Bio261 Lecture 6 Q's- Synapses

Front 1

What are the only two types of tissues that are considered to have excitable membranes?

Back 1

Nerve and muscle cells.

Front 2

What experiment did Otto Loewi do and what did it demonstrate?

Back 2

Stimulated the vagus nerve of a frog heart… it slowed…. Then he took some of the saline that perfused that heart, and put it on another frog heart, and it slowed, too. This demonstrated that the signals from the neurons were being transmitted by chemicals that are released from the neuron.

Front 3

What is a synapse?

Back 3

The gap between two cells into which the signaling cell releases chemicals to signal the second cell.

Front 4

Where are they found?

Back 4

Between two neurons, or a neuron and its target cell, such as a muscle cell.

Front 5

Is synaptic conduction considered to be an electrical or chemical event?

Back 5

Chemical.

Front 6

Can a single neuron have both a presynaptic and a postsynaptic membrane?

Back 6

Yes, almost all do.

Front 7

Where are presynaptic and a postsynaptic membranes found?

Back 7

The dendrites or cell body is considered to be postsynaptic, because it is receiving information… the axon terminal (or bouton) is considered presynaptic as it will transmit info across the synapse.

Front 8

Where are synaptic vesicles found?

Back 8

Within presynaptic axon terminal (or boutons).

Front 9

What do synaptic vesicles contain?

Back 9

Neurotransmitters.

Front 10

What triggers the fusion of synaptic vesicles with the membrane and the consequent release of its contents?

Back 10

The influx of Ca++ through voltage-gated Ca++ channels that are opened when the AP's reach the axon terminal.

Front 11

When neurotransmitter (NT) binds to its receptor on the postsynaptic membrane what type of change occurs in the postsynaptic cell?

Back 11

Ion channels open.

Front 12

Is the change localized to the area of the receptor or does it spread?

Back 12

It spreads away; the stronger the stimulus, the longer the channel is open and the farther away it spreads.

Front 13

At what location on a nerve cell are the neurotransmitter’s receptors found?

Back 13

Dendrites or cell body.

Front 14

Does a neuron have more than one synapse?

Back 14

Yes, there are generally many, many synapses.

Front 15

Can the binding of NT to its receptor cause a postsynaptic neuron to be closer to the threshold membrane potential?

Back 15

Yes… this is considered excitatory.

Front 16

Can the binding of NT to its receptor cause a postsynaptic neuron to be farther from the threshold membrane potential?

Back 16

Yes… this is considered inhibitory.

Front 17

What type of ion permeability change could depolarize a membrane?

Back 17

Positive ions move into the cells like, sodium (Na+) and calcium (Ca++).

Front 18

What type of ion permeability change could hyperpolarize a membrane?

Back 18

Negative ions moving into cells like chloride (Cl-). Or movement of K+ out of the cell.

Front 19

Can a brief change in a cell’s membrane potential be used as a communication signal from one cell to another?

Back 19

Yes.

Front 20

Is there more than one type of NT?

Back 20

Yes... i.e. NE, ACh, etc.

Front 21

Is it possible to have more than one type of receptor for a single type of NT?

Back 21

Yes….i.e. ACh has two types of
receptors, nicotinic and muscarinic. (Although a single neuron will ONLY produce one type of receptor.)

Front 22

Can a neuron have more than one active synapse at the same time?

Back 22

Definitely, and most of the time it does.

Front 23

To what does summation refer?

Back 23

The ability of EPSP's and/or IPSP's to add together.

Front 24

How can summation increase the possibility of a neuron reaching threshold?

Back 24

The more excitatory signals coming in over a short period of time, the closer the membrane gets to threshold.

Front 25

Does a graded potential have a threshold?

Back 25

No.

Front 26

What causes a graded potential?

Back 26

The opening of ion channels in the cell body at the synapse.

Front 27

Does a graded potential have a refractory period? Why?

Back 27

No. Because the channels can remain open as long as the chemicals (NT’s) are around. This allows the info, both excitatory and inhibitory, to be continuously processed and added together as needed.

Front 28

Does a refractory period prevent summation?

Back 28

Yes, it would.

Front 29

How does a synaptic transmission cease?

Back 29

First, the presynaptic neuron stops firing (no more AP's)… also the neurotransmitter in the cleft is quickly broken down by enzymes, either in the synapse itself or in the presynaptic neuron (and sometimes the postsynaptic neuron).

Front 30

How is NT removed from the synaptic cleft?

Back 30

Re-uptake or degredation .

Front 31

Is it important that the NT leave? Why?

Back 31

Yes. To stop the synaptic signal.

Front 32

Do you think if a chemical were found that delayed the re-uptake of NT in the synapse, it could have any medical use?

Back 32

Yes, as an example, in depression, we have found out that patients neurons either aren’t making enough serotonin or it is removed too quickly (producing very short signals), so antidepressant like Zoloft or Paxil block the re-uptake of serotonin – this allows the signal to be longer and/or stronger and alleviates the depression.

Front 33

Do you think if there was a chemical that delayed the re-uptake of NT in synapses of neurons which cause us to experience pleasure, that the chemical could become addictive?

Back 33

Absolutely! As an example, cocaine blocks the re-uptake of the monoamine NT's and is extremely addictive!

Front 34

Which NT pathways does Prozac affect, and what does it do?

Back 34

Serotonin - it acts as an antidepressant.

Front 35

What is a MAO, and what does it do?

Back 35

Monoamine oxidase… MAO is the enzyme that is responsible for degrading (breaking apart) the monoamine NTs once they are re-uptaken into the presynaptic neuron.

Front 36

What are the symptoms and causes of Parkinson’s disorder?

Back 36

A tremor of the resting muscles… not enough dopamine producing neurons in the substantia nigra.

Front 37

Why does treatment of Parkinson’s occasionally cause symptoms of schizophrenia?

Back 37

Parkinson's is treated by trying to increase
dopamine activity, however, dopamine is also used in the mesolimbic dopamine pathway, when the mesolimbic pathway is overactive it is associated with schizophrenia.

Front 38

What is Alzheimer’s disease?

Back 38

The most common cause of senile dementia (including loss of memory)… brain lesions contain lots of deposits of beta-amyloid protein and degenerating nerve fibers, with the most extensive damage to cholinergic neurons (neurons which use ACh) in the hippocampus.

Front 39

Synapse

Back 39

-a functional connection b/n a neuron (presynaptic) & another cell (postsynaptic)

-Chemical synaptic transmission is via the release of neurotransmitters (NT)

Front 40

Synaptic Potentials

Back 40

-

Front 41

Graded potential

Back 41

-

Front 42

EPSP (Excitatory Postsynpatic Potential)

Back 42

-the change in postsynaptci potential occurring at an excitatory synapse ( the receptor channgels to which the NT binds are nonspecific cation channels that permit simultaneous pasage of Na+ & K+ through them)

-A single EPSP only depolarizes the membrane a little bit, not to threshold.

Front 43

IPSP (Inhibitory Postsynaptic Potential

Back 43

-the small hyperpolarization of the postsynaptic cell

Front 44

Neurotransmitter (NT)

Back 44

- specific chemical messenger that is packaged and synthesized by he presynaptic neuron to be received by the postsynaptic neuron

Front 45

Presynaptic neuron

Back 45

-the neuron at the synapse sending the signal to the postsynaptic neuron

Front 46

Postsynaptic neuron

Back 46

-The neuron at the synapse receiving the signal from the presynaptic neuron

Front 47

Synaptic vesicles

Back 47

-Store neurotransmitters

Front 48

Synaptic cleft

Back 48

-The space b/n the presynaptic & postsynaptic neurons

-too wide for the direct spread of current from one cell to another, & therefore prevents APs from electrically passing b/n the neurons

Front 49

Votage-gated channels

Back 49

-open/close in response to changes in membrane potential

-have a 'timer': refractory period

Front 50

ACh (acetylcholine)

Back 50

-Most widely used NT

-at all neuromuscular junctions

-used in brain

-used in ANS: where can be excitatory/inhibitory

Front 51

Nicotinic ACh channel receptors

Back 51

-Ligand-gated channels

-Accept ACh or nicotine

-ALWAYS DEPOLARIZE THE MEMBRANE= EXCITATORY SIGNAL

Front 52

Muscarinic ACh receptors

Back 52

-Ligand-sensitive molecule;not a channel

-Accept ACh or muscarine

-GIVES EXCITATORY/INHIBITORY RESPONSE

-activates G-protein, which activates the cell to make whatever it makes.

Front 53

AChE (acetylcholinesterase)

Back 53

-Inactivates ACh, terminating its action; located in cleft

-found in postsynaptic cell membrane

Front 54

NMJ (Neuromuscular Junction)

Back 54

- connects the nervous system to the muscular system via synapses between efferent nerve fibers andmuscle fibers

-this is where ACh is passed from the presynaptic neuron to he postsynaptic neuron

Front 55

Curare

Back 55

-found in snake venom or black widows

-causes weak muscles and paralysis of diaphragm if extreme doses

-Used in eye & hand surgeries to paralyze muscles.

Front 56

Monoamine NT's

Back 56

-Include serotonin, norepinephrine & dopamine

Front 57

Serotonin

Back 57

-derived from tryptophan

-a monoamine NT

-involved in regulation of mood, behavior, appetite, & cerebral circulation

-associated w/depression; ppl w/depression don't have as much serotonin in their body as there should be.

Front 58

Norepinepherine (NE)

Back 58

-Used in PNS & CNS

-Sypathetic NT in PNS

-in CNS, affects general level of arousal (being awake & alert to things)

-Meth activates all pathway of brain that use NE.

Front 59

Dopamine

Back 59

-Involved in motor control & emotional reward

Front 60

Catecholamines

Back 60

-NE, Dopamine, & Epinephrine

Front 61

MAO (Monoamine Oxidase)

Back 61

-a presynaptic neuron that inhibits serotonin and catecholamines

-destroys/degrades them

Front 62

MAOI (Monoamine Oxidase Inhibitor)

Back 62

-inhibits MAO

Front 63

COMT (catachol-o-methyl Transferase)

Back 63

-inactivates NE and dopamine

Front 64

SSRI (serotonin-specific Reuptake inhibitors)

Back 64

-Antidepressants that prevent serotonin from being taken back into the cell from the junction; prolonging its action.

Front 65

Prozac

Back 65

-an SSRI

-

Front 66

Zoloft

Back 66

-an SSRI

Front 67

Paxil

Back 67

-an SSRI

Front 68

Luvox

Back 68

-an SSRI

Front 69

Parkinson's/Dopamine

Back 69

-Caused by not enough Dopamine in the motor control pathway of Dopamine.

-treated by L Dopa in some cases, which can lead to Schizophrenia

Front 70

Amphetamines

Back 70

-a potent central nervous system stimulant of the phenethylamine class that is used in the treatment of attention deficit hyperactivity disorder and narcolepsy

Front 71

Amino acid NT’s

Back 71

-NTs that are amino acids

-Including Glutamic acid, asparitic acid, glycine, & GABA

Front 72

Glutamic aicd

Back 72

-major CNS excitatory NT

Front 73

Aspartic acid

Back 73

-major CNS excitatory NT

Front 74

Glycine- Inhibited by Strychnine

Back 74

-an inhibitory NT; opens Cl- channels which hyperpolarize

-Strychnine blocks glycine receptors

Front 75

GABA - gamma aminobutyric acid

Back 75

-inhibitory NT; opens Cl- channels

-most common NT in brain

Front 76

Schzophrenia

Back 76

-Caused by too much Dopamine in the emotional reward pathway of Dopamine.

-treated by anti-dopamine drugs

Front 77

Similarities b/n EPSPs & IPSPs

Back 77

-graded in magnitude

-have no threshold (can stay open)

-summate

-have no refractory period