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Unit 2 Study Guide Questions Flashcards

(60 cards)

1
Q

physiological sensory processing, driven by sensation

A

Bottom-up processing

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2
Q

perception is driven by cognition

A

Top-down processing

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3
Q

Olfactory Transduction Pathway

A

inhale odorants –> bind to olfactory receptors (on cilia) –> trigger cell changes –> action potential down axon –> project info about pattern of activation to olfactory bulb –> bypasses thalamus –> some info goes to amygdala and hypocampus; some info goes to olfactory cortex where messages coded by location –> perceptions of different smells

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4
Q

Taste Transduction Pathway

A

tastants enter taste pores (taste bud openings) in oral cavity –> interact with taste receptors –> taste nerves on each side of tongue (chorda tympani, glossopharyngeal, greater superficial petrosal, superior pharyngeal) –> solitary nucleus (in brain stem) –> crosses over to other side of brain –> ** thalamus** –> gustatory cortex

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5
Q

What are the four taste nerves?

A
  • chorda tympani
  • glossopharyngeal
  • superior laryngeal
  • greater superficial petrosal
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6
Q

Vision Pathway

A

light hits pupil–> focused by lens and cornea onto –> rods and cones at back of retina –> reduces NT release, hyperpolarizes receptor –> passes through horizontal/bipolar/amacrine cells –> ganglion –> produce action potentials –> down axon via optic nerve –> leave eye through optic disk –> half of axons from each eye cross to other side of brain at optic chiasm –> portion of axons synapse in lateral geniculate nucleus (in thalamus); the rest go to primary visual cortex (in occipital lobe)

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7
Q

Auditory Pathway

A

Air to pinna –> through ear canal –> sound waves vibrate tympanic membrane –> ossicles (malleus, incus, stapes) amplify sound waves –> vibrations through cochlea’s fluid-filled tunnels (scala vestibule, scala tympani, cochlear duct) –> excite auditory nerve –> hair cells/receptors (receptors) move due to tectorial membrane (mechanical stimulation) –> ion channels open –> depolarization due to influx of K+ –> GLUT and ACh released to cochlear nerve afferents –> crosses midline at cochlear nucleus –> superior olivary nucleus –> inferior colliculus –> medial geniculate nucleus –> auditory cortex

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8
Q

Somatosensory pathway

A

Skin/touch receptors send action potentials –> unipolar axon (in dorsal root ganglion) –> enter spinal cord dorsal horn –> joins dorsal column in spine –> in medulla, periphery axon makes synapse to neuron of dorsal column nuclei –> sends axon across midline –> up to thalamus –> thalamus receives info contralaterally –> send info to primary somatosensory cortex

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9
Q

particular neurons that are, right from the outset, labeled for distinctive sensory experiences

A

labeled lines

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10
Q

region of space in which stimulus will alter neurons’ firing rate

A

receptive field (why photoreceptors only transmit info as light)

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11
Q

progressive loss of receptor response as stimulation is maintained

A

sensory adaptation

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12
Q

recept in which frequency of action potentials drops rapidly as stimulation is maintained

related to sensory adaptation

A

phasic receptor

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13
Q

receptor in which frequency of action potentials declines slowly or not at all as stimulation is maintained

A

tonic receptors

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14
Q

Pain Pathway

A

Damaged cells release substances –> stimulate nociceptors –> action potentials in periphery –> excite blood cells and mast cells/produce inflammation/ mast cells release histamine –> info from periphery enters through **dorsal root ** and synapses on neurons in dorsal horn –> pain fibers release glutamate NT and substance P neuromodulator in spinal cord –> then dorsal horn cells send info across midline and up to thalamus –> form spinothalamic system (different than somatosensory)

In spinothalamic pathway:

Nerve fibers send axons into dorsal horns of spinal cord  synapse on spinal interneurons  project across midline  ascend to thalamus

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15
Q

Hypovolemic thirst pathway

A

triggered when fluid volume is low

cardiac baroreceptors –> via vagus nerve –> brain stem –> Preoptic Area (POA)–>

kidney baroreceptors –> angiotensin II restricts blood vessels, reabsorbs water –> subfornical organ –> Preoptic Area (POA) –>

From Preoptic Area (POA) –> paraventricular and supraoptic nucleus –> vasopressin –> water conservation

From Preoptic Area (POA) –> Hypothalamic thirst network –> drinking behavior

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16
Q

Osmotic thirst pathway

A

triggered when solute concentration is too high

Osmosensory neurons in OVLT –> POA –>
- hypothalamic thirst pathway –> drinking behavior
- paraventricular and supraoptic nucleus –> vasopressin –> water conservation

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17
Q

Hunger hormones

A

leptin: in fat cells, provide info about long-term energy stores
ghrelin: in stomach; appetite stimulant
PYY3-36: in intestines; appetite suppressant
Cholecystokinin: in gut; acts on vagus nerve to inhibit appetite

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18
Q

When blood sugar is low, signals release of ——-

Explain cycle.

A

glucagon

glucodetectors in liver recognize low blood sugar –> signal *glucagon release from pancreas –> breaks down glycogen to glucose (glycogenolysis) –> released into circulatory system –> raises blood sugar

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19
Q

When blood sugar is high, signals release of ——-. Explain cycle.

A

insulin

glucodetectors in liver detect high blood sugar –> pancreas releases insulin –> helps get glucose into cells (acts as receptor “key”) AND signals liver to store excess glucose as glycogen (glycogenesis) –> lowers blood sugar in circulation

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20
Q

Thermoregulatory system for mammals

A

Thermoreceptors (TRP receptors) in skin, body core, hypothalamus detect temp and transmit info –> spinal cord –> brainstem –> hypothalamus

Body temp outside of set zone?
neural regions initiate physiological and behavioral responses to return temp to set zone

Physiological:
- increase temp: shiver, fluff out fur, decrease blood flow to skin
- decreatse temp: pant, sweat

Behavioral:
- increase or decrease temp: change exposure of body surface, change insulation, change surroundings

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21
Q

Hunger in hypothalamus (brain lesions)

A

VMH lesion: caused obesity due to increase in food intake; thought to be satiety center

LH lesions: caused weight loss due to refusal to eat; thought to be hunger center

BUT weight/eating went back to normal after awhile = neither VMH or LH is solely responsible for appetite signaling

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22
Q

Neither —– or —- is completely responsible for hunger or satiety.

A

LH or VMH

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23
Q

——– drive hypothalamic appetite control

How?

A

hormones

  • arcuate nucleus circuit integrates hormones
  • digestive organs and fat tissue release hormonal signals (energy balance)
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24
Q

What do neurotrophins do?

A
  • axon guidance
  • cell growth/survival
  • stimulate synaptogenesis
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25
How do bird brains change from breeding to non-breeding seasons?
HVC and Area X = important for male songbirds to learn/maintain mating longs In non-breeding season: - HVC neurons are less active In breeding season: - HVC neurons are more active and lead to larger HVC brain area during breeding When birds no longer need those songs, those areas die off -- neurogenesis is done better in these birds
26
CNS Divisions Early in Development
18 days: - 3 cell layers are ectoderm (skin, neural tissue), mesoderm (skeletal, cardia), endoderm (digesting, respiratory) - thickening of dorsal surface tissue (ectoderm) develops neural plate 20 days: - neural plate starts to fold in to make neural groove 22 days: - neural tube forms when neural groove closes (beginning of CNS) - neural tube = spinal cord - anterior end = brain 25 Days: - spinal cord and 3 brain divisions (forebrain, midbrain, hindbrain) are discernable 50 days: - from forebrain, 5 main divisions of brain become visible (cortex, basal ganglia, limbic, thalamus, hypothalamus) 100 Days: - cerebral hemispheres more developed - hindbrain is differentiated into cerebellum, pons, medulla
27
Explain divisions of CNS at 25 days.
**spinal cord** - formed from neural tube **forebrain**(front of neural tube) - Telencephalon = cerebral hemispheres - diencephalon = thalamus and hypothalamus **midbrain** - middle of neural tube **hindbrain** (rear of neural tube) - cerebellum, pons, medulla
28
What are the three classes of hormones?
proteins, amines (or peptides), steroids
29
Explain tropic hormones.
**Hypothalamus** *regulates release of **tropic hormones*** by *sending "**releasing hormones"*** to **anterior pituitary** --> **endocrine cells in pituitary** *make/release **tropic hormones*** --> hormones *enter circulation*, *affect endocrine organ secretion throughout body*
30
Explain gonadal hormone release.
hypothalamus controls gonadal hormone release via anterior pituitary (brain/pituitary regulation) **Hypothalamus** releases ***GnRH*** --> stimulates **anterior pituitary** to release ***tropic hormones*** (LH, FSH) --> enter **circulatory system** --> stimulate **gonads** to release ***gonadal hormones*** (testosterone, estrogen, progesterone)
31
Endocrine feedback loops work secrete hormones through either ----- regulation or ----- and ------- regulation hormone release in both systems is regulated by ------ cells
neuroendocrine
32
How are the two types of regulation in endocrine feedback loops different?
brain regulation -- biological response in target tissue tells hypothalamus to shut down brain and pituitary regulation -- circulating hormones in blood stream tell hypothalamus to shut down
33
Sexual Differentiation in Bird Brains
looks at organizational effects of steroid hormones Takeaways before looking at genetics: - Area X, HVC, and RA are all larger with more dense/larger neurons in males. These difference give us male vs. female brain. - significant differences in brain area size, neuron size, # of neuron - cannot create male-typic brain in female by altering hormones - estrogen masculinizes better than testosterone - blocking estrogen has no significant effect on masculizination of brain in males or females Genetic role (using gynandromorph) - test genetics + hormones - in gynandromorph, genetic sex differences only act on one side, hormones act on both sides - takeaway: **genetically male side is more "male typic" than female side. This means combo of genes/hormones (epigenetics) contribute to sex diff early in prenatal development**
34
Which gene is responsible for sex dimorphism in humans?
SRY
35
more than two sizes of gametes
anisogametic
36
only one gamete size
isogametic
37
two sizes of gametes but no sex dimorphisms (both males and females pass on both sizes of gametes)
monecious
38
no fusion of gametes or combination of chromosomes; genetic info directly passed on from parent
Asexual reproduction
39
some individuals have no gametes
infertility
40
XXY genes
Kleinfelter syndrome
41
X0 gene (no Y gene)
Turner syndrome
42
XX but male phenotype
De la Chappelle
43
XY but female phenotype, including fertility
Sawyer Syndrome
44
Why are multiples no longer an issue in in vitro fertilization?
PGT testing
45
Diurnal Cortisol release
Wake up: cortisol peaks throughout day: declines Evening: steady Next morning: peaks again, restarts
46
Diurnal testosterone release
- hormone levels vary within day - hormone amount changes with age - diurnal pattern of hormone changes with age (is less variable)
47
hormonal variation in women
Menstrual cycle = hormone release pattern over several weeks instead of one day Pregnancy = hormone release pattern over several months
48
Epigenetics and effect on development
Study #1: Black6 mice raised/carried by either Albino or Black6 mom; groups: - carried/raised by Albino mom: acted more like Albino male (explored less, slower mazes, more anxious) - carried by Albino mom but raised by Black6: acted somewhat like albino males (more anxious, slower at mazes) - carried by Black6 mom but raised by Albino: acted more like Black6 males but still were more anxious (like albino males) **Black6 male mice were genetically identical, so changes have to be due to prenatal environments and postnatal experiences. Type of mothering received influenced gene expression. ** Rodent Methylation study attentive rodent mother prevent methylation of stress hormone receptor gene in offspring (leading to lower stress hormones, low anxiety, high licking/grooming) --> female offspring grew to be attentive mothers themselves. Effect can be carried across generations. - in humans, same gene more likely to be methylated in suicide victims but only those who experienced child abuse
49
Sympathetic nervous system prompt you to rehydrate through ------- and -------.
thirst; salt hunger
50
What does aldosterone do?
in thirst system, signals **kidneys to conserve sodium** and aid in water retention
51
What does angiotensin II do?
increases blood pressure
52
Osmosensory neurons in OVLT relay information to -------------- and -----------------, and control rate at which posterior pituitary releases -------------.
supraoptic nucleus, paraventricular nucleus, vasopressin
53
What does vasopressin do in thirst pathway?
raises blood pressure (constricts blood vessels) and helps kidney absorb water
54
How does entrainment of SCN cells happen? | different than melatonin
- system is triggered by binding of glutamate receptors - retinal ganglion cells signal SCN (helps entrain/set clock)
55
How is melatonin production triggered?
SCN is entrained by light/dark and regulates pineal gland secretion of melatonin.
56
How is entrainment of SCN cell (partially) triggered?
retinal ganglion cells **(ipRCGs)** detect light --> glutamate released ---> binds to SCN neurons --> Per is stimulated Within cell: - Clock and cycle form a dimer and enter nucleus to - tell per and cry genes to make per and cry proteins - per and cry proteins bind and - inhibit Clock/Cycle dimer (negative feedback system) - Per/cry proteins break down over time - when Per/cry no longer active, Clock/Cycle dimer reforms and system restarts
57
What do ipRCGs do?
(intrinsically photosensitive ganglion cells) light stimulates ipRCGs --> signals SCN and other brain areas to send signals through rest of body works through retinohypothalamic pathway - ipRCGs (contain light-sensitve melanopsin) carry light from eye to SCN. **This is pathway for entraining to light or dark.** - light suppresses melatonin production; ipRCGs signal SCN to send message to pineal gland to produce melatonin
58
What parts of brain keep us awake?
- pontomesencephalon (projects to thalamus, basal forebrain, hypothalamus): releases ACh (wake) and glutamate (wake) - locus coeruleus (in pons) - typically dormant during sleep but releases GABA and glycine which inhibit movement during REM - hypothalamus - releases histamine (wake) - basal forebrain - releases ACh (wake) but also releases GABA (sleep)
59
During REM there is low blood flow in --------------------------.
inferior frontal cortex
60
Theories for sleep
- restorative (metabolism and waste removal) - energy conservation - learning and memory (do synaptogenesis/pruning happen in sleep)