre-synaptic neuron or broken down into a metabolite. Such neuromodulators end up spending a significant amount of time in the cerebrospinal fluid (CSF), influencing (or “modulating”) the activity of several other neurons in the brain. For this reason, some neurotransmitters are also considered to be neuromodulators, such as serotonin and acetylcholine.