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NEUR 10 > Part 3? > Flashcards

Part 3? Flashcards

1
Q

What is direct synaptic transmission?

A

Transmission of signals directly from one neuron to another.

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2
Q

What are diffuse modulatory systems?

A

Divergent axonal projections using specific neurotransmitters, found only in the CNS.

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3
Q

How does neuroendocrine signaling work?

A

It involves secreting chemicals directly into the bloodstream.

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4
Q

What do autonomic nervous system networks innervate?

A

Organs, blood vessels, and glands.

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5
Q

What is the characteristic of core neurons?

A

They form widely divergent axons that can each form up to 100k synapses broadly throughout the brain.

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6
Q

Where do most neurons originate from?

A

Brainstem nuclei.

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7
Q

What type of receptors do they typically activate?

A

CNS metabotropic receptors.

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8
Q

Apart from synaptic neurotransmitter release, where else do they release neurotransmitters?

A

Into the extracellular fluid, leading to effects broader than a single synapse.

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9
Q

Name the main neurotransmitters involved in this process.

A

Norepinephrine, Dopamine, Acetylcholine, Serotonin.

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10
Q

Where is the origin of the noradrenergic system?

A

In the pons at the locus coeruleus.

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11
Q

Where does the noradrenergic system have wide projections?

A

Throughout the brain, especially in the cortex, thalamus, and cerebellum.

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12
Q

What is the main function of the noradrenergic system?

A

Regulating attentiveness/wakefulness.

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13
Q

Is the noradrenergic system generally excitatory or inhibitory?

A

Generally excitatory.

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14
Q

What type of stimuli do neurons of the noradrenergic system respond most to?

A

New, unexpected stimuli.

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15
Q

What effect does the noradrenergic system have on neuron responsiveness?

A

Increases it.

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16
Q

What is the function of Raphe nuclei?

A

Modulates sleep/wake cycle and mood control.

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17
Q

Where do the large projections from Raphe nuclei go?

A

To the forebrain.

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18
Q

Where does the caudal part of Raphe nuclei send projections?

A

To the spinal cord to modulate pain.

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19
Q

What is the origin of the Pontomesencephalotegmental complex?

A

Pons + midbrain + tegmentum

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20
Q

Where does the Pontomesencephalotegmental complex project to?

A

Dorsal thalamus and telencephalon

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21
Q

What is the function of the Pontomesencephalotegmental complex in the dorsal thalamus?

A

Regulate excitability of sensory relay nuclei

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22
Q

What is the function of the Pontomesencephalotegmental complex in the telencephalon?

A

Acts as an ACh link between brainstem and basal forebrain complex

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23
Q

What type of receptors are present at the neuromuscular junction in the context of the Pontomesencephalotegmental complex?

A

Nicotinic receptors

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24
Q

Where do the cholinergic neurons in the basal forebrain complex originate?

A

Telencephalon.

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25
Q

What are the projections of the basal forebrain complex’s cholinergic neurons to the neocortex?

A

Basal nucleus of Meynert.

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26
Q

Where do the cholinergic neurons of the basal forebrain complex project to in the hippocampus?

A

Medial septal nuclei.

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27
Q

What are the functions of the basal forebrain complex?

A

Learning and memory, coordinating activity in large brain areas, and degeneration in Alzheimer’s disease.

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28
Q

Which brain areas’ activity does the basal forebrain complex coordinate?

A

Large brain areas such as arousal, sleep/wake cycles, etc.

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29
Q

What neurotransmitter reuptake does cocaine block?

A

Dopamine (DA) reuptake.

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30
Q

What neurotransmitter reuptake does methamphetamine block?

A

Norepinephrine (NE) and dopamine (DA) reuptake.

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31
Q

How does methamphetamine affect dopamine (DA) release?

A

It stimulates dopamine (DA) release.

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32
Q

What are the effects of NE/DA reuptake blockage?

A

Prolonged effects of increased alertness, self-confidence, exhilaration, euphoria, and decreased appetite.

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33
Q

What sympathetic activation effects do cocaine and methamphetamine mimic?

A

Increase in heart rate, blood pressure, pupil dilation, etc.

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34
Q

What is the function of the cells in the periventricular hypothalamus?

A

Coordinating neuroendocrine signaling.

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35
Q

What does the periventricular hypothalamus help regulate?

A

ANS outflow and circadian rhythms.

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36
Q

What type of neurons does the periventricular hypothalamus contain?

A

Neurosecretory neurons.

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37
Q

Where do the neurosecretory neurons in the periventricular hypothalamus send axons for hormone signaling?

A

To the pituitary gland.

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38
Q

What is the main role of the periventricular hypothalamus in maintaining body function?

A

Maintaining homeostasis.

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39
Q

What signals does the periventricular hypothalamus integrate to drive behavior?

A

Hormones, somatic/visceral sensation, etc.

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40
Q

What kind of neurons innervate the posterior pituitary and release neurohormones directly onto its capillaries?

A

Magnocellular secretory neurons.

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41
Q

What are the two neurohormones released by the magnocellular secretory neurons?

A

Oxytocin and vasopressin (ADH).

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42
Q

Where do the neurohormones oxytocin and vasopressin circulate in the body?

A

In the blood from the capillaries.

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43
Q

What is the role of oxytocin when a mother sees her baby?

A

Responsible for uterine contractions.

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44
Q

What is the role of vasopressin in males?

A

Regulating blood volume and salinity.

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45
Q

What are the two types of voles with different distributions of oxytocin and vasopressin receptors?

A

Prairie voles and Montane voles.

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46
Q

Which type of voles has more oxytocin and vasopressin receptors in reward areas and exhibits more monogamy?

A

Prairie voles.

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47
Q

Which type of voles has less oxytocin and vasopressin receptors in reward areas and does not pair bond?

A

Montane voles.

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48
Q

What is the mnemonic for remembering the difference in pair bonding between prairie and montane voles?

A

MP, PM (montane polygamy, prairie monogamy).

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49
Q

What effect did blocking vasopressin have on prairie voles?

A

Made them less monogamous.

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50
Q

What effect did overexpression of vasopressin have on montane voles?

A

Made them monogamous.

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51
Q

What genetic component is present in prairie voles related to vasopressin receptor DNA sequence?

A

V1aR subtype gene variant.

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52
Q

What effect did transgenically introducing the V1aR subtype gene variant into montane voles have?

A

Made them more monogamous.

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53
Q

What releases hypophysiotropic hormones onto anterior pituitary cells?

A

Parvocellular secretory neurons in the hypothalamus.

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54
Q

How do hypophysiotropic hormones reach anterior pituitary cells?

A

Through local blood circulation (portal circulation).

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55
Q

Where do the hormones released by the anterior pituitary go?

A

They are released into the bloodstream.

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56
Q

What is the function of the hormones released by the anterior pituitary?

A

To affect organs in the body.

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57
Q

Name some of the hormones released by the anterior pituitary.

A

FSH, LH, TSH, ACTH, GH, prolactin.

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58
Q

What is the relationship between cortisol levels and stress?

A

Higher cortisol levels are associated with higher stress.

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59
Q

What does the HPA axis involve?

A

The anterior pituitary hormone cortisol.

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60
Q

What hormone does the hypothalamus release onto the anterior pituitary?

A

CRH (corticotrophin-releasing hormone).

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61
Q

Where does the anterior pituitary release ACTH?

A

Onto the adrenal cortex (kidney).

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62
Q

Where does the adrenal cortex release cortisol?

A

Into the bloodstream.

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63
Q

What is the mechanism of negative feedback in the HPA axis?

A

Cortisol inhibits CRH and ACTH release.

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64
Q

What negative effects does chronic stress have on baboons low in the social hierarchy?

A

Hypertension, ulcers, and depression.

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65
Q

What is the abbreviation for adrenocorticotropic hormone?

A

ACTH.

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66
Q

What happens to the hippocampus during chronic stress?

A

Constant inhibition of hippocampal dendrites, cell death, and reduced hippocampal size.

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67
Q

What is the role of the hippocampus in regulating the HPA axis?

A

It inhibits the HPA axis through negative feedback.

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68
Q

How does chronic stress affect the HPA axis regulation by the hippocampus?

A

Hippocampal degeneration leads to less HPA inhibition, allowing cortisol to keep building up.

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69
Q

What are the two divisions of the autonomic nervous system?

A

Sympathetic and Parasympathetic.

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70
Q

Where do sympathetic nervous system fibers originate?

A

Thoracic and lumbar segments.

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71
Q

Where do parasympathetic nervous system fibers originate?

A

Brainstem and sacral segment.

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72
Q

What is the primary neurotransmitter released by sympathetic preganglionic fibers?

A

ACh (Acetylcholine).

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73
Q

What is the primary neurotransmitter released by sympathetic postganglionic fibers?

A

NE (Norepinephrine).

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74
Q

What neurotransmitter is released by both pre and postganglionic fibers in the parasympathetic nervous system?

A

ACh (Acetylcholine).

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75
Q

What is the name of the division that functions relatively independently in the gastrointestinal system?

A

Enteric Division

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76
Q

What type of cells communicate gut information to the brain?

A

Enterochromaffin cells

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77
Q

What is the function of the Enteric Division in the gastrointestinal system?

A

Works with viscera and gets some input from the ANS

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78
Q

What is the similarity between the gut and the tongue?

A

Both have taste receptors

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79
Q

Where do sympathetic nerves originate from?

A

Middle ■ of the spinal cord: lumbar and thoracic.

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80
Q

Where do parasympathetic nerves originate from?

A

Brainstem and sacral spinal cord.

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81
Q

What do sympathetic preganglionic fibers release onto the autonomic ganglion?

A

ACh (Acetylcholine).

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82
Q

What do parasympathetic preganglionic fibers release onto the autonomic ganglion?

A

ACh (Acetylcholine).

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83
Q

Is the sympathetic ganglion closer or further from the target?

A

Further from the target.

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84
Q

Is the parasympathetic ganglion closer or further from the target?

A

Closer to the target.

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85
Q

What do sympathetic postganglionic fibers release onto the target?

A

NE (Norepinephrine).

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86
Q

What do parasympathetic postganglionic fibers release onto the target?

A

ACh (Acetylcholine) (muscarinic).

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87
Q

What types of cells do sympathetic and parasympathetic nerves innervate?

A

Smooth muscle, cardiac muscle, and gland cells.

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88
Q

What is the subject of Chapter 16?

A

Motivation, Eating, Drinking, and Temperature.

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89
Q

What is homeostasis?

A

The balance/equilibrium of an internal environment, even in the face of external changes.

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90
Q

What does homeostasis help to maintain?

A

Set points.

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91
Q

What is a set point?

A

A narrow, defended range.

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92
Q

How is feedback used in homeostasis?

A

To bring the variable back to a set point.

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93
Q

What is the term used to describe warm-blooded mammals and birds?

A

Homeothermic.

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94
Q

What is the set point for the internal body temperature of mammals and birds?

A

98.6°F (37°C).

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95
Q

What rhythm do mammals and birds follow with their internal body temperature?

A

Circadian rhythm.

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96
Q

What temperature range can humans maintain a fixed core temperature in?

A

From around -40°F to 130°F.

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97
Q

What are the advantages of being a homeotherm?

A

Ability to stay active in both cold and hot weather, and a larger geographical range.

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98
Q

At what temperature do biochemical reactions evolve to take place?

A

Around 37 degrees Celsius.

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99
Q

What are the disadvantages of being a homeotherm?

A

It takes more energy and is not as successful when food is scarce, as it requires moving around to find food and expending energy to maintain temperature.

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100
Q

What are the two kinds of thermoreceptors?

A

Warm receptors and cold receptors.

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101
Q

What do warm receptors respond to?

A

Heat stimuli.

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102
Q

What do cold receptors respond to?

A

Cold stimuli.

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103
Q

Where are thermoreceptors largely located for body temperature regulation?

A

In the CNS (hypothalamus).

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104
Q

Apart from the CNS, where else can thermoreceptors be found?

A

In the skin.

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105
Q

Which fibers follow the contra spinothalamic tract to the brain?

A

Aδ and C fibers.

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106
Q

In the prioritization of thermoreceptors, what comes first?

A

TRs in the hypothalamus.

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107
Q

What comes next in the prioritization of thermoreceptors after the hypothalamus?

A

TRs in the body core.

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108
Q

What comes last in the prioritization of thermoreceptors?

A

TRs in the skin.

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109
Q

What area is crucial for temperature regulation and located above the optic chiasm?

A

Preoptic area (POA).

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110
Q

Where are the temperature-sensitive cells located in the brain?

A

Hypothalamus, specifically in the preoptic area (POA).

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111
Q

What happens with stimulation of the preoptic area (POA)?

A

It leads to sweating or panting.

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112
Q

What happens with a lesion in the preoptic area (POA)?

A

It results in the loss of thermoregulation.

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113
Q

What is the focus of the body’s temperature regulation system?

A

Temperature of the brain, specifically the hypothalamus.

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114
Q

What does the hypothesis suggest about the input from cold/warm receptors and the set point of the POA?

A

They are compared, and then warm/cool behaviors are initiated accordingly.

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115
Q

What happens when the POA is cooled?

A

Needs to warm the body.

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116
Q

What happens when the POA is heated?

A

Needs to cool the body.

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117
Q

What does the hypothalamus cause to be released from the anterior pituitary when the body needs to bring temperature back to set point?

A

Thyroid Stimulating Hormone (TSH).

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118
Q

What does an increased sympathetic activity lead to in terms of blood vessels?

A

Constriction (vasoconstriction).

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119
Q

What response is associated with an increase in parasympathetic activity?

A

Goosebumps (piloerection).

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120
Q

What is the somatic motor response to cooling of the body?

A

Seek warmth and shiver.

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121
Q

What is the somatic motor response to heating of the body?

A

Seek shade and sweat (panting in other mammals).

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122
Q

What are pyrogens?

A

Fever-inducing agents.

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123
Q

What are the two general categories of pyrogens?

A

Proteins released by bacteria/virus and Proteins produced by body cells in reaction to bacteria or virus.

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124
Q

What happens when the set point increases during fever?

A

The hypothalamus attempts to heat the body, leading to chills and shivering.

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125
Q

Why can fever be fatal if it gets too high?

A

Proteins denature and organ failure can occur.

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126
Q

Should you take Tylenol during fever according to the information provided?

A

The evidence isn’t clear, as fever may serve to kill bacteria.

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127
Q

Give an example of a substance that is released by white blood cells to drive the hypothalamus to increase temperature.

A

Prostaglandins.

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128
Q

What are the two main reasons for eating?

A

Liking (for enjoyment) and wanting (for energy).

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129
Q

What happens during digestion?

A

Macronutrients (carbs, protein, fat) are broken down.

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130
Q

Where is glucose stored in limited amounts?

A

As glycogen in the liver and skeletal muscle.

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131
Q

What happens if food intake + storage is greater than energy expenditure?

A

Weight gain.

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132
Q

What happens if food intake + storage is less than energy expenditure?

A

Weight loss.

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133
Q

What are the different uses of energy in the human body?

A

Basal metabolic rate, thermic effect of food, exercise, and non-exercise activity thermogenesis (NEAT).

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134
Q

What is the role of leptin in the body’s energy expenditure?

A

Leptin is the signal that informs the brain about the body’s fat level and helps regulate energy expenditure.

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135
Q

What does the ob gene code for in mice?

A

Leptin.

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136
Q

What happens to ob/ob mice due to the absence of the ob gene?

A

They become obese.

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137
Q

What effect does injecting leptin have on ob/ob mice?

A

They return to typical body weight.

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138
Q

In humans, what is the effect of injecting leptin on weight?

A

It only decreases weight if there is a genetic mutation or low leptin levels.

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139
Q

What produces leptin in levels proportional to body fat?

A

Fat (adipose) cells.

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140
Q

Where are leptin receptors located?

A

Arcuate nucleus of the hypothalamus.

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141
Q

What does the lateral hypothalamus incite?

A

Feeding behavior.

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142
Q

What effect does a lesion to the lateral hypothalamus cause?

A

Loss of hunger.

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143
Q

What effect does a lesion to the ventromedial hypothalamus cause?

A

Increased hunger.

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144
Q

What peptides are released by the arcuate nucleus to decrease appetite?

A

αMSH and CART

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145
Q

What peptides are released by the arcuate nucleus to increase appetite?

A

AgRP, MCH, Orexin, NPY

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146
Q

What are the effects of anorexia?

A

Extreme weight loss and higher than normal ghrelin levels

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147
Q

What are the effects of obesity?

A

High BMI, lower than normal ghrelin levels, and being more sensitive to ghrelin

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148
Q

What do fat cells release into the bloodstream?

A

Leptin

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149
Q

Where do leptin receptors bind?

A

Arcuate nucleus (hypothalamus)

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150
Q

What do arcuate neurons release in response to leptin binding?

A

αMSH and CART

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151
Q

What is the effect of increased TSH/ACTH release by the pituitary due to leptin?

A

Increased metabolism (burn fat)

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152
Q

How does increased sympathetic ANS activity respond to leptin?

A

Increased temperature/metabolism (burn fat)

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153
Q

What is the effect of inhibition of MCH/Orexin neurons in the lateral hypothalamus due to leptin?

A

Decreased feeding behavior

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154
Q

What happens when there is a decrease of leptin in the blood stream?

A

Arcuate neurons release NPY/AgRP.

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155
Q

What are the effects of arcuate neurons stopping the release of αMSH and CART?

A

Inhibition of TSH (thyrotropin)/ACTH release by the pituitary → decreased metabolism.

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156
Q

What is the result of the release of MCH/Orexin neurons in the lateral hypothalamus?

A

Increased feeding behavior.

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157
Q

What effect does dieting have on ghrelin levels?

A

Significantly increases ghrelin levels.

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158
Q

What is the impact of bariatric surgery on ghrelin levels?

A

Ghrelin levels decrease as a result of the surgery.

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159
Q

How does bariatric surgery affect the size of the stomach?

A

It decreases the size of the stomach or allows bypass of a portion of it.

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160
Q

What is the potential impact of epigenetic factors on obesity in children?

A

Children of mothers who have undergone starvation are more likely to be obese due to epigenetic factors.

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161
Q

Why are children of mothers who have undergone starvation more likely to be obese?

A

Possibly due to a change in defended range in the children.

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162
Q

What promotes eating?

A

Sight, smell, taste, and act of eating.

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163
Q

What peptide is released by the empty stomach to activate neurons in the arcuate nucleus?

A

Ghrelin.

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164
Q

What inhibits eating?

A

Gastric distension and CCK (cholecystokinin).

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165
Q

What does gastric distension activate to inhibit feeding?

A

Vagus nerve and nucleus of solitary tract.

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166
Q

Where is CCK released from to suppress feeding?

A

Cells of intestines and enteric system.

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167
Q

What type of foods cause the release of CCK from the intestines?

A

Fatty foods.

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168
Q

What hormone is associated with increased appetite and elevated ghrelin levels?

A

Ghrelin.

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169
Q

What is the most common genetic cause of obesity?

A

Prader-Willi Syndrome.

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170
Q

What is responsible for the psychological effects of marijuana?

A

THC

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171
Q

What does THC cause in ghrelin levels?

A

A surge

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172
Q

What is the common term for the increased appetite caused by THC?

A

The munchies

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173
Q

In what condition can marijuana be a helpful therapy for suppressed appetites?

A

Cancer/chemo and HIV/AIDS

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174
Q

What triggers VOLUMETRIC thirst?

A

Decrease in blood volume (hypovolemia).

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175
Q

What triggers OSMOMETRIC thirst?

A

Increase in tonicity of blood (hypertonicity).

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176
Q

What is volumetric thirst also known as?

A

Hypovolemia.

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177
Q

What triggers volumetric thirst?

A

Inadequate blood flow or low blood pressure.

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178
Q

What is the end result of volumetric thirst?

A

An increase in ADH (Antidiuretic Hormone).

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179
Q

What are the two factors that trigger the release of ADH?

A

Stimulation of magnocellular neurosecretory cells in the hypothalamus and mechanoreceptors in major blood vessels and heart.

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180
Q

What does ADH do to the kidneys?

A

Increases water uptake, decreasing urine production and increasing urine concentration.

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181
Q

What does reduced blood volume drive in terms of sympathetic activity?

A

Increases sympathetic activity to constrict arterioles and increase blood pressure.

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182
Q

What does reduced blood volume drive in terms of behavior?

A

Increases motivation to seek and consume water.

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183
Q

What is the first response of the kidneys to lower blood volume/pressure?

A

Secreting hormone renin.

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184
Q

What does renin lead to the production of?

A

Angiotensin II.

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185
Q

Where is Angiotensin II detected?

A

Subfornical organ.

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186
Q

What is activated in the subfornical organ upon detecting Angiotensin II?

A

Magnocellular neurosecretory cells.

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187
Q

What is released by the activated cells?

A

ADH (Antidiuretic hormone).

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188
Q

What is the effect of ADH on the kidneys?

A

Causes kidneys to hold onto water / inhibit urine.

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189
Q

What do mechanoreceptors in the heart and major blood vessels detect?

A

Decreased blood pressure.

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190
Q

Where does the signal from mechanoreceptors via the vagus nerve go?

A

Nucleus of the solitary tract in the medulla.

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191
Q

What does the nucleus of the solitary tract in the medulla project to?

A

Hypothalamus.

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192
Q

What does the hypothalamus activate in response to decreased blood pressure?

A

Sympathetic ANS.

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193
Q

What is the role of the lateral hypothalamus in response to hypovolemia?

A

Initiates behaviors to seek water.

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194
Q

What is the response to hypovolemia known as?

A

Cardiac phase.

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195
Q

What does hypertonicity refer to?

A

Increased ion concentrations in the blood.

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196
Q

What is hypernatremia?

A

Excess sodium in the blood.

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197
Q

What hormone is associated with hypernatremia and triggers osmometric thirst?

A

Oxytocin (love hormone).

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198
Q

Where are neurons that detect hypernatremia located?

A

In the vascular organ of the lamina terminalis (OVLT).

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199
Q

What does OVLT excite in response to hypernatremia?

A

Magnocellular secretory neurons.

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200
Q

What does ADH (vasopressin) do in response to hypernatremia?

A

Causes kidneys to retain water and inhibits urination.

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201
Q

What type of thirst is triggered by hypertonicity?

A

Osmometric Thirst.

202
Q

What are the possible causes of Diabetes Insipidus?

A

Genetics, autoimmune disease, tumor, etc.

203
Q

What are the symptoms of Diabetes Insipidus?

A

Incredibly thirsty all the time, excreting 20 liters of urine a day (normal is 1-2).

204
Q

What is the role of ADH in Diabetes Insipidus?

A

ADH doesn’t hold up its role, causing excessive urination and thirst.

205
Q

What is the brain’s response in Diabetes Insipidus?

A

The brain accurately signals the need for water.

206
Q

What does the Medial preoptic area of hypothalamus respond to?

A

Temperature and mediates humoral + visceromotor response.

207
Q

What does the Arcuate nucleus of hypothalamus respond to?

A

Blood levels of leptin and ghrelin.

208
Q

What is the Paraventricular nucleus of hypothalamus involved in?

A

Long-term regulation of eating (release hypophysiotropic hormones, receives input from arcuate nucleus, affects sympathetic ANS).

209
Q

What signals does the Nucleus of solitary tract respond to?

A

Gastric distension signals of stomach (eating) and mechanoreceptors in blood vessel walls (drinking).

210
Q

What does the Subfornical organ respond to?

A

Elevated angiotensin II blood levels (drinking) because it is outside the blood-brain barrier (BBB).

211
Q

What does the OVLT respond to?

A

Tonicity of blood because it is outside the BBB.

212
Q

What does the Suprachiasmatic nucleus of PVZ mediate?

A

Circadian rhythms.

213
Q

What does the Supraoptic nucleus of PVZ contain?

A

Magnocellular secretory neurons.

214
Q

What is Declarative/Explicit Memory?

A

Facts and events that can be consciously remembered.

215
Q

Where is Declarative/Explicit Memory localized?

A

Medial temporal lobe, especially hippocampus, and diencephalon.

216
Q

What is Nondeclarative/Implicit Memory?

A

Procedural memory for skills and habits that operates without conscious recollection.

217
Q

Where is Procedural Memory localized?

A

Striatum.

218
Q

What are the two parts of classical conditioning as a type of procedural memory?

A

Skeletal musculature (cerebellum) and Emotional responses (amygdala).

219
Q

What are the timespans of memory?

A

Working, Short-term, Long-term

220
Q

What is the duration of short-term memory?

A

Seconds to hours (depends on context)

221
Q

What is the duration of long-term memory?

A

Many years

222
Q

What is the capacity/storage of working memory?

A

Very small

223
Q

What is the capacity/storage of short-term memory?

A

Medium

224
Q

What is the capacity/storage of long-term memory?

A

Very large

225
Q

What is the fidelity/reliability of working memory?

A

Bad – must be rehearsed or gone in seconds

226
Q

What can cause the loss of short-term memory?

A

Head trauma

227
Q

Is long-term memory resistant to head trauma?

A

Yes

228
Q

What is the synapse change in working memory?

A

No permanent change

229
Q

What is the synapse change in short-term memory?

A

Structural synaptic change

230
Q

What is the synapse change in long-term memory?

A

Long-term changes in synapse strength

231
Q

Which brain area is associated with working memory?

A

Frontal Cortex

232
Q

Which brain area is associated with short-term memory?

A

Hippocampus (HPPC)

233
Q

What does the hippocampus do in relation to short-term memory?

A

May link new sensory info to pre-existing info in cortex

234
Q

What is an example of working memory?

A

Holding a person’s address in mind

235
Q

What is an example of long-term memory?

A

Childhood memories

236
Q

What is the purpose of the delayed response task?

A

To test the ability to hold information in working memory.

237
Q

Where is the prefrontal cortex activity observed during the delay period?

A

During the delay period of the delayed response task.

238
Q

What does the monkey have to do during the delay period in the delayed response task?

A

Hold information in working memory.

239
Q

What evidence exists regarding the brain areas involved in different delay-period tasks?

A

Different types of delay-period tasks use different (but overlapping) areas of the brain.

240
Q

What is the process that converts a few memories into long-term memories?

A

Memory consolidation.

241
Q

What influences the process of memory consolidation?

A

Salience (significance) and emotion.

242
Q

Where is sensory information initially stored?

A

In working and short-term memory.

243
Q

Where is short-term memory converted to long-term memory?

A

In the cortex (from the hippocampus).

244
Q

From where do we retrieve information during the retrieval process?

A

Long-term memory.

245
Q

What is amnesia?

A

Abnormal memory loss or loss of ability to form new memories.

246
Q

What are the causes of amnesia?

A

Concussion, tumor, stroke, viral encephalitis.

247
Q

How many types of amnesia are there?

A

2 types.

248
Q

What is retrograde amnesia?

A

Forgetting past memories but being able to make new ones.

249
Q

How is retrograde amnesia graded temporally?

A

Older memories are more likely to be retained.

250
Q

What is anterograde amnesia?

A

Inability to make new memories.

251
Q

Do people usually have a combination of both types of amnesia?

A

Yes.

252
Q

What are the functions of the hippocampus and nearby cortical areas?

A

Declarative memory formation and storage.

253
Q

Who discovered that electrically stimulating the temporal lobe evokes specific memories?

A

Wilder Penfield.

254
Q

What is the result of damage to the temporal lobe?

A

Amnesia.

255
Q

What do hippocampal recordings show some cells are sensitive to?

A

Categories of objects.

256
Q

What are some examples of specific things that some hippocampal cells respond to?

A

Household objects, Jennifer Aniston.

257
Q

What areas are related to recall in the nearby lateral temporal lobe?

A

Area IT for face/object recognition.

258
Q

What condition was the patient treated for?

A

Epilepsy.

259
Q

What surgical procedure was performed on the patient?

A

Bilateral removal of parts of MTL (including HPPC, amygdala, and surrounding cortex).

260
Q

What type of amnesia did the patient experience after the surgery?

A

Absolute anterograde amnesia and partial retrograde amnesia.

261
Q

What memory functions remained intact in the patient?

A

Working memory and procedural memory.

262
Q

What type of memory does the test assess?

A

Declarative memory.

263
Q

What happens in the experiment?

A

An animal is trained to displace an object covering a well, then after a delay, the animal must displace a new object on a new well to get a reward.

264
Q

What effect does lesioning the MTL have?

A

Decreased performance.

265
Q

What is the function of the hippocampus in memory?

A

Declarative memory consolidation, possible key role in spatial memory, face and object selectivity, integrating/associating important sensory information, and linking different pieces of information together.

266
Q

What is the Morris Water Maze?

A

A test for spatial memory in rats.

267
Q

How does the Morris Water Maze work?

A

Rat placed in a pool of opaque liquid and swims to find a hidden platform.

268
Q

What does the performance of rats in the Morris Water Maze test indicate?

A

Their spatial memory.

269
Q

What happens when rats improve in the Morris Water Maze test?

A

They remember the location of the hidden platform.

270
Q

What is the impact of a bilateral HPPC lesion on the Morris Water Maze test?

A

Inability to learn the platform location or understand the task.

271
Q

Which brain region is associated with spatial memory in the context of the Morris Water Maze test?

A

Hippocampus.

272
Q

What is a place field in rat HPPC cells?

A

A place field is an area where the cell responds maximally when the rat is at a specific location.

273
Q

How can a rat’s place field be modified?

A

By exploration and by expanding the rat’s cage to include new areas.

274
Q

What may place fields be used for?

A

Navigation and spatial memory.

275
Q

What do intracellular recordings of individual hippocampal cells show during a water-maze-esque task?

A

Certain cells respond to certain areas preferentially.

276
Q

What is the function of grid cells in the entorhinal cortex?

A

To activate at locations that can be laid out in a grid, functioning as an internal GPS.

277
Q

What is the cognitive map theory related to the entorhinal cortex?

A

One of the purposes is to create a map of the environment through grid cells and place cells.

278
Q

What happens when hippocampal input is silenced in relation to grid cells?

A

The grid pattern is lost.

279
Q

In what condition is the entorhinal cortex often damaged early?

A

Alzheimer’s.

280
Q

What part of the brain is affected when the navigational ability of London taxi drivers is damaged?

A

Hippocampus.

281
Q

What happens to the size of the hippocampus with more taxi driver work experience?

A

Increases.

282
Q

When are the human place cells active in taxi drivers?

A

While actually navigating routes (in simulation).

283
Q

What happens to the hippocampus when taxi drivers are just watching someone else drive around?

A

Not active.

284
Q

What are the two models of memory storage?

A

Linear, unchanged with retrieval and Multiple trace model.

285
Q

What role does the hippocampus play in memory storage?

A

It may retain some memory trace.

286
Q

What happens each time you retrieve a memory?

A

You can add a little strength to the memory.

287
Q

What makes memories moldable again?

A

Reconsolidation by recalling/reactivating a memory.

288
Q

When does reconsolidation occur?

A

After consolidation, recalling/reactivating a memory makes it plastic again.

289
Q

What is the significance of reconsolidation?

A

It is important for adapting to new information.

290
Q

What is the effect of benzodiazepines on memory consolidation?

A

Inhibit consolidation from HPPC to cortex.

291
Q

How do GABAA receptors affect memory?

A

They inhibit memory.

292
Q

What is the impact of benzodiazepines on the hippocampus?

A

They ‘shut down’ the hippocampus.

293
Q

In what context are benzodiazepines sometimes administered to block memory formation?

A

During surgeries.

294
Q

What is the role of HDAC2 (histone deacetylase 2) in memory modification?

A

It shuts off plasticity genes.

295
Q

How was the traumatic experience created for the mouse in the experiment?

A

By pairing a sound with an electric shock.

296
Q

What was the end result of inhibiting HDAC2 in the experiment?

A

Plasticity was turned on, allowing the memory to become non-traumatic.

297
Q

What was the outcome of presenting the sound in a safe environment after inhibiting HDAC2?

A

The animal no longer feared the foot shock.

298
Q

What is the phenomenon described in the given text?

A

Creating false memories.

299
Q

What was done in Box A in the given experiment?

A

Labeled neurons that were active in a neutral box.

300
Q

What was done in Box B in the given experiment?

A

Reactivated the Box A neurons by shining light on them, paired with foot shock.

301
Q

What was the result when the mouse was back in Box A?

A

Mouse showed fear response to being in Box A, even though no shock was given in Box A previously.

302
Q

What was the significance of the experiment in Box A and B?

A

Box A neuron activation in Box B paired with shock was enough to create false memory of Box A and foot shock.

303
Q

What type of information does the Inferotemporal Cortex receive?

A

Information from the ventral stream.

304
Q

What kind of stimuli causes the Inferotemporal Cortex to fire?

A

Faces.

305
Q

What can happen to the response of neurons in the Inferotemporal Cortex after multiple presentations of faces?

A

They can change and acquire stimulus selectivity.

306
Q

Which brain area communicates with the cortex to consolidate memories, including area IT?

A

Hippocampus.

307
Q

What is distributed memory?

A

Representation of a single memory stored in a population of neurons, not a single neuron.

308
Q

How is memory stored in distributed memory?

A

Changes in synaptic strength in a population of neurons.

309
Q

Explain the concept of graceful degradation in distributed memory.

A

It ensures that the loss of a single neuron does not result in the complete loss of a specific memory, as memory representations blend together and get confused for each other as neurons are removed.

310
Q

What are the two sheets of neurons in the hippocampus?

A

Dentate gyrus and Ammon’s horn.

311
Q

What are the four divisions of Ammon’s horn?

A

Including CA1 and CA3.

312
Q

What is the major input to the hippocampus?

A

Entorhinal cortex.

313
Q

Where does the entorhinal cortex send perforant path axons?

A

To the dentate gyrus.

314
Q

Which region sends mossy fiber axons to CA3?

A

Dentate gyrus.

315
Q

Which region sends Schaffer collateral axons to CA1?

A

CA3.

316
Q

What has been studied with Schaffer collateral synapses on CA1?

A

LTP (Long-Term Potentiation).

317
Q

What is Long-Term Potentiation (LTP)?

A

Long-lasting enhancement of synaptic transmission effectiveness.

318
Q

How is LTP measured?

A

As elevated EPSP compared to measurements in a baseline period.

319
Q

At what level does LTP operate?

A

At the level of individual synapse.

320
Q

How is LTP induced experimentally?

A

By tetanus (brief burst of high-frequency stimulation).

321
Q

What can lead to very prolonged LTP?

A

A brief tetanus (less than a minute).

322
Q

What is the first characteristic of LTP?

A

Specificity

323
Q

How are individual synapses strengthened via LTP?

A

Through specificity

324
Q

What are the two types of glutamate receptors mentioned?

A

AMPA receptor and NMDA receptor.

325
Q

What ions does the AMPA receptor conduct?

A

Only Na+ ions.

326
Q

What ions does the NMDA receptor conduct?

A

Na+ and Ca++ ions.

327
Q

What is the main requirement for ion conduction in the AMPA receptor?

A

Glutamate binding.

328
Q

What are the two requirements for ion conduction in the NMDA receptor?

A

Glutamate binding and postsynaptic membrane depolarization.

329
Q

Why is the NMDA receptor called a coincidence detector?

A

Because it signals when the presynaptic and postsynaptic elements are active simultaneously.

330
Q

What is the impact of elevated postsynaptic Ca++ on LTP?

A

It is important for LTP as it can be prevented if NMDA receptors are inhibited or if the rise in Ca++ is prevented by injection of a Ca++ chelator into the postsynaptic neuron.

331
Q

What are the two kinases activated by the rise in postsynaptic [Ca++]?

A

Protein kinase C and calcium-calmodulin-dependent protein kinase II (CAMKII).

332
Q

What are the two effects of the activation of these kinases?

A

Phosphorylation of existing AMPA receptors to increase their effectiveness and insertion of entirely new AMPA receptors into the membrane, which can change synaptic structure.

333
Q

What happens when Ca++ activates kinases through NMDA receptors?

A

Phosphorylation of AMPA receptors leading to more effective ionic conductance and addition of new AMPA receptors to the postsynaptic membrane.

334
Q

Who discovered the BCM Theory?

A

Bienenstock, Cooper, and Munro.

335
Q

What does the BCM Theory account for?

A

Bidirectional change in synaptic strength.

336
Q

When does synaptic weakening occur according to the BCM Theory?

A

When synapses are active at the same time as weak depolarization of the postsynaptic neuron.

337
Q

What is the end result of synaptic weakening according to the BCM Theory?

A

Long-term depression (LTD).

338
Q

What experimental evidence supports the BCM Theory?

A

Low-frequency tetanic stimulation causing weak depolarization of postsynaptic neuron.

339
Q

What happens when synaptic transmission occurs at the same time as strong depolarization of the postsynaptic neuron according to the BCM Theory?

A

Long-term potentiation (LTP) of the active synapses.

340
Q

What happens when synaptic transmission occurs at the same time as weak depolarization of the postsynaptic neuron according to the BCM Theory?

A

Long-term depression (LTD) of the active synapses.

341
Q

What is the abbreviation for this synaptic phenomenon?

A

LTD

342
Q

What happens to the magnitude of the EPSP during LTD?

A

Prolonged decrease compared to a measured baseline

343
Q

Is LTD input-specific or non-specific?

A

Input-specific

344
Q

How is LTD different from LTP in terms of input specificity?

A

Only the stimulated synapse experiences LTD

345
Q

What causes LTD (Long-Term Depression)?

A

Weak NMDA receptor activation and low Ca++ entry.

346
Q

What does low/modest prolonged Ca++ activation lead to in LTD?

A

Activation of protein phosphatases instead of kinases.

347
Q

What are the two effects of low/modest prolonged Ca++ activation in LTD?

A

Dephosphorylation of AMPA receptors and internalization of AMPA receptors at the synapse.

348
Q

What is associated with spine shrinkage in LTD?

A

Internalization of AMPA receptors at the synapse.

349
Q

Does LTD still require NMDA activation?

A

Yes, but at a low level instead of a high one.

350
Q

What impact does the activation of NMDA receptor have on synaptic strength?

A

It impacts changes in synaptic strength.

351
Q

What type of synaptic modification is associated with weak NMDA activation?

A

Long-term depression (LTD).

352
Q

What type of synaptic modification is associated with strong NMDA activation?

A

Long-term potentiation (LTP).

353
Q

Where is synaptic plasticity found, in addition to the CA1 of the hippocampus?

A

Areas in the neocortex such as area IT (memories of familiar faces stored).

354
Q

What does the BCM theory posit about synaptic modification?

A

It posits that bidirectional modification of synapses suggests that they can store memories.

355
Q

What evidence supports the link between plasticity and memory?

A

Stimulation of area IT tissue produces similar LTD → LTP pattern as NMDA activation.

356
Q

Why can’t phosphorylation alone explain memory consolidation?

A

Phosphorylation is not permanent as phosphate groups are eventually removed.

357
Q

What evidence suggests a mechanism to account for the impermanence of phosphorylation in memory consolidation?

A

Some evidence suggests that protein kinases can be made persistently active.

358
Q

What is required for the consolidation of long-term memories?

A

New protein synthesis.

359
Q

What is inhibited in the case of inhibitory avoidance memory?

A

Avoidance behavior.

360
Q

How is the strength of memory quantified?

A

By the amount of latency.

361
Q

What happens to the latency in mice when protein synthesis is inhibited?

A

It decreases, indicating that the memory was not consolidated into long-term memory.

362
Q

What process consolidates Long-Term Potentiation (LTP)?

A

New protein synthesis.

363
Q

What happens if protein synthesis is inhibited during inhibitory avoidance training?

A

Rats forget avoidance behavior.

364
Q

What is the effect of inhibiting protein synthesis during tetanus or training on LTP?

A

Typically has no effect on LTP.

365
Q

What does inhibiting protein synthesis during tetanus or training affect?

A

Consolidation.

366
Q

What happens to memories as the interval between training and injection of synthesis inhibitor increases?

A

They become more resistant to the injection of synthesis inhibitor.

367
Q

How is protein synthesis triggered in the context of long-term potentiation (LTP)?

A

Stronger stimulation, such as 1000 Hz, triggers more synapses to activate, leading to long-lasting LTP by stimulating new protein synthesis.

368
Q

What is synaptic tagging and capture?

A

A phenomenon where weakly stimulated synaptic input captures newly-synthesized proteins caused by a strongly stimulated input to consolidate its own LTP.

369
Q

What are the key players in synaptic tagging and capture?

A

Protein synthesis, phosphorylation of protein by kinases like CaMKII and PKM zeta.

370
Q

What role does salience play in memory consolidation?

A

Salience is registered by activation neuromodulatory systems that have a broad reach, act through G protein-coupled receptors, and can cause biochemical changes, including new gene expression, which leads to synaptic protein synthesis and consolidation.

371
Q

What is the role of AMPAkines or D-cycloserine in memory enhancement?

A

Enhance initial synaptic modification (experience → STM).

372
Q

What is the role of Levo-amphetamines and bifunctional stigmines in memory enhancement?

A

Enhance neuromodulatory systems during adaptive demand for consolidation.

373
Q

How do PDE inhibitors contribute to memory enhancement?

A

Enhance new gene expression occurring during consolidation.

374
Q

What does an EEG measure?

A

Brain rhythms.

375
Q

What picks up the electrical signals in an EEG?

A

Scalp electrodes.

376
Q

Where do electrodes record the signals from in an EEG?

A

Scalp, skull, and meninges.

377
Q

What primarily generates the EEG signals?

A

Pyramidal cells with dendrites extending across cortical layers.

378
Q

How is the activity represented in an EEG?

A

As negative.

379
Q

Why does the activity appear negative in an EEG?

A

Due to the rush of sodium into depolarizing cells, making the extracellular fluid more negative.

380
Q

What type of brain activity is associated with a low-frequency and large-amplitude EEG?

A

Relaxed or sleeping brain.

381
Q

What type of brain activity is associated with a high-frequency and low-amplitude EEG?

A

Active brain.

382
Q

What type of activity is reflected in an EEG?

A

Coordinated activity.

383
Q

What type of brain waves have high amplitude and low frequency?

A

Synchronized neural activity.

384
Q

When are synchronized neural activities commonly observed?

A

During sleeping.

385
Q

What type of brain waves have low amplitude and high frequency?

A

Desynchronized neural activity.

386
Q

When are desynchronized neural activities commonly observed?

A

During active/awake brain and REM sleep.

387
Q

What are pacemaker neurons characterized by?

A

Multiple types of VG channels that allow neurons to fire APs in self-sustaining rhythmic bursts.

388
Q

How are pacemakers synchronized?

A

Pacemakers interact and synchronize themselves.

389
Q

What is the role of thalamic neurons in synchronizing cortical neurons?

A

Thalamic neurons synchronize cortical neurons.

390
Q

What are oscillator circuits responsible for?

A

Generating rhythmic patterns using the aggregate behavior of neurons that collectively excite or inhibit each other.

391
Q

How are oscillator circuits synchronized?

A

Synchronized by each other.

392
Q

What leads to synchronous rhythms in oscillator circuits?

A

Alternating pattern of excitation and inhibition leads to synchronous rhythms.

393
Q

What is a seizure?

A

Abnormal synchronized brain activity.

394
Q

What percentage of people experience a seizure in their lifetime?

A

Approximately 5-10%.

395
Q

What is epilepsy?

A

Recurrent seizures.

396
Q

What percentage of people have epilepsy?

A

About 1%.

397
Q

Is epilepsy a disease or a symptom?

A

Disease.

398
Q

Name some potential causes of seizures and epilepsy.

A

Head trauma, tumors, stroke, Alzheimer’s, genetic mutations, drug withdrawal, convulsants.

399
Q

What are some treatments for seizures and epilepsy?

A

Anticonvulsive drugs, surgical resection.

400
Q

What are the characteristics of generalized seizures?

A

Involves all of the brain, patient generally loses consciousness, and may include tonic-clonic seizures (grand mal, motor) and absence seizure (petite mal seizure/non-motor).

401
Q

What are the characteristics of tonic-clonic seizures?

A

Sudden onset + offset, all brain areas affected at once, recovery takes minutes to hours, patient falls, and muscles spasm.

402
Q

What are the characteristics of absence seizures?

A

Patient is completely dissociated from everything around them, with only subtle motor signs.

403
Q

What are the characteristics of partial seizures?

A

Affects a small portion of the brain or one hemisphere, often preceded by an ‘aura’, and may be simple or complex.

404
Q

What are the general symptoms of seizures?

A

Muscle jerk, distortions/hallucinations, pupil dilation/breathing and heart rate changes, fear/anxiety.

405
Q

What is the effect of a ketogenic (high fat) diet on neuron excitability?

A

Decrease in neuron excitability.

406
Q

How do anticonvulsants shift the balance to help with epilepsy?

A

By blocking Na+ or Ca2+ channels, blocking glutamate receptors, or inhibiting metabolism or increasing GABA release.

407
Q

What percentage of people are helped by anticonvulsant drugs for epilepsy?

A

■ (two-thirds).

408
Q

What are the alternative treatments if anticonvulsant drugs are not effective for epilepsy?

A

DBS (deep brain stimulation) or TMS (transcranial magnetic stimulation).

409
Q

What is the last resort treatment for severe epilepsy if other methods are not effective?

A

Surgery.

410
Q

What does NREM stand for?

A

Non-Rapid Eye Movement.

411
Q

What percentage of sleep does NREM constitute?

A

75%.

412
Q

What is the percentage of sleep that REM constitutes?

A

25%.

413
Q

What kind of activity increases during NREM sleep?

A

Increased parasympathetic activity.

414
Q

What happens to the temperature and energy consumption of the body during NREM sleep?

A

They are lowered.

415
Q

What kind of activity increases during REM sleep?

A

Increased sympathetic activity.

416
Q

How many stages make up NREM sleep?

A

3-4 stages.

417
Q

What is the name for the phenomenon in which the EEG looks awake during REM sleep?

A

Paradoxical sleep.

418
Q

What kind of eye movements are seen in NREM sleep?

A

Slow or no eye movements.

419
Q

What kind of eye movements are seen in REM sleep?

A

Rapid eye movements.

420
Q

What does the EEG show during NREM sleep?

A

Low frequency and high amplitude activity.

421
Q

What is the approximate duration of a sleep cycle?

A

About every 90 minutes.

422
Q

What are the two main types of sleep within a sleep cycle?

A

Non-REM and REM sleep.

423
Q

In which stage of sleep do you first enter when sleeping?

A

NREM stage 1.

424
Q

What characterizes the sleep cycles as ultradian rhythms?

A

They repeat faster than circadian rhythms.

425
Q

At what point during the night does 50% of REM sleep occur?

A

In the last 1/3 of the night.

426
Q

How many cycles of sleep do individuals typically experience per night?

A

5-7 cycles.

427
Q

What is the duration of the first REM (Rapid Eye Movement) sleep?

A

10 minutes/short.

428
Q

What is the duration of the longest stretches of REM sleep?

A

60-90 minutes.

429
Q

What happens when subjects are prevented from reaching REM sleep?

A

They experience REM rebound.

430
Q

What occurs when individuals are allowed to sleep uninterrupted after being deprived of REM sleep?

A

They spend more time in REM sleep.

431
Q

What are the symptoms sleep-deprived rats show?

A

Weight loss, disruption of temperature regulation, dysregulated immune system, eventual death in 2-3 weeks.

432
Q

What is the link between most symptoms and the hypothalamus?

A

The symptoms are linked to the hypothalamus.

433
Q

What were the effects on Randy Gardner after staying awake for 11 days?

A

Fatigue, irritability, tremors, motor problems, nausea, memory difficulty, speech problems, hallucinations.

434
Q

What happened to Randy Gardner after catching up on rest?

A

Back to normal, but experienced insomnia throughout life.

435
Q

What was the result of the experiment on memory and sleep?

A

Hippocampus activity increased after sleep, and sleep improved performance.

436
Q

What is the advice given regarding sleep and finals?

A

The advice is to ensure proper sleep before finals.

437
Q

What are the physiological effects of 5 hours of sleep instead of 8?

A

Higher heart rate, blood pressure, and cortisol levels (stress hormone), leading to increased heart attack risk.

438
Q

How does sleep deprivation affect hunger and weight?

A

Leptin decreases and ghrelin increases, leading to an increase in eating behavior by about 300 calories per day.

439
Q

What hormonal changes occur due to inadequate sleep?

A

Reduced testosterone in men and decreased levels of progesterone, estrogen, and FRH in women, leading to lower fertility. The drop in testosterone is equivalent to aging men 10-15 years.

440
Q

What impact does inadequate sleep have on glucose absorption?

A

Humans with no sign of diabetes put on a low sleep regimen had 40% lower glucose absorption and a significant number became pre-diabetic.

441
Q

What are the long-term effects of medium sleep deprivation?

A

Elevated blood pressure, stroke, depression, obesity, Alzheimer’s, and type II Diabetes.

442
Q

What is the name of the rare genetic disease that affects 40 families in the world?

A

Fatal Familial Insomnia

443
Q

What is the cause of Fatal Familial Insomnia?

A

Misfolded prion protein

444
Q

Where in the brain does Fatal Familial Insomnia cause lesions?

A

Especially in the thalamus

445
Q

At what age does the onset of symptoms typically occur in Fatal Familial Insomnia?

A

50s

446
Q

What are the common symptoms of Fatal Familial Insomnia?

A

Insomnia, weight loss, confusion, dementia, motor difficulties

447
Q

What is the typical outcome for individuals with Fatal Familial Insomnia?

A

Inability to sleep, walk, or talk, leading to death 1-3 years after diagnosis

448
Q

What is sleep?

A

A readily reversible state of reduced responsiveness to, and interaction with, the environment resulting in rapidly reversible loss of consciousness.

449
Q

Is sleep universal?

A

Yes, all animals sleep.

450
Q

Name one reason for why we sleep.

A

To conserve energy at night when not doing anything.

451
Q

What is memory consolidation?

A

The process of strengthening and stabilizing memories during sleep.

452
Q

How does sleep help in disease prevention and maintaining body homeostasis?

A

It helps prevent diseases like Alzheimer’s disease and obesity, and maintains overall body balance.

453
Q

What is the relationship between replay and spatial planning for navigation?

A

Replay underlies spatial planning for navigation towards a goal.

454
Q

How does more replays correlate with performance?

A

More replays shown to correlate with better performance.

455
Q

What is the effect of electric interruption on rat’s acquisition of spatial memory task?

A

Electric interruption reduces the rate at which rats acquired a spatial memory task.

456
Q

What is the impact of sleep on hippocampus activity and performance?

A

Sleep allows for greater hippocampus activity during navigation and leads to better performance after sleep.

457
Q

According to the Sleep-Replay Consolidation Hypothesis, what does sleep facilitate?

A

Sleep facilitates memory consolidation through replay.

458
Q

What does the lymphatic system remove from the body?

A

Excess plasma, dead blood cells, and waste.

459
Q

What does the glymphatic system consist of?

A

Glia and lymphatic.

460
Q

When is the glymphatic system mainly active?

A

During non-REM sleep.

461
Q

What does the glymphatic system help in preventing?

A

Neurological diseases.

462
Q

What happens in animal studies when the glymphatic system is impeded?

A

More aggregation and cognitive decline.

463
Q

Why do older people tend to have more build-up of toxins in the brain?

A

Due to reduced glymphatic system activity.

464
Q

What is adenosine?

A

An endogenous sleep factor.

465
Q

What causes the build-up of adenosine in the body?

A

Breakdown of ATP.

466
Q

What happens to adenosine levels during the day while awake?

A

They increase.

467
Q

What happens to adenosine levels during sleep?

A

They decrease.

468
Q

What effect does binding adenosine to adenosine receptors have on neurons?

A

Hyperpolarization (quieting effect).

469
Q

What modulatory systems involved in wakefulness may be inhibited by adenosine?

A

NE (Norepinephrine), 5-HT (Serotonin), ACh (Acetylcholine).

470
Q

What does the concentration of adenosine in the body indicate?

A

Sleep pressure.

471
Q

What is the effect of adenosine agonists?

A

They promote sleep.

472
Q

What does caffeine do to adenosine receptors?

A

Blocks them.

473
Q

When is the peak caffeine effect after ingestion?

A

30 minutes.

474
Q

How long is the half-life of caffeine?

A

5-7 hours.

475
Q

Does caffeine affect the production of adenosine?

A

No.

476
Q

What happens once caffeine clears out from the body?

A

Accumulated adenosine comes back in and binds to receptors, causing a ‘caffeine crash’.

477
Q

What gland releases melatonin?

A

Pineal gland.

478
Q

When does melatonin release start and peak?

A

Starts around dusk and peaks at around 4 AM.

479
Q

How does melatonin affect blood flow and core temperature?

A

Increases blood flow, especially to limbs/hands, and causes a drop in core temperature.

480
Q

What is the relationship between melatonin release and core body temperature?

A

Inversely related.

481
Q

What does melatonin indicate by its release?

A

That it’s dark.

482
Q

What does melatonin regulate in relation to sleep?

A

Sleep timing, not sleep production.

483
Q

What is the most effective melatonin dose?

A

Between 0.5-5 mg.

484
Q

What is melatonin a derivative of?

A

Tryptophan.

485
Q

What is the primary visual cortex’s activity level during awake and REM sleep?

A

Equally active.

486
Q

How does V1 activity in REM compare to non-REM sleep?

A

V1 is less active in REM than NREM.

487
Q

What is associated with high activity in higher visual areas with no corresponding increase in V1 activity?

A

REM sleep.

488
Q

What does high activity in higher visual areas during REM sleep suggest about dreams?

A

It suggests that dreams may be the result of the brain putting together random brain activity.

489
Q

What is the cause of REM Sleep Behavior Disorder?

A

Loss of REM atonia.

490
Q

What happens to muscles in REM Sleep Behavior Disorder?

A

They are not inhibited, leading to movement during dreams.

491
Q

Who is most commonly affected by REM Sleep Behavior Disorder?

A

Older men (90% of affected people).

492
Q

What percentage of people with REM Sleep Behavior Disorder may develop Parkinson’s disease?

A

40%.

493
Q

What is the function of the hypocretin/orexin system?

A

Associated with wakefulness.

494
Q

What are the REM sleep attacks characterized by in narcolepsy?

A

Immediate REM sleep instead of slow wave sleep first.

495
Q

What is cataplexy in the context of narcolepsy?

A

Sudden atonia triggered by intense emotions, leading to muscle weakness and slurred speech.

496
Q

What is sleep paralysis in the context of narcolepsy?

A

Atonia extends into wakefulness.

497
Q

What request is made to everyone regarding discussions on mental illness?

A

To be mindful and respectful towards others.

498
Q

What assurance is given to the students regarding the support system?

A

TAs and professors are available for support.

499
Q

What potential pitfall is mentioned when discussing mental illness from a neuroscientist’s perspective?

A

Generalized data may not encompass every individual experience.

500
Q

What incorrect notion has prevailed for a long time regarding conditions affecting the mind?

A

That they don’t have a biological basis.

NEUR 10 (5 decks)

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