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1
Q

1906, Charles Scott Sherrington physiologically demon-

strated

A

that communication between one neuron and the next
differs from communication along a single axon. He inferred a
specialized gap between neurons and introduced the term
synapse to describe it.

2
Q

reflexes

A

—automatic muscular responses

to stimuli.

3
Q

Reflex arc: In a leg flexion reflex

A

a sensory neuron excites a
second neuron, which in turn excites a
motor neuron, which excites a muscle,
as in Figure 3.1 (p. 40) The circuit from sen-
sory neuron to muscle response is called
a reflex arc.

4
Q

Sherrington observed several properties of reflexes sug-
gesting special processes at the junctions between neurons: (3)

A

(a) Reflexes are slower than conduction along an axon.
(b) Several weak stimuli presented at slightly different times
or locations produce a stronger reflex than a single stimulus
does. (c) When one set of muscles becomes excited, a different
set becomes relaxed. Let’s consider each of these points and
their implications.

5
Q

What evidence led Sherrington to conclude that transmis-
sion at a synapse is different from transmission along an
axon?

A

Sherrington found that the velocity of conduction
through a reflex arc was significantly slower than the
velocity of an action potential along an axon. There-
fore, some delay must occur at the junction between
one neuron and the next.

6
Q

temporal summation

A

repeated stimuli within a brief time
have a cumulative effect. He referred to this phenomenon as
temporal summation (summation over time). A light pinch
of the dog’s foot did not evoke a reflex, but a few rapidly re-
peated pinches did. Sherrington surmised that a single pinch
did not reach the threshold of excitation for the next neuron.

7
Q

presynaptic neuron

A

The neuron that delivers transmission is the presynaptic neuron.

8
Q

postsynaptic neuron

A

The neuron that receives transmission is the postsynaptic neuron.

9
Q

excitatory postsynaptic potential (EPSP)

A

A graded depolarization is
known as an excitatory postsynaptic potential (EPSP).
Partial depolarization is a graded potential.
Unlike action potentials, which are always depolarizations.
It results from a flow of sodium ions into the neuron. If an EPSP does not cause the cell to reach its threshold, the depolarization decays quickly.

10
Q

spatial summation

A

that is, summation over space. Synap-

tic inputs from separate locations combine their effects on a neuron.

11
Q

What is the difference between temporal summation and

spatial summation?

A

Temporal summation is the combined effect of
quickly repeated stimulation at a single synapse.
Spatial summation is the combined effect of several
nearly simultaneous stimulations at several synapses
onto one neuron.

12
Q

inhibitory postsynaptic potential (IPSP)

A

That is, it increases the negative charge within the
cell, moving it further from the threshold and decreasing the
probability of an action potential (point 5 in Figure 3.3, p. 54).
This temporary hyperpolarization of a membrane—called
an inhibitory postsynaptic potential, or IPSP—resembles
an EPSP. An IPSP occurs when synaptic input selectively
opens the gates for potassium ions to leave the cell (carrying
a positive charge with them) or for chloride ions to enter the
cell (carrying a negative charge).

13
Q

What was Sherrington’s evidence for inhibition in the nervous system?

A

Sherrington found that a reflex that stimulates a
flexor muscle prevents contraction of the extensor
muscles of the same limb. He therefore inferred that
an axon sending an excitatory message for the flexor
muscle also sent an inhibitory message for the extensor muscle.

14
Q

What ion gates in the membrane open during an EPSP?

What gates open during an IPSP?

A

During an EPSP, sodium gates open. During

an IPSP, potassium or chloride gates open.

15
Q

Can an inhibitory message flow along an axon?

A

No. Only
action potentials propagate along an axon. Inhibitory
messages—IPSPs—decay over time and distance.

16
Q

spontaneous firing rate

A

a periodic
production of action potentials even without synaptic input.
In such cases, the EPSPs increase the frequency of action po-
tentials above the spontaneous rate, whereas IPSPs decrease
it.

17
Q

What was Loewi’s evidence that neurotransmission de-

pends on the release of chemicals?

A

When Loewi stimulated a nerve that increased or
decreased a frog’s heart rate, he could withdraw some
fluid from the area around the heart, transfer it to
another frog’s heart, and thereby increase or decrease
its rate also.

18
Q

Every year, research-
ers discover more and more details about synapses, their
structure, and how those structures relate to function. Here
are the major events (6):

A
  1. The neuron synthesizes chemicals that serve as
    neurotransmitters. It synthesizes the smaller
    neurotransmitters in the axon terminals and synthesizes
    neuropeptides in the cell body.
    2. Action potentials travel down the axon. At the
    presynaptic terminal, an action potential enables
    calcium to enter the cell. Calcium releases
    neurotransmitters from the terminals and into the
    synaptic cleft, the space between the presynaptic and
    postsynaptic neurons.
    3. The released molecules diffuse across the cleft, attach to
    receptors, and alter the activity of the postsynaptic neuron.
    4. The neurotransmitter molecules separate from their
    receptors.
    5. The neurotransmitter molecules may be taken back into the
    presynaptic neuron for recycling or they may diffuse away.
    6. Some postsynaptic cells send reverse messages to control
    the further release of neurotransmitter by presynaptic cells.
    Figure 3.13 (p. 60) summarizes these steps.
19
Q

neurotransmitters

A

At a synapse, a neuron releases chemicals that affect another
neuron. Those chemicals are known as neurotransmitters.

20
Q

major categories of neurotransmitters:

A
"amino acids"
acids containing an amine group (NH 2 )
"monoamines"
chemicals  formed  by  a change in certain amino acids "acetylcholine"
 (a one-member “family”) a chemical similar to an amino acid, except that it includes an N(CH 3 ) 3  group 
instead of an NH 2
"neuropeptides"
chains of amino acids 
"purines"
a  category  of  chemicals  including  adenosine  and several  of  its derivatives
"gases"
nitric oxide and possibly others

The oddest transmitter is “nitric ox-
ide” (chemical formula NO), a gas re-
leased by many small local neurons. (Do
not confuse nitric oxide, NO, with ni-
trous oxide, N(small2)O, sometimes known as
“laughing gas.”) Nitric oxide is poison-
ous in large quantities and difficult to
make in a laboratory. Yet, many neurons
contain an enzyme that enables them to
make it efficiently. One special function
of nitric oxide relates to blood flow:
When a brain area becomes highly ac-
tive, blood flow to that area increases.
How does the blood “know” which
brain area has become more active? The
message comes from nitric oxide. Many neurons release nitric oxide when they are stimulated. In addi-
tion to influencing other neurons, nitric oxide dilates the nearby
blood vessels, thereby increasing blood flow to that brain area

21
Q

What does a highly active brain area do to increase its

blood supply?

A

In a highly active brain area, many stimulated neurons
release nitric oxide, which dilates the blood vessels in
the area and thereby increases blood flow to the area.

22
Q

catecholamines

A

compounds known as catecholamines,

because they contain a catechol group and an amine group ( epinephrine, norepinephrine, and dopamine)

23
Q

tryptophan

A

The amino acid tryptophan, the precursor to serotonin, crosses the blood–brain barrier by a special transport system that it shares with other large amino acids. The amount of tryptophan in the diet controls the amount of serotonin in the brain

24
Q

how to increase tryptophan entry in the brain

A

eat foods
richer in tryptophan, such as soy, and fall after something low in
tryptophan, such as maize (American corn). However, trypto-
phan has to compete with other, more abundant large amino
acids, such as phenylalanine, that share the same transport sys-
tem. One way to increase tryptophan entry to the brain is to
decrease consumption of phenylalanine. Another is to eat car-
bohydrates. Carbohydrates increase the release of the hormone
insulin, which takes several competing amino acids out of the
bloodstream and into body cells, thus decreasing the competi-
tion against tryptophan

25
Q

vesicles

A

Most neurotransmitters are synthesized in the presynaptic
terminal, near the point of release. The presynaptic terminal
stores high concentrations of neurotransmitter molecules in
vesicles, tiny nearly spherical packets (Figure 3.15, p. 62). (Nitric
oxide is an exception to this rule. Neurons release nitric oxide
as soon as they form it instead of storing it.)

26
Q

, MAO (mono-amine oxidase)

A

It is possible for a neuron to accumulate excess levels of a neurotransmitter. Neurons that release serotonin, dopamine, or norepinephrine contain an enzyme, MAO (mono-amine oxidase), that breaks down these transmitters into inactive chemicals.

27
Q

how does an action potential lead to the release of a neurotransmitter (exocytosis)?

A

At the end of an axon, the action potential itself does not
release the neurotransmitter. Rather, the depolarization
opens voltage-dependent calcium gates in the presynaptic terminal. Within 1 or 2 milliseconds (ms) after calcium en-
ters the presynaptic terminal, it causes exocytosis—release
of neurotransmitter in bursts from the presynaptic neuron
into the synaptic cleft that separates one neuron from an-
other. An action potential often fails to release any trans-
mitter, and even when it does, the amount varies

28
Q

For many years, investigators believed that each neuron released just one neurotransmitter, but later researchers found that

A

many, perhaps most, neurons release a combination of two or more transmitters.

29
Q

Why does a neuron release a combination of transmitters instead of just one?

A

The combination makes the neuron’s message

more complex, such as brief excitation followed by slight but prolonged inhibition

30
Q

Motor neurons in the spinal chord release what transmitters?

A

different transmitters from different branches of its axon.
Motor neurons in the spinal cord have one branch to the muscles, where they release acetylcholine, and another branch to other spinal cord neurons, where they release both acetylcholine and glutamate

31
Q

Although a neuron releases only a limited number of neu-

rotransmitters, it may receive and respond to

A

many neu-
rotransmitters at different synapses. For example, at various
locations on its membrane, it might have receptors for gluta-
mate, serotonin, acetylcholine, and others.

32
Q

When the action potential reaches the presynaptic ter-
minal, which ion must enter the presynaptic terminal to
evoke release of the neurotransmitter?

A

Calcium.

33
Q

ionotropic effects (receptor, neurotransmittter)

A

brief on/off effect: when a neurotransmitter binds to the receptor it opens its central channel to let ions pass (transmitter gated/ ligand gated channels)
well suited to conveying visual information, auditory information, and anything else that needs to be updated as quickly as possible.

34
Q

transmitter gated/ ligand gated channels

A

when a neurotransmitter attaches, it opens a channel

35
Q

Most of the brain’s excitatory ionotropic synapses use which neurotransmitter?

A

glutamate

36
Q

which is the most abundant neurotransmitter in the nervous system?

A

glutamate

37
Q

Most of the inhibitory ionotropic synapses use which neurotransmitter?

A

GABA (gamma-aminobutyric acid)

38
Q

how does GABA (gamma-aminobutyric acid) work as neurotransmitter in the synapse as an inhibitor?

A

opens chloride gates, enabling chloride ions, with their negative charge, to cross the membrane into the cell more rapidly than usual.

39
Q

Which inhibitory neurotransmitter is mostly in the spinal cord?

A

Glycine

40
Q

Acetylcholine, a transmitter at many ionotropic synapses, is

in most cases inhibitory or excitatory?

A

excitatory

41
Q

metabotropic effects

A

longer lasting than ionotropic effects (30 ms or longer) neurotransmitter bend the receptor and detaches a g protein which activates a second messanger, which may open or close ion channels in the membrane or activate a portion of a chromosome

42
Q

g protein

A

a protein coupled to guanosine triphos-

phate (GTP), an energy-storing molecule.

43
Q

second messenger (metabotropic receptors)

A

The result of that G protein is increased concentration of a second messenger, such as cyclic adenosine monophosphate (cyclic AMP), inside the cell. Just as the “first messenger” (the neurotransmitter) carries information to the postsynaptic
cell, the second messenger communicates to many areas
within the cell. It may open or close ion channels in the mem-
brane or activate a portion of a chromosome.

44
Q

metabotropic synapses contribute to behaviour like: (examples)

A

metabotropic synapses are suited for enduring effects such as taste , smell, and pain where the exact timing isn’t important anyway. Metabotropic synapses are also important for many aspects of arousal, attention, pleasure, and emotion

45
Q

Neuropeptides, where are they produced and where are they released?

A

a) or neuromodulators. b) synthesized in the cell body c) released mainly by dendrites, cell body, and sides of the axon

46
Q

How do neuropeptides work?

A

after a few dendrites release a neuropeptide, the released chemical primes other nearby dendrites to release the same neuropeptide also, including dendrites of other cells. Neuropeptides diffuse widely, slowly affecting many neurons in their region of
the brain. In that way they resemble hormones.

47
Q

Neuropeptides are important for..? (functions)

A

hunger, thirst, and other long-term

changes in behavior and experience

48
Q

How do ionotropic and metabotropic synapses differ in speed and duration of effects?

A

Ionotropic synapses act more quickly and more

briefly.

49
Q

What are second messengers, and which type of

synapse relies on them?

A

At metabotropic synapses, the neurotrans-
mitter attaches to its receptor and thereby releases a
chemical (the second messenger) within the postsyn-
aptic cell, which alters metabolism or gene expression
of the postsynaptic cell.

50
Q

How are neuropeptides special compared to other

transmitters?

A

Neuropeptides are released only after prolonged stimulation, but when they are released, they are released in large amounts by all parts of the neuron, not just the axon terminal. Neuropeptides diffuse widely, producing long-lasting effects on many neurons.

51
Q

ondansetron

A

blocks serotonin receptor type 3 that mediates

nausea to help cancer patients to undergo treatment

52
Q

hallucinogenic drugs

A

drugs

that distort perception

53
Q

lysergic acid diethylamide

(LSD) chemically resembles

A

serotonin

54
Q

Nicotine, a compound present in tobacco, stimulates which family of receptors?

A

acetylcholine receptors, conveniently known as

nicotinic receptors.

55
Q

Nicotinic receptors are abundant on neu-

rons that release

A

dopamine, so nicotine increases dopamine

release there

56
Q

Typical antipsychotic drugs block

A

dopamine receptors

57
Q

examples for opiate drugs

A

morphine, heroin, and methadone

58
Q

how are the “natural” produced opiates in the human body called?

A

endorphines- endogenous morphines

59
Q

How do LSD, nicotine, and opiate drugs influence

behavior?

A

LSD binds to one type of serotonin receptor. Nicotine binds to one type of acetylcholine receptor. Opiates bind to endorphin receptors.

60
Q

acetylcholinesterase and what does it do?

A

After acetylcholine activates a receptor, it is broken down by this enzyme into two fragments: acetate and choline

61
Q

Serotonin and the catecholamines (dopamine, norepinephrine, and epinephrine) inactivate through

A

reuptake

62
Q

reuptake occurs through special membrane proteins called

A

transporters

63
Q

Any transmitter molecules not taken up by transporters are broken down by

A

an enzyme called COMT (catechol-o-methyltransferase)

64
Q

COMT (catechol-o-methyltransferase)

A

Any transmitter molecules not taken up by transporters are broken down by this enzyme

65
Q

Stimulant drugs, including amphetamine and cocaine,

inhibit

A

the transporters for dopamine, thus decreasing reup-
take and prolonging dopamine’s effects. Amphetamine
also blocks the serotonin and norepinephrine transporters

66
Q

Metamphetamine are like amphetamine, but… antidepressants are like amphetamine, but…

A

stronger

weaker

67
Q

Methylphenidate

A

(Ritalin) and cocaine block the reuptake of

dopamine in the same way at the same brain receptors.

68
Q

Difference methylphenidate and cocaine

A

dose and time course. Co-
caine users typically sniff it or inject it to produce a rapid rush of
effect on the brain. People taking methylphenidate pills experi-
ence a gradual increase in the drug’s concentration over an hour
or more, followed by a slow decline. Therefore, methylphenidate
does not produce the sudden rush of excitement that cocaine
does.

69
Q

What happens to acetylcholine molecules after they

stimulate a postsynaptic receptor?

A

The enzyme acetylcholinesterase breaks acetyl-
choline molecules into two smaller molecules, acetate
and choline, which are then reabsorbed by the presyn-
aptic terminal.

70
Q

What happens to serotonin and catecholamine

molecules after they stimulate a postsynaptic receptor?

A

Most serotonin and catecholamine
molecules are reabsorbed by the presynaptic terminal.
Some of their molecules are broken down into inactive
chemicals, which then diffuse away.

71
Q

How do amphetamine and cocaine influence dopamine

synapses?

A

They interfere

with reuptake of released dopamine.

72
Q

Why is methylphenidate generally less disruptive to
behavior than cocaine is despite the drugs’ similar
mechanisms?

A

The effects of
a methylphenidate pill develop and decline in the brain
much more slowly than do those of cocaine.

73
Q

autoreceptors and what are they doing?

A

receptors that respond to the released
transmitter by inhibiting further synthesis and release.
They provide negative feedback

74
Q

Nitric oxide, anandamide and 2-AG (sn-2 arachidonylglycerol) give negative feedback in/to the synapse by

A

traveling from the postsynapses to the presynaptic terminal and inhibit further release of transmitter

75
Q

Cannabinoids function by

A

binding to anandamide or 2-AG receptors on presynaptic neurons or GABA. By attaching to these receptors, they inhibit the presynapse to send. Thereby they inhibit excitatory and inhibitory messages from neurons

76
Q

How do cannabinoids affect neurons?

A

Cannabinoids released by the postsynaptic
neuron attach to receptors on presynaptic neurons,
where they inhibit further release of both glutamate
and GABA.

77
Q

gap junction

A

At an electrical synapse, the membrane of one neuron comes into direct contact with the membrane of another. This contact is called gap junction. Large pores on the pre- connect with pores on the postsynaptic neuron and allow sodium at depolarization quickly to pass, make the neurons act almost as one neuron

78
Q

hormone

A

chemical secreted by cells in one part of the body and conveyed by the blood to influence other cells

79
Q

endrocrine glands

A

hormon producing glands

80
Q

Which two types of hormones are composed by chains of amino acids and attach to membrane receptors, activating a second messenger?

A

protein hormones and peptide hormones
(Proteins are longer chains and peptides are shorter.)
act like metabotropic synapses

81
Q

what does the pituitary gland consist of and what is their function?

A

anterior pituitary and posterior pituitary. The posterior pituitary can be seen as extension of the hypothalamus (neural tissue), takes in antidiuretic hormones from hypothalamus and releases them in the blood. The anterior pituitary gland produces hormones itself (glandular tissue), but is controlled by hypothalamus, which releases releasing hormones

82
Q

what and where are antidiuretic hormones?

A

Neurons
in the hypothalamus synthesize the hormones oxytocin and
vasopressin, also known as antidiuretic hormones

83
Q

Which part of the pituitary—anterior or posterior—is
neural tissue, similar to the hypothalamus? Which part
is glandular tissue and produces hormones that control
the secretions by other endocrine organs?

A

The posterior pituitary is neural tissue, like the
hypothalamus. The anterior pituitary is glandular tis-
sue and produces hormones that control several other
endocrine organs.

84
Q

In what way is a neuropeptide intermediate between

neurotransmitters and hormones?

A

Most neurotransmitters are
released in small amounts close to their receptors.
Neuropeptides are released into a brain area in larger
amounts or not at all. When released, they diffuse
more widely. Hormones are released into the blood for
diffuse delivery throughout the body.