Unit 5 Flashcards

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1
Q

Arousal

A

the physiological and psychological state of being awoken or of sensory organs stimulated to a point of perception. It involves activation of the ascending reticular activating system (RAS) in the brain (which mediates wakefulness and relays arousal info), the autonomic nervous system, and the endocrine system, leading to increased heart rate and blood pressure and a condition of sensory alertness, mobility, and readiness to respond.

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2
Q

Increased arousal

A

Highly active, alert, ready to respond to changes in the environment, prep to fight/flee

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3
Q

Decreased arousal

A

Sleepy, lethargic, difficulty concentrating

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4
Q

How is arousal regulated

A

Several NT and neuromodulators are produced in specific groups of cell bodies (nuclei) in brainstem and surrounding areas
These nuclei project brain wide, all over the CNS, PNS,ANS to modulate arousal

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5
Q

Neurotransmitter

A

 signaling molecule released by a neuron, used to communicate with another neuron across a synapse (often use ionotropic receptors)
 Released from presynaptic neuron moving across the cleft of post synaptic neuron
 Cell to cell communication

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6
Q

Criteria to be a neurotransmitter

A

1) The substances must be present within the presynaptic neuron
2) The substance must be released in response to presynaptic depolarization (AP) and the released must be Ca dependent (involves influx of calcium)
3) specific receptors for the substance must be present on the postsynaptic cell
(Punitive NT do 2 out of the 3 things)

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7
Q

Neurotransmitter types

A

1) small molecule NT
2) peptide NT (string of animo acids put together)
3) Unconventional NTs (not released the same as NT)

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8
Q

Neuromodulator

A

 signaling molecule released by a neuron that potentiates or inhibits the transmission of a nerve impulse in a group of neurons but is not the actual means of transmission itself (often use metabotropic receptors; ex: axo-axonic synapses)
 Causing an influence to increase/decrease transmission at the synaptic cleft
 Not acting as chemical signaling itself

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9
Q

Types of synapses: Axo Axonic

A

1) Pain neuron releases NT called substance P to signal injury
2) Activity along pain neuron activates endorphin cells
3) In turn, endorphin cells release endogenous opioids as a modulator onto terminal of pain axon to turn off pain signal

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10
Q

Hormone

A

signaling molecule produced by glands in multicellular organisms, that are transported by the circulatory system (blood supply) to target distant organs to regulate physiology and behavior (neurohormone = in brain)
Chemicals that act at a greater distance away from where they’re produced causing a change/regulating behavior

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11
Q

Reticular formation

A

 Contains various interconnected nuclei along with numerous ascending and descending tracts located throughout the brainstem
 Nuclei involved in NT production
 Ascending tracts integral to arousal and consciousness
 to the cortex in the ascending reticular activating system (ARAS or RAS)
 Descending tracts involved in modulating sensory and motor functions
 descending pathways to the spinal cord via the reticulospinal tracts
 Nuclei associated with the cranial nerves
 Fibers give the region a net like appearance (reticular means net-like)
 Was thought to lack organization, but is actually highly organized, just very intricate and complex

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12
Q

Reticular formation NT

A

 FT neuronal populations have extensive connections throughout the central nervous system and are involved in the regulation/modulation of activity throughout the brain
 Acetylcholine: pedunculopontine nucleus (PPM) & laterodorsal tegmental nucleus (LDT)
 Norepinephrine: locus coeruleus (LC)
 Dopamine: ventral tegmental area (VTA)
 Serotonin: raphe nuclei (RN)
 Histamine: Hypothalamus (posterior: TMN)
 Orexin: Hypothalamus (lateral)
 GABA & Ach: Basal forebrain

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13
Q

Reticular formation terminology

A

 ARAS=RAS=ascending RF
 ARAS/RAS also may refer to entire RF
 Nonspecific sensory projection system throughout RAS relays arousal

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14
Q

RAS: Ascending reticular activating system

A

composed of several groups of cells that produce neurotransmitters; these neuronal populations have extensive connections throughout the central nervous system and are involved in the regulation of activity throughout the brain. ‘Nonspecific’ sensory projection system through RAS relays ‘arousal’ information via the thalamus to cortex, where this info meets up with primary sensory specific inputs to produce conscious perception of a sensory event. (See associated neurotransmitter charts for breakdown of specific NT, brain regions, and roles.) Functions in parallel with the flow of specific sensory input through the primary sensory thalamic nuclei that is then relayed to the cortex
 Ascending pathways controlling arousal, attention, sleep cycle
 Includes numerous nuclei and NTs/NMs
 Temporal summation in cortex of nonspecific inputs with primary sensory specific inputs > conscious perception of a sensory event

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15
Q

Reticulospinal tracts

A

Descending pathway that arise from the RF that influences spinal motor neurons based on changes in arousal. Motor control includes voluntary and reflexive movements (esp. stereotyped movements like stepping), modulation of muscle tone to either aid or inhibit movement, postural control, and autonomic functions.

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16
Q

Pain pathway

A

descending pathway that arise from the raphe nuclei of the RF to the dorsal horn of spinal cord. The nerve fibers in these pathways act in the spinal cord to block/inhibit the transmission of some pain signals to the brain, especially during traumatic events.
(we’re able to ignore a painful injury in order to run away)

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17
Q

Cranial nerves

A

a set of 12 paired nerves that arise directly from the brain. The first two nerves (olfactory and optic) arise from the cerebrum, whereas the remaining ten emerge from the brain stem. RF circuitry helps coordinate activity of neurons in these CN nuclei, and thus is involved in the regulation of simple motor behaviors, including eye movements.

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18
Q

External influences on arousal

A

 Diet (Adenosine) provides precursors for making NT/NM/Hormones can effect lv. of NT
 Drugs directly affect synapses
- Mimics NT/NM at receptor
- Changes NT/NM amount in synapse (reuptake changes)
 Trauma (Mild, severe, more severe damage)
- Damaged RF interrupts normal arousal circuitry

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19
Q

Diet effect on arousal

A

 Provides precursors for NTs/NMs/Hormones.
 Increases intake of a particular type of amino acid
 Increases production of related NT
 Example: amino acid tryptophan from food like turkey is a precursor for serotonin, which itself is a precursor for melatonin = makes us sleepy.

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20
Q

Adenosine

A

a naturally occurring purine nucleoside that forms from the breakdown of adenosine triphosphate (ATP). It is thus a metabolic that builds up in cells while we are awake.

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21
Q

Drugs effect on arousal

A

Directly affect synapses by either mimicking the NT/NM at the receptor or by changing the NT/NM amount within the synaptic cleft (e.g., reuptake changes). Example: caffeine blocks adenosine inhibition of acetylcholine, doesn’t inhibit ACh cells which raises arousal, suppressing GABA, keeping you awake

22
Q

Trauma effect on arousal

A

Damaged RF interrupts normal arousal circuitry
 Mild damage: fatigue, changes in sex arousal, disrupted sleep patterns
 Severe damage: coma or vegetative state from inhibited ability to wake up
 More severe: fatal

23
Q

Sleep

A

a naturally recurring state of mind and body, characterized by altered consciousness, relatively inhibited sensory activity, reduced muscle activity and inhibition of nearly all voluntary muscles during rapid eye movement (REM) sleep, and reduced interactions with surroundings. It is distinguished from wakefulness by a decreased ability to react to stimuli, but more reactive than a coma or disorders of consciousness, with sleep displaying very different and active brain patterns.
 Consists of multiple repeating phases
 Non-REM sleep (several stage)
 REM sleep (rapid eye movemement)
 Dreams occur in this phase

24
Q

EEG

A

 Electroencephalogram
 Gross average change in electrical potentials in area under electrode
 Amplitude = voltage (how large the signal is)
 Frequency = Cycles per second (Hz) (how rapidly signals are changing)

25
Q

Sleep Stages

A

Wake – Active, Wake - Relaxed, NREM Stage 1, NREM Stage 2, NREM Stages 3 & 4, Rapid eye movement (REM)

26
Q

Wake – Active

A

EEG is dominated by low-voltage fast-activity in the beta (~16–30 Hz) and gamma (>30 Hz); active muscles
 Small hyper frequencies happen

27
Q

Wake - Relaxed

A

Alpha waves (8–12 Hz) – from synchronous electrical activity of thalamic pacemaker cells
 More regular pattern of osculation, sign that we are relaxing

28
Q

NREM Stage 1

A

transitional role, 1 to 7 minutes, easily interrupted by a disruptive noise; low-voltage, mixed-frequency waves with theta waves (4-7Hz)
 Lightest stage of sleep, loss of alpha waves

29
Q

NREM Stage 2

A

10 to 25 minutes or more in later cycles; requires more intense stimuli to wake; has a further decrease in frequency and increase in amplitude, together with intermittent high-frequency spike clusters called sleep spindles and low-frequency/high amplitude K-complexes
 Memory consolidations

30
Q

NREM Stages 3 & 4:

A

(now considered one deep-sleep stage) low frequency (1–4 Hz), high-amplitude delta waves = slow wave sleep
Mostly considered to be a single stage of deep sleep
 Increase amplitude and decrease frequency

31
Q

Rapid eye movement (REM) sleep

A

Also called paradoxical sleep
EEG desynchronized (low-voltage, mixed/high-frequency) EEG like wake, includes sawtooth waves, muscle atonia (genitals active but muscles are paralyzed) with variable heart rate and breathing and bursts of rapid eye movements; primary dreaming stage

32
Q

EEG synchronization

A

 Goes from desynchronized (awake to stage 2)
 Highly active and uncoordinated
 Unregulated
 Synchronized (stage 2 &3)
 Desynchronized (REM)

33
Q

Physiological changes in sleep

A

 Interim between consciousness and sleep
 Move to stage 2 after 5-15 min
 Heart rate slows, brain does less complicated tasks
 After another 15 minutes move into non-REM sleep, the Delta stage
 Body makes repairs
 Body temperature and BP decreases
 Move into REM sleep approx. 90 minutes after first feeling sleepy
 Increase eye movement, heart rate, breathing, BP and temperatures

34
Q

How long does a sleep cycle last

A

90 minutes

35
Q

Sleep Switch: VLPO

A

 Ventral lateral preoptic area

36
Q

Functions of Sleep and REM

A

Sleep is restorative
 Engage in critical metabolic processes, process waste, etc
REM may have cognitive/psychological advantages
 REM deprived have poorer memory for previous days learning
 Dreams may be involved in helping to resolve psychological conflicts
Slow-wave/REM cycle may also involve temperature regulation
 Brain cools down during slow wave sleep
 REM warms brain (cooling can help with cleaning process)
- Enzymes may be efficient at different temperatures

37
Q

Sleep spindles

A

8–12 Hz EEG waves that generally last 1 or 2 seconds and arise as a result of interactions between thalamic and cortical neurons; may be important for memory consolidation

38
Q

K-complexes

A

low frequency, high amplitude: largest event in healthy human EEG; two proposed functions: (1) suppressing cortical arousal in response to stimuli that the sleeping brain evaluates not to signal danger; and/or (2) aiding sleep-based memory consolidation.

39
Q

Atonia

A

a condition in which a muscle has lost its strength; associated here with the lack of muscle movements in REM sleep.

40
Q

Hypnogram

A

is a form of polysomnography (EEG sleep measurement); it is a graph that represents the stages of sleep as a function of time.

41
Q

Pontogeniculo-Occipital Waves

A

the EEG signature of REM sleep. Neural activity spreads from pons (P) to the lateral geniculate nucleus (G) of the thalamus to the visual cortex in the occipital lobe (O) and convey information about upcoming eye movements.

42
Q

Sleep deprivation

A

short-term and long-term periods of sleep deprivation cause numerous detrimental cognitive and physiological effects

43
Q

Sleep deprivation short term effects

A

 Increased tolerance of risk
 Decline in working memory
 Decreased psychomotor performance
 Increased error in commission and omission
 Increased incidence of microsleeps
 Impaired performance on attention intensive tasks
 Increased distractibility

44
Q

Sleep deprivation long term effects

A

Increased risk of
 Hypertension, heart attack/stroke, weight gain/obesity, diabetes, depression/anxiety, faulty brain function, memory loss, immune system deficiency, decreased fertility/sex issues, psychiatric/mood disorders

45
Q

Effect of oscillation and fluid during sleep

A

 In NREM: low freq oscillations in neural activity support memory consolidation and neuronal computation
 Sleep is also associated with increased interstitial fluid volume and clearance of metabolic waste products
 Slow oscillation neuronal activity leads to oscillations in blood volume, drawing cerebrospinal fluid into and out of the brain facilitating the removal of potentially damaging waste production

46
Q

Circadian rhythm

A

Physical, mental, and behavioral changes that follow a daily cycle
Clock maintains a close to 24 hour rhythm of activity
Genetically controlled and driven by daylight cycles
Cycle tends to drift in the absence of night/day cues

47
Q

Biological clocks

A

An organism’s innate timing device composed of specific intracellular proteins that are found in nearly every tissue and organ

48
Q

Master clock

A

coordinates all the biological clocks in vertebrates, composed of about 20,000 neurons that form the suprachiasmatic nucleus (SCN)

49
Q

Pineal gland

A

a small endocrine gland in the brain of most vertebrates that produces melatonin, a serotonin-derived hormone which modulates sleep patterns in both circadian and seasonal cycles

50
Q

Retinohypothalamic tract (RHT)

A

a photic neural input pathway involved in the circadian rhythms of mammals. The origin of the retinohypothalamic tract is the intrinsically photosensitive retinal ganglion cells (ipRGC), which contain the photopigment melanopsin. The axons of the ipRGCs belonging to the retinohypothalamic tract project directly, monosynaptically, to the suprachiasmatic nuclei (SCN) via the optic nerve.
 Specialized visual receptors react to ambient light levels
 These ganglions send their axons to the SCN of hypothalamus
 SCN informs pineal gland, so daylight decreases/nightfall increases its release of melatonin
 Pineal gland releases melatonin inhibiting SCN regulating its active/inactive cycle

51
Q

Jet lag

A

a temporary disorder of circadian rhythms that causes fatigue, insomnia and other symptoms as a result of air travel across time zones; Only occurs when flying East-West or West-East (not North-South): changing time zones. Treatments include bright morning light, daily activity, taking melatonin before sleep.