Unit 2 Study Guide Questions Flashcards

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
Q

How do bird brains change from breeding to non-breeding seasons?

A

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
Q

CNS Divisions Early in Development

A

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
Q

Explain divisions of CNS at 25 days.

A

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
Q

What are the three classes of hormones?

A

proteins, amines (or peptides), steroids

29
Q

Explain tropic hormones.

A

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
Q

Explain gonadal hormone release.

A

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
Q

Endocrine feedback loops work secrete hormones through either —– regulation or —– and ——- regulation

hormone release in both systems is regulated by —— cells

A

neuroendocrine

32
Q

How are the two types of regulation in endocrine feedback loops different?

A

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
Q

Sexual Differentiation in Bird Brains

A

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
Q

Which gene is responsible for sex dimorphism in humans?

A

SRY

35
Q

more than two sizes of gametes

A

anisogametic

36
Q

only one gamete size

A

isogametic

37
Q

two sizes of gametes but no sex dimorphisms (both males and females pass on both sizes of gametes)

A

monecious

38
Q

no fusion of gametes or combination of chromosomes; genetic info directly passed on from parent

A

Asexual reproduction

39
Q

some individuals have no gametes

A

infertility

40
Q

XXY genes

A

Kleinfelter syndrome

41
Q

X0 gene (no Y gene)

A

Turner syndrome

42
Q

XX but male phenotype

A

De la Chappelle

43
Q

XY but female phenotype, including fertility

A

Sawyer Syndrome

44
Q

Why are multiples no longer an issue in in vitro fertilization?

A

PGT testing

45
Q

Diurnal Cortisol release

A

Wake up: cortisol peaks
throughout day: declines
Evening: steady
Next morning: peaks again, restarts

46
Q

Diurnal testosterone release

A
  • hormone levels vary within day
  • hormone amount changes with age
  • diurnal pattern of hormone changes with age (is less variable)
47
Q

hormonal variation in women

A

Menstrual cycle = hormone release pattern over several weeks instead of one day

Pregnancy = hormone release pattern over several months

48
Q

Epigenetics and effect on development

A

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
Q

Sympathetic nervous system prompt you to rehydrate through ——- and ——-.

A

thirst; salt hunger

50
Q

What does aldosterone do?

A

in thirst system, signals kidneys to conserve sodium and aid in water retention

51
Q

What does angiotensin II do?

A

increases blood pressure

52
Q

Osmosensory neurons in OVLT relay information to ————– and —————–, and control rate at which posterior pituitary releases ————-.

A

supraoptic nucleus, paraventricular nucleus, vasopressin

53
Q

What does vasopressin do in thirst pathway?

A

raises blood pressure (constricts blood vessels) and helps kidney absorb water

54
Q

How does entrainment of SCN cells happen?

different than melatonin

A
  • system is triggered by binding of glutamate receptors
  • retinal ganglion cells signal SCN (helps entrain/set clock)
55
Q

How is melatonin production triggered?

A

SCN is entrained by light/dark and regulates pineal gland secretion of melatonin.

56
Q

How is entrainment of SCN cell (partially) triggered?

A

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
Q

What do ipRCGs do?

A

(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
Q

What parts of brain keep us awake?

A
  • 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
Q

During REM there is low blood flow in ————————–.

A

inferior frontal cortex

60
Q

Theories for sleep

A
  • restorative (metabolism and waste removal)
  • energy conservation
  • learning and memory (do synaptogenesis/pruning happen in sleep)