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PSL300 > Term Test 2 > Flashcards

Term Test 2 Flashcards

1
Q

What are the two glands that make up the pituitary gland?

A

Posterior Pituitary and Anterior Pituitary

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2
Q

What is the posterior pituitary gland? What does it excrete?

A

Neural Tissue that secretes two hormones: Vasopressin (ADH) and Oxytocin

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3
Q

What is the anterior pituitary? What does it excrete?

A

Endocrine tissue: prolactin, thyrotropin, adrenocorticotropin, growth hormone, follicle-stimulating hormone, luteinizing hormone

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4
Q

What is the pathway of secretion of posterior hormones?

A
  1. neurohormone made and packaged in the hypothalamus
  2. vesicles transported down the cell
  3. Vesicles are stored in the posterior pituitary
  4. neurohormones are released into the blood
    * first goes to posterior then blood
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5
Q

What is the pathway of anterior hormone secretion?

A
  1. neurons synthesizing trophic neurohormones release them into the capillaries of the portal system (hypothalamic hormones that tell the anterior pituitary when to release hormones)
  2. Portal veins carry the trophic neurohormones directly to the anterior pituitary, where they act on the endocrine cells
  3. Endocrine cells release their peptide hormones into the second set of capillaries for distribution to the rest of the body
    *hypothalamus–>portal veins–>endocrine cells–> blood
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6
Q

What are the hypothalamic hormones?

A

Dopamine, Thyrtropin-releasing hormone (TRH), Corticotropin-releasing hormone (CRH), GHRH, Gonadotropin-releasing hormone (GnRH), Somatostatin (GHIH)

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7
Q

What does Dopamine do? What is its target?

A

Inhibit prolactin, breast

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8
Q

What does TRH do? Target? Further hormones?

A

Stimulate the release of Thyrotropin, or Thyroid-stimulating hormone (TSH), Thyroid gland –> thyroid hormones (T3/4)

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9
Q

What does CRH do? Target? Further hormones?

A

Simulate the release of Adrenocorticotropin, Adrenocorticotrophic hormone (ACTH), Adrenal Cortex–>Cortisol

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10
Q

what does GHRH do? Target? Further hormones?

A

stimulate GH (Somatotropin) release, liver–> Insulin like growth factor

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11
Q

What does GnRH do? Target? Further?

A

Stimulate the release of FSH and LH, Endocrine cells on the gonands–>androgens, estrogens, progesterones–>germ cells on the gonands

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12
Q

What are bones like in utero?

A

they are soft, cartilage is not fully ossified, active growth plates

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13
Q

What are adolescent bones like?

A

Bones are fully ossified, growth plates are closing towards the end of puberty

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14
Q

What are adult bones like?

A

Growth plates are closed, fully ossified, bone loss occurs around 35-40

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15
Q

What are the epiphyseal growth plates?

A

Epiphyseal bone plate is a flat bony structure located between the epiphysis and the metaphysis of the long bones. It holds the growth plate cartilage, providing the weakest area of the growing bone with strength and stability. It is the blue that contains chondrocytes

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16
Q

What is ossification and what is required for it?

A

Bone formation, needs osteoblasts

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17
Q

What direction does bone growth take place?

A

The growth plates are growing towards the compact bone

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18
Q

What is a chondrocyte?

A

produce new cartilage

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19
Q

How does bone growth work?

A
  1. Closest to the newly calcified growth plate osteoblasts lay down new bone on top of cartilage (foundation for bone from Ca2+) from the chondrocytes
  2. Old chondrocytes disintegrate and are replaced by bone as the bone grows
  3. Chondrocytes (from media) produce cartilage
  4. Dividing chondrocytes add length to the bone
    *compact bone is the walls, the epiphyseal growth plate is chondrocytes, cartilage, and dying chondrocytes (it is a layer)
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20
Q

What is the stimulatory growth hormone pathway?

A
  1. Circadian rhythm, stress and cortisol, and fasting signal the hypothalamus to produce GHRH
  2. GHRH increases GH release from the anterior pituitary to signal on the the liver
  3. IGF is secreted from the liber signaling for cartilage growth (inc. in chondrocytes)
  4. IGF also signals a negative feedback mechanism on the anterior pituitary and hypothalamus to stop GH and GHRH production
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21
Q

What is the inhibitory growth hormone pathway?

A
  1. Circadian rhythm, stress and cortisol, and fasting signal the hypothalamus to produce Somatostatin (GHIH)
  2. Stops GH release from the anterior pituitary
  3. Blood glucose increases and bone and tissues grow
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22
Q

What is IGF-1

A

Insulin-Like Growth Factor
- growth-promoting effects on almost every cell in the body
- anabolic effects (growth)

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23
Q

How does GH stimulate bone growth?

A

Chondrocytes inc in:
- recruitment
- proliferation
- matrix

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24
Q

What are the catabolic, glucose sparing effects of GH?

A

Stimulates adipose cells to break down stored fat, fueling growth effects (lipolysis)

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25
Q

What are the catabolic growth effects of GH?

A
  1. Increases the uptake of amino acids from the blood
  2. Enhances cellular proliferation and reduces apoptosis (targets: bone, muscle, nervous system, and immune cells)
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26
Q

What are the catabolic diabetogenic effects of GH?

A

GH stimulates liver to break down glycogen into glucose, fueling growth effects (gluconeogenesis, glycogenolysis)

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27
Q

What would you expect to see in a person with too much growth hormone because of a pituitary tumor?

A

increased number of chondrocytes

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28
Q

What does growth depend on?

A
  1. Diet and Genetics
    - adequate nutrition and no chronic stress
  2. Hormones and growth factors like:
    - GH and IGF-1
    - Thyroid Hormones
    - Insulin
    - Sex steroids
    - Cortisol
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29
Q

What is gigantism?

A

Too much GH in childhood (adds to the growth plates)

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30
Q

What is acromegaly?

A

Too much GH in adulthood (adds to the ends of irregularly shaped/flat bones and affects the skin and lips)

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31
Q

Where is the Thyroid?

A

By adams apple, middle of neck

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32
Q

What cell types and things make up the thyroid?

A
  1. Follicles (produce the hormones)
  2. C cells
  3. Follicular cells surrounding the colloid
  4. Capillaries
  5. Connective tissue
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33
Q

How are thyroid hormones made?

A
  1. Na+ I- symporter (transport both the same way) brings I- into the follicular cell
  2. The pendrin transporter moves the I- into the colloid
  3. Follicular cells synthesize enzymes and thyroglobulin for colloid
  4. Thyroid peroxidase adds iodine to tyrosine to make T3 and T4 (thyroid hormones)
  5. Thyroglobulin is taken back into the cell in vesicles to be recycled
  6. Intracellular enzymes T3 and T4 from the thyroglobulin protein
  7. Free T3 and T4 enter circulation
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34
Q

What are all the names of the thyroid hormone variants?

A

1 iodine: monoiodotyrosine
2 iodine: diiodotyrosine
3: triiodothyronine
4. thyroxine

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35
Q

What is Iodine used for in humans?

A

Just thyroid hormone

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36
Q

What is the stimulatory pathway of Thyroid hormone?

A
  1. TRH is made in and released from the hypothalamus at a constant rhythmic release without stimulation
  2. TSH is released from the anterior pituitary signaling for T3/4 to be made
  3. Thyroid hormone sends negative feedback mechanisms to the Hypothalamus for TRH and anterior pituitary for TSH
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37
Q

What is TSH and its function?

A
  • Activates G-protein linked membrane receptors acting via Adenylate cyclase
  • Stimulates synthesis and activity of enzymes involved in T3 and T4 synthesis
  • activates TFs
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38
Q

What is the mechanism of action of thyroid hormones?

A
  • T3/4 circulate in blood bound to plasma proteins
  • T3 more potent than T4
  • T4 converted to T3 in target tissues
  • alter gene transription
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39
Q

What do T3 and T4 bind to?

A

Both bind to nuclear thyroid receptors (form dimers with retinoic acid receptor)

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40
Q

What are the metabolic functions of thyroid hormones?

A

metabolic rate, oxygen consumption, heat production, protein degradation, lipolysis

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41
Q

What are the nervous system functions of thyroid hormones?

A

enhance speech, thinking, reflexes

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42
Q

What are the growth and development functions of thyroid hormones?

A

essential in children, works with GH to promote growth

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43
Q

What are the cardiovascular functions of thyroid hormones?

A

enhances heart rate and contractility, peripheral blood flow, works in part by increasing numbers of B adrenergic receptors and other proteins

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44
Q

What are the muscular functions of thyroid hormones?

A

too much causes muscle weakness,

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45
Q

What is Hyperthyroidism and its causes?

A

Excess thyroid hormone
- causes: tumors, thyroid stimulating immunoglobulins

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46
Q

Symptoms of hyperthyroidism?

A

goiter, nervousness, insomnia, anxiety, high heart rate, graves disease, weight loss

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47
Q

Treatments of hyperthyroidism?

A

remove part of thyroid, block synthesis of T3 and T4 or block T4 conversion to T3

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48
Q

What is Graves disease and its symptoms?

A

Autoimmune disease: abnormal antibodies against the TSH receptor are produced
- no known cause
- most common cause of hyperthyroidism
- immune system produces antibodies that look like TSH and bind to the TSH receptor
- TSH receptor turns on mistakenly

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49
Q

What is hypothyroidism and its causes?

A
  • Thyroid hormone deficiency
    Causes:
  • under active thyroid gland
  • no iodine in diet
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50
Q

Symtoms and treatments of hypothyroidism?

A
  • goiter, slowed heart rate, slowed speech, fatigue, cold-intolerance, cretinism, stunted growth, weight gain
  • exogenous thyroid hormone (T4) thyroxin
  • the goiter is caused by parts of the thyroid trying to compensate
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51
Q

Iodine definiciency causes…

A
  • no ability to make T3/4
  • lack of negative feedback inc. TSH secretion
  • TSH stimulates growth of thyroid gland=goiter
  • causes death, retards, poor growth, stupidity
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52
Q

Without iodine what happens to a dude?

A

High TRH, TSH, low TH (no negative feedback)

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53
Q

what re the commonalities found between sexes?

A
  1. Gamete formation
  2. Hypothalamic/Pituitary control of reproduction
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54
Q

What is gametogensis?

A
  • gametes with 23 chromosomes produces from cells in gonads with 46 chromosomes
  • Involves meiosis
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55
Q

What is meiosis?

A

DNA replicated once and undergoes division twice

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56
Q

What is nonhomologous recombination?

A
  1. random assortment of genetic material
  2. reassortment of the genes so the products are a unique combo when fertilized
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57
Q

What is GnRH and how does it work?

A
  • Gonadotropin Releasing Hormone
  • Secreted in pulses from neuroendocrine cells in the hypothalamus
  • stimulates synthesis and secretion of LH and FSH
  • Pulsality is critical for reproductive function
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58
Q

What is the pulsality of GnRH

A
  • regulated by hormonal feedback and higher brain centers
  • Pulse frequency/amplitude changes during development and during periods in adult life
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59
Q

What happens if GnRH pulses are low?

A
  • FSH released
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60
Q

What happens if GnRH pulses are high?

A
  • LH released
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61
Q

Which is correct regarding the regulation of reproductive hormone secretion?

A

LH stimulates the release of steroid hormones from the gonads

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62
Q

How are sperm produced?

A
  • in the testis
  • optimally at 2-3C lower than body temp
  • Takes 64 days
  • 200 million produced a day
  • Further mature in the epididymis
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63
Q

What do sertoli cells do?

A
  • also called sustentacular cells
  • Support sperm development
  • filter and absorb nutrients
  • provide tight junctions between early stages/initial germ cells and actual developing sperm
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64
Q

What do leydig cells do?

A
  • secrete testosterone
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65
Q

How are the seminiferous tubules organized?

A
  • sertoli cells inside tubule
  • Leydig cells outside
  • Spermatogonium (sperm precursors) inside as as the move to the center they mature to sperm
  • capillaries are not in the tubule, just outside
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66
Q

What are the tight junctions responsible for?

A

blood testis barrier because immune cells would recognize sperm as novel proteins + only 1/2 genetic material and kill them

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67
Q

Process of Spermatogenesis

A
  1. Spermatogonia undergo mitosis, one stays behind to produce more spermatogonia
  2. The other is the primary spermatocyte that undergoes meiosis 1 forming the 2 secondary spermatocytes
  3. The secondary spermatocytes undergo meiosis 2 forming four spermatids
  4. These mature into spermatozoa (loss of cytoplasm, formation of the tail)
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68
Q

What are spermatozoa and their structure?

A

from the top:
- acrosome with enzymes derived from golgi apparatus
- nucleus
- centrioles
- mitochondrial spiral (for swim energy)
- microtubules

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69
Q

What does the acrosome contain?

A
  • hyaluronidase and acrosin which breakdown the zona pellucida, a glycoprotein coat that covers the oocyte
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70
Q

What is semen?

A

Water
Lubricant: mucous
Buffers: neutralize acid
Nutrients: fructose, citric acid, vitamin C, Carnitine (for energy)
Enzymes
Zinc
Prostaglandins: Smooth muscle contractions (aid muscle contractions)

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71
Q

What are the exocrine organs in the male repro system?

A

seminal vesicle, prostate gland, bulbourethral gland (alkaline secretions)

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72
Q

What is the system of stimulatory hormonal control of gametogenesis in males?

A
  1. GnRH from hypo stimulates FSH and LH in anterior
  2. FSH signals for secondary messengers to make cell products
  3. The cell products make androgen-binding protein (ABP)
  4. ABP interacts with testosterone from LH stimulating Leydig cells to support sperm development
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73
Q

What in the inhibitory control of male gametogenesis?

A
  1. Cell products produced by FSH’s secondary messengers signals for Inhibin, which stops FSH production
  2. LH production and GnRH production are stopped by Testosterone production
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74
Q

FSH role

A

stimulates sertoli cells
- support sperm development
- secrete inhibin (inhibits FSH release)
- Secrete androgen-binding protein (helps to concentrate androgens in testis)

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75
Q

LH role

A

Stimulates Leydig cells to secrete testosterone

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76
Q

Testosterone secretion throughout life

A
  1. burst in fetus
  2. burst in neo-natal
  3. nothing pre-puberty
  4. HUGE burst in puberty to adult then steady decline
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77
Q

Hormone levels of men throughout their life…

A

LH, T, FSH, and INSL3:
- high-second and third trimester, 0-6 months, puberty
- low/rising: first trimester, childhood
AMH:
- high: first, second, third trimester, childhood
- low: steep drop at puberty
Inhibin:
- high: first, second, third trimester, childhood (first half), rises at puberty
- low: second half of childhood

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78
Q

What is hypogonadism?

A
  • decreased function of the testis
  • decreased production of androgens, inhibin B, AMH, and/or impaired sperm production
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79
Q

What is primary hypogonadism’s pathway?

A
  1. Inc in GnRH
  2. Inc. FSH and LH
  3. Dec. testosteron b/c testis damaged
  4. no negative feedback lots of GnRH, FSH, and LH still
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80
Q

What is secondary hypogonadism?

A
  1. damaged hypothalamus
  2. low GnRH
  3. affects anterior pituitary
  4. low FSH and LH
  5. low testosterone
    * one can be given supplementary testosterone
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81
Q

What does testosterone do in sex-specific tissues?

A
  • promotes spermatogenesis
  • maintains and stimulates secretion from prostate and seminal vesicles
  • Maintains reproductive tract
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82
Q

Other reproductive effects of testosterone?

A
  • Inc. sex drive
  • negative feedback on LH, FSH, GnRH
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83
Q

Secondary sex characteristics of testosterone?

A
  • male pattern hair growth, baldness
  • promotes muscle growth
  • Increases sebaceous gland secretion (odors)
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84
Q

Non-reproductive effects of testosterone

A
  • promotes protein synthesis
  • Increases aggression (side effects of steroids)
  • Stimulates erythropoiesis (make new blood)
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85
Q

What else can testosterone make?

A

cholesterol–>testosterone–>+5a-reductase–>DHT–>important for prostate, external male genitalia, and baldness

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86
Q

What happens when you inhibit 5a-reductase

A
  • treatment for benign prostate enlargement
  • increased hair growth
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87
Q

How are oocytes produced?

A

Oogenesis:
1. Before birth: oogonia undergo meiosis 1, duplicate their DNA then STOP resulting in primary oocytes
2. at puberty 300,00 primary oocytes remain
3. After puberty, one primary oocyte completes meiosis 1 and enters meiosis 2 to become a secondary oocyte every 28 days
4. Secondary oocyte released at ovulation
5. Secondary oocyte completes meiosis 2 only if fertilized, dies if not

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88
Q

What are the differences between oogenesis and spermatogenesis?

A
  • asymmetric cell division (only one secondary oocyte produced from each oogonium), remove polar bodies
  • Limited duration (menopause)
  • Limited number of primary oocytes
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89
Q

What is the process of oocyte maturation?

A
  • primary oocytes are surrounded by granulosa and theca cells in what is called primary follicles
  • Maturation recruits 5-10 follicles in each ovary, only one will fully mature
  • remaining oocytes die (atresia)
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90
Q

What is the structure of the primary follicle?

A
  • Theca externa
  • Theca interna
  • basement membrane
  • granulosa cells
  • atrium is also in the primary follicle
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91
Q

What are theca cells for?

A
  • secrete steroid hormone precursors
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92
Q

What are granulosa cells for?

A

support oocyte development

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93
Q

Explain the ovarian cycle, follicular phase…

A

Days 1-14:
1. 5-10 follicles per ovary are selected to mature
2. The granulosa cells surrounding the primary oocyte proliferate
3. the theca cell proliferate and produce androgens–>estrogens as well and the atrium forms
4. All cells have proliferated a ton and the atrium is a huge fluid filled cavity with estrogen and enzymes (now a tertiary follicle)
5. the oocyte is now secondary and a dominant follicle is selected

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94
Q

What is the LH surge and what does it do?

A

The release of the tertiary dominant follicle (secondary oocyte and cumulus) to the fimbria of the fallopian tubes to be picked up and ovulated
1. Follicular cells (granulosa/theca) release collagenase: connective tissue to the ovary is digested
2. Progesterone is release aiding in smooth muscle contractions

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95
Q

Explain the luteal phase of the ovarian cycle…

A
  • Follicular cells left behind in the ovary become corpus luteum
  • This releases progesterone and estrogen
    IF NOT FERTILIZED:
  • corpus luteum degenerates into the corpus albicans
    IF FERTILIZED:
  • the corpus luteum continues to make progesterone and estrogen until the end of the first trimester
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96
Q

Describe the Menses phase of the uterine cycle

A

Blood vessels supplying the endometrium undergo constriction causing shedding of the endometrial lining because of declining levels of progesterone and estrogen

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97
Q

Describe the proliferative phase of the uterine cycle…

A

Endometrium develops in response to estrogen. The endometrial lining thickens as the blood supply to the tissue is re-established and cells proliferate

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98
Q

Describe the secretory phase of the uterine cycle…

A

Glands in the endometrium secrete more viscous fluid. Endometrial cells deposit lipid and glycogen in cytoplasm under the influence of progesterone and estrogen

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99
Q

Estrogen and Progesterone levels during the menstrual cycle

A

High during luteal/secretory phase, and estrogen high at the end of the follicular phase/proliferative because of atrium

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100
Q

Hypothalamic/Pituitary control of Early-mid follicular phase…

A

This is during the menses/proliferative phase of uterine
1. GnRH in hypothalamus turns on LH and FSH which begin to RISE, system still at a low
2. LH stimulates the release of androgens from theca cells
3. FSH stimulates conversion to estrogen by granulosa cells
4. Granulosa cells also secrete AMH which prevents recruitment of additional follicles
5. Estrogens exert positive feedback on granulosa cells increasing proliferation and estrogen
6. Estrogens exert negative feedback on ant pituitary and hypo to shut down LH and FSH

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101
Q

Hypothalamic/Pituitary control of late follicular phase and ovulation…

A

This is during the uterine proliferative phase
1. The tertiary follicle is now present
2. follicular cells secrete inhibin (inhibits FSH), progesterone, and estrogen
3. Progesterone increases pituitary sensitivity to GnRH (positive feedback for GnRH and LH)
4. High estrogens increase frequency of GnRH pulses to one every 65 min (positive feedback)
5. FSH being inhibited, LH surge occurs triggering meiosis 1 and ovulation

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102
Q

Hypothalamic/Pituitary control of Early-mid luteal phase…

A

This is during the beginning of the secretory phase of the uterine cycle
1. After ovulation the corpus luteum, under the influence of LH and FSH releases progesterone, inhibin, and estrogen
2. These hormones exert negative feedback at the hypothalamus and pituitary stopping LH and FSH production
3. Progesterone and Estrogen inhibits GnRH pulses (now once every 3-4 hours)

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103
Q

Hypothalamic/Pituitary control of late luteal phase…

A

This is during the end of he secretory phase of the uterine cycle:
1. The intrinsic life-span of the corpus luteum is 12 days
2. If not fertilization, the corpus luteum undergoes apoptosis

THE CYCLE REPEATS: This is during the menses phase of the uterine cycle
- FSH begins to rise to recruit new follicles
- Estrogen and progesterone are low so GnRH turns back on to make more

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104
Q

What is the process of estrogen regulation?

A
  1. In the theca cell LH signals for the conversion of cholesterol to androstenedione
  2. In the granulosa cell the FSH signals for the conversion of androstenedione to estrone via aromatase
  3. Estrone is converted to estradiol and then estrogens to be secreted
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105
Q

What are the sex-specific tissue actions of estrogen?

A
  • promote follicular development and ovulation
  • stimulates growth of the endometrium
  • maintains reproductive tract
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106
Q

What are the other reproductive actions of estrogen?

A

Negative feedback effects on GnRH, LH and FSH secretion

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107
Q

What are the secondary sex characteristics actions of estrogen?

A
  • stimulates development and growth of breast tissue
  • increase sebaceous gland secretion
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108
Q

What are the non-reproductive actions of estrogen?

A
  • promotes fat deposition around the hips and thighs
109
Q

What are the functions of adrenal androgens in adult females?

A
  • Increase sex drive
  • body hair
110
Q

What is the correlation between age and pregnancy?

A
  • The alignment of chromosomes is defected overtime and can cause deformities/disabilities
  • Oocyte quality declines with age
  • Sharp decline in success after age 33
  • number of follicles also declines
111
Q

What is menopause?

A
  • The end of the female reproductive cycle
  • Ovaries lose their ability to respond to FSH and LH
  • Estradiol and progesterone levels fall
  • There is a lack of negative feedback causing LH and FSH to rise, but the ovaries can’t respond
112
Q

What happens when a woman is on birth control?

A
  1. LH and FSH will remain low due to artificial estrogen and progesterone production
  2. Without FSH there is no follicle progression
  3. Ovulation is inhibited (no dominant follicle)
113
Q

Describe the process of sperm maturation…

A
  1. sperm must pass through cervical mucous, and travel to the egg
  2. Although uterine and oviduct contractions aid their transport, they need help
  3. They undergo capacitation to become hyperactive
114
Q

What is capacitation?

A

Capacitation is the process of albumin, enzymes, and lipoproteins binding to the sperm to remove the glycoprotein coat, induce intracellular changes, and develop a strong whip like motion
- this has to happen in the female reproductive tract

115
Q

Where does fertilization occur?

A

in the fallopian tubes
- oocyte viable for 24 hours
- sperm can live inside a woman for 4-6 days and still be viable

116
Q

What is the process of fertilization?

A
  • Fertilization is when about 100 sper reach the oocyte guided by the chemotaxis of the progesterone in the cumulus cells
  • The sperm tunnel through barriers using their acrosomal enzymes
  • The removal of those final layers allows the sperm to penetrate to the egg and the genetic content to be released
  • The first sperm to unite with the egg wins
117
Q

What are the specifics of fertilization?

A
  1. Sperm and egg plasma membranes fuse triggering the cortical reaction (depolarization of oocyte)
  2. Fusion of cortical granules (oocyte intracellular vesicles) with outer membrane
  3. This coats the oocyte and prevents penetration by additional sperm (polyspermy)
  4. The sperm nucleus moves into the cytoplasm of the egg
  5. Oocyte nucleus completes meiotic division
  6. The sperm and egg nuclei fuse to form the zygote nucleus (the second polar body is expelled)
118
Q

What happens after fertilization?

A
  1. Ovulation
  2. Fertilization
  3. Cell division
  4. Blastocyst reached the uterus becoming the trophoblast
  5. Blastocyst/trophoblast implants
119
Q

What is the fertilization hormone?

A

Human chorionic gonadotropin (hCG) secreted from the trophoblast
- it takes over from the pituitary to maintain corpus luteum and prevent the next menstrual cycle
- This maintenance keeps the endometrium intact and the production of progesterone, estrogen, and inhibin suppress the pituitary

120
Q

What is the placenta and what does it do?

A
  • Performs the role of digestion, respiration, and renal systems for the fetus
  • Provides an exchange of nutrients, waste, oxygen/CO2, proteins, chemical, etc
  • Temporary endocrine gland
121
Q

Describe placental circulation

A
  1. Maternal vasculature not physically linked to the fetal vasculature
  2. Maternal blood forms a lacunae (lake)
  3. Fetal chorionic villi transfer gases and solutes between mother and fetus
  4. Chorionic villi contain embryonic blood vessels, the maternal blood bathes these villi allowing the proper movement of oxygenated and non-oxygenated blood to and from the infant via the umbilical
122
Q

What are the hormone secretion patterns of the placenta?

A
  1. Cholesterol
    - Mothers blood (and vice versa)–>placenta where it is converted to progesterone–> back to mothers blood
  2. Cholesterol cont.
    - Mothers blood–>placenta–>fetal blood–>fetal adrenal cortex where it is converted to DHEA
  3. DHEA
    - fetal adrenal cortex–>fetal blood–>placenta where it is converted to estrogen
  4. Estrogen
    - placenta–>mothers blood
123
Q

What are the functions of placental hormones?

A
  1. Human chorionic gonadotropin
    - maintains corpus luteum, stimulates fetal testis
  2. Progesterone
    - suppresses uterine contractions, cervical plug, mammary gland development
  3. Estrogen
    - Uterine development (growth, blood supply, oxytocin receptors), breast duct development
  4. Human placental lactogen
    - structurally related to growth hormone and prolactin
    - High in mother/low in fetus
    - Decreases maternal cellular uptake of glucose, enhances maternal lipolysis
124
Q

What are the normal terms of pregnancy

A
  1. First trimester 0-12 weeks
  2. Second trimester 12-28 weeks
  3. Third trimester 28 weeks to delivery
  4. Normal birth 37-42 weeks after last menstrual cycle
  5. Preterm fetus born before 28 weeks
  6. Postterm after 42 weeks
125
Q

What are the maternal adaptations to pregnancy?

A
  1. Renal
    - Increased vasopressin levels increase blood volume
    - increased activity RAS sodium and fluid retention
  2. Cardiovascular
    - increased output
  3. Immune system: partially suppressed
  4. Calcium homeostasis:
    - pregnancy associated hyperparathyroidism (inc in PTH)
    - calcium transfer to fetus
    - Increased calcitonin to limit mobilization of maternal bone
126
Q

How is labor triggered?

A

Before the feedback mechanisms, relaxin released from the ovary and placenta loosens the ligaments in the pelvic bone and causes the cervix to soften dropping the fetus lower in the uterus
1. Cervical stretch increases oxytocin release and uterine contractions pushing the fetus further down
2. There is a positive feedback mechanism that keeps the contractions happening
3. The oxytocin increases prostaglandins (smooth muscle contractions) from uterine wall
4. There is an increase in estrogen and oxytocin receptors in the uterus
5. Fetal cortisol increases
6. Placental corticotropin-releasing hormone (CRH)
7. Prostaglandins inc.

127
Q

What hormones are necessary for breast milk?

A

Estrogens and progesterones are needed for the development of mammary glands but inhibit milk production thus, before pregnancy mammary glands have the capacity to make milk, but don’t, after pregnancy they can

128
Q

Following birth what hormones are necessary for breast milk?

A
  • Prolactin increases epithelial milk producing cells
  • Oxytocin increases myoepithelial cells (muscle cells to squeeze out milk)
129
Q

What is the oxytocin feedback regulation?

A
  1. Stimulus like baby crying or suckling on the nipple
  2. Higher brain centers signal for the hypothalamus to release oxytocin
  3. Oxytocin is released out of the posterior pituitary and stimulates smooth muscle contractions to release milk
130
Q

What is the prolactin feedback regulation?

A
  1. Same stimulus
  2. PIH (dopamine) inhibits oxytocin pathway
  3. Hypothalamus signals for the AP to remove the inhibitor of prolactin cells
  4. prolactin increases and milk is made for secretion
131
Q

Which gamete is responsible for the sex of the child?

A

sperm
XX girl
XY boy

132
Q

What type of repro system does a fetus have at 6 weeks

A

bipotential primordium and rudimentary reproductive tracts

133
Q

What is the development process of XX structures?

A
  1. Gonadal cortex becomes ovary in the absence of SRY proteins and under the influence of female specific genes
  2. Absence of testosterone causes Wolffian duct to degenerate
  3. At birth the absence of AMH allows the Mullerian duct to become the Fallopian tube, uterus, upper vagina,, cervix
134
Q

What is so special about the Y chromosome?

A
  • encodes for testes determining factor (TDF)
  • Has SRY gene that promotes testes development
135
Q

What is the function of SRY?

A
  • SF1 (TF) increases SRY which increases SOX9 which increases AMH stopping the development of female structures and encouraging sertoli and leydig cells and testes
  • converts embryonic gonad to a testis without it it becomes an ovary
136
Q

What do the testis do once developed?

A
  • secrete AMH and testosterone leading to wolffian duct development and male genitalia
  • No AMH and testosterone= Mullerian ducts persis and develop into female stuff
137
Q

What happens with and without SRY

A

With: Lots of SOX9, lots of AMH, inhibition of B-catenin, male go, female suppressed
Without: No SOX9, no AMH, B-catenin further inhibits SOX9, female go, male suppressed, no testosterone

138
Q

What does SOX9 do?

A
  • stimulate the production of AMH
  • Initiate Sertoli cell differentiation
  • Sertoli precursors proliferate
  • They organize around clusters of germ cells
  • proliferation, migration, organization, vascularization, leydig cell differentiation
  • SOX9 rapidly organizes testis structure after sertoli cell differentiation
139
Q

What is the development of XY structures?

A
  • SRY protein in male emryo directs the medulla of the bipotential gonad to develop into testies
  • AMH causes the Mullerian ducts to disappear
  • Testosterone from tesis converts Wolffian duct into the seminal vesicle, vas deferens, epididymis. DHT=prostate development
140
Q

How do sertoli and leydig cells help with fetus differentiation?

A

S: AMH=no mullerian duct
L: testosterone=development of wolffian duct and other male parts

141
Q

What do T and DHT develop?

A

T: internal male stuff
DHT: external male stuff and prostate

142
Q

Atypical hormone levels or action in a person:

A

XY: atypical androgen synthesis ex. no 5a-reductase= lack of outer male genitalia
XX: excessive exposure to androgens during early gestation

143
Q

What happens to an individual with complete androgen insensitivity?

A
  • testes undescenced
  • closed vag, no ovaries, infertile
  • High androgens, high LH (no negative feedback)
  • no pubic hair, but can have breast development
144
Q

How is puberty regulated?

A
  • earlier start in girls than boys, but no known stimulus
  • start LH FSH, begin next developmental stage
145
Q

What makes up the CNS

A

Brain and spinal cord (protect by spinal column)

146
Q

What makes up the peripheral nervous system?

A
  • All neurons and parts of neurons outside of the CNS
147
Q

What are the parts of the peripheral nervous system?

A

somatic nervous system (controlling voluntary action via skeletal muscle), autonomic nervous system (visceral functions such as heart rate and breathing)
- autonomic also includes the enteric nervous system which controls digestion and movements of the gut
- It gets input from the spinal cord, but can also work independently

148
Q

How many neurons are in the CNS?

A

Brain: 86 BILLION
Spinal Cord: 1 BILLION
Enteric nervous system: 100-600 million
PNS: 100-600 million
* there are also glial cells in the CNS and PNS which support and protect neurons

149
Q

What are the ventricles and what do they contain?

A
  • Cerebrospinal fluid (CSF)
    top:
    1. lateral ventricles
    2. third ventricle
    3. Fourth ventricle
    4. Central canal of spinal cord
150
Q

What is grey matter?

A
  • part of the CNS
  • consists of nerve cell bodies, unmyelinated axons, and dendrites
  • Cell bodies arranged in layers ir clusters called NUCLEI or NUCLEUS (singular)
151
Q

What is white matter?

A
  • In the CNS
  • Consists of MYELINATED axons running in bundles called TRACTS
152
Q

In the PNS was are the different names?

A
  • Clusters of NEURONS= GANGLIA (singular=GANGLION)
  • Bundles of axons=NERVES
153
Q

How much energy does the CNS use?

A
  • the brain gets 15% of the hearts blood pumped to it
  • Uses 1/2 of the bodies glucose
  • It runs on 40 watts (not much, very efficient)
154
Q

How is the CNS so efficient?

A
  • Neurons communicate with energy needing action potentials
  • The energy supply to the CNS can only support a low rate of firing
    Ex. the cortex permits an average rate per cell of just one spike every 6 seconds
  • only about 4% of your neurons are firing at any given moment
155
Q

How many spinal segments are there are what do they contain?

A

31 spinal segments, each with a PAIR of spinal nerves

156
Q

What is a spinal nerve and what is their structure?

A
  • Each spinal nerve has a dorsal root facing behind a person, which carries afferent (incoming, sensory signals)
  • The dorsal root ganglion contains the cell bodies (in PNS) of the neurons carrying these signals
  • the ventral root (facing out) carries efferent (outgoing, exit) signals from the CNS to the body, including motor signals (skeletal muscles)
157
Q

Where is grey matter in the spinal cord usually found?

A
  • Mainly in the middle of the spinal cord
  • It has a dorsal and ventral horn in its butterfly shape
158
Q

What are the divisions of the grey matter in the spinal cord?

A
  • This is in the CNS
    1. Sensory nuclei are in the dorsal horn because sensory signals arrive at the dorsal root
  • Somatic sensory nuclei gets signals from the skin
  • Visceral sensory nuclei get signals from the viscera (internal organs)
    2. Efferent nuclei are ventral
  • Autonomic efferent nuclei send commands to glands and smooth muscle
  • Motor nuclei send commands to skeletal muscle
159
Q

What is the structure and division of white matter in the spinal cord?

A
  1. Ascending tracts carry sensory signals to the brain. They are mainly dorsal because sensory signals arrive at the dorsal root
  2. Descending tracts carry signals from the brain. They are mainly ventral, where outgoing signals leave the CNS
  3. Propriospinal tracts stay in the spinal cord
160
Q

What happens during a spinal reflex?

A
  1. The spinal cord responds to the stimuli without consulting the brain
    Ex. Knee jerk reflex, a ligament is stretched below the kneecap. Sensory fibers carry the news of this into the dorsal horn via dorsal root ganglion
    - These fibers send branches up to the brain, but also excite neurons in the ventral horn that send signals out to the leg muscles to contract and counter the stretch
    - Brain gets the info, but spinal cord does not wait for brain input
161
Q

What are the brains 6 major divisions?

A
  1. Medulla
  2. Pons
  3. Cerebellum
  4. Midbrain
  5. Diencephalon
  6. Cerebrum
162
Q

What makes up the brain stem and what does it do?

A

In ascending order:
1. Medulla
2. Pons
3. Midbrain
- The brains stem is the main control center for many autonomic functions and reflexes such as breathing, swallowing, vomiting, and regulating blood pressure
- Cranial nerves 3-10 and 12 arise from the brain stem

163
Q

What are cranial nerves?

A
  • nerves that enter or leave the brain rather than the spinal cord
  • There are 12 pairs
164
Q

What is cranial nerve 0?

A

Where info arrives from or leaves to the periphery

165
Q

What is the diencephelon?

A

It is composed of the thalamus, hypothalamus, pituitary gland, and pineal gland (glands secrete hormones)

166
Q

What does the thalamus do?

A

Processes info going to and from the cerebral cortex

167
Q

What does the hypothalamus do?

A

Regulates behavioral drives, and endocrine and autonomic homeostasis

168
Q

What is the cerebrum composed of?

A
  1. Has two hemispheres connected by the corpus callosum
  2. The cerebral grey matter includes the outer layer called the cortex, the limbic system, and the basal ganglia which help control movement
  3. The white matter is all on the inside surrounded by the grey matter, except for the basal ganglia which is also in the middle
  4. Corpus callosum is a large bundle of myelinated axons (giant track)
169
Q

What are the different functions of each hemisphere?

A

L: writing, speech, math, language
R: spatial analysis, analysis by touch

170
Q

What are the four lobes in the brain

A

Frontal, Parietal, Occipital, Temporal (near temple)

171
Q

What does each hemisphere have?

A
  • a cingulate gyrus, which is part of the limbic system
172
Q

What is the limbic system?

A
  • old group of brain regions
  • Cingulate gyrus, amygdala, hippocampus
  • concerned with motivation, emotion, and memory
  • ex. monkeys with lesioned amygdala were not afraid of snakes
173
Q

What are the five special senses?

A

vision, hearing, equilibrium, taste, and smell

174
Q

What are the 4 somatic sense?

A

touch, temperature, proprioception, and nociception (pain and itch)

174
Q

What is transduction?

A

The conversion of stimuli into electrical signals

175
Q

What are we conscious and unconscious of?

A

Conscious: 9 senses ish
Unconscious: blood pressure, lung inflation, blood-glucose concentration, internal body temp, pH etc.

176
Q

What are the types of receptor cells?

A

in some systems such as vision they are called neurons, in others such as hearing they are non-neuronal epithelial cells

177
Q

What is a receptor potential?

A
  • Recetor cells can convert stimulus energy into a graded membrane potential
  • the receptor may then release neurotransmitter to affect a neuron
  • If the receptor is itself a neuron, it may fire action potentials
  • not all neurons fire action potentials
178
Q

What is an adequate stimulus?

A
  • the form of energy to which it is most responsive
  • ex. thermoreceptors respond most sensitive to temperature
  • However, many receptors also respond to other forms of energy as well, if those other forms are powerful enough
    ex. some thermoreceptors also respond to certain chemicals, or fans vibrating at the same vibration of a human eyeball can cause people to see things
179
Q

What are chemoreceptors?

A

they respond to specific molecules or ions, ex. to glucose, oxygen, or H+

180
Q

What are mechanoreceptors?

A

Respond to mechanical energy such as pressure, vibration, gravity, and sound

181
Q

What are thermoreceptors?

A

They respond to tempurature

182
Q

What are photoreceptors?

A

Respond to light

183
Q

What is a receptor threshold?

A

The weakest stimulus that will cause a response in the receptor, but its not enough for the person themselves to perceive the stimulus
- ex. some photoreceptors can detect a single photon of light, or chemoreceptors to one molecule of odorant

184
Q

What is the perceptual threshold?

A

the weakest stimulus that will cause a conscious perception in the organism
ex. it takes 40 odorant molecules for you to perceive a smell

185
Q

What is the series of neurons needed to sense something?

A
  1. first neurons are called the primary sensory neurons
  2. secondary sensory neurons
  3. Tertiary, etc
    - many presynaptic cells may contact any one post synaptic cell
    - This convergence allows secondary and higher neurons to combine data from many receptors
186
Q

What is stimulus modality and how is it indicated?

A
  • modality is whether a stimulus is a light, sound, touch, etc.
  • sensory systems indicate modality via labeled lines, meaning modality is revealed by which axons carry the signal
187
Q

What are the two ways intensity can be represented?

A
  1. stronger stimuli may activate more neurons, this is called POPULATION CODING OF INTENSITY
  2. Stronger stimuli may also make the individual neurons fire at a faster rate=FREQUENCY CODING
    * both mechanisms may operate together, a stronger stimulus may increase the firing rates of neurons and also cause more neurons to be active
188
Q

What are dynamics?

A

receptors and neurons activities may not only depend on the stimulus right now, but how it changes over time, cells signal changes in stimuli not steady levels

189
Q

What are phasic cells?

A

they respond briefly to any change and then cease firing

190
Q

What are tonic cells?

A

they maintain their activity when the stimulus is not changing, signaling its present level

191
Q

What are phasic-tonic cells?

A

react to change, but don’t return all the way to zero firing when the stimulus is constant, also carry info about steady level
- a change can happen and then it settles into a new tonic level

192
Q

What is a type of phasic cell?

A
  • mant retinal cells are phasic
  • they report changes in you visual world as when something moves
  • phasic cells lose activity when nothing changes
193
Q

how do phasic cells make communication more efficient?

A
  • because our world is fairly stable, it is more efficient to report changes then to repeat similar messages
194
Q

What are temporal changes?

A

changes through time between one moment and the next

195
Q

What are spatial changes?

A
  • they are the differences between neighboring regions in space
  • spatial change is also called contrast
196
Q

What happens away from the edge?

A

Excitation and inhibition cancel out in cells away from the edge, thus they are near baseline activity and contribute to the edge contrast
- only cells near the edge have activity that isn’t baseline

196
Q

What are edges?

A

locations where there is strong contrast

197
Q

What is lateral inhibition?

A
  • cells inhibit their neighbors, or they inhibit the cells their neighbors excite
  • cells can have different levels of activity depending on how close they are to the stimulus
  • secondary neurons can inhibit tertiary neurons
198
Q

How do most sensory pathways run?

A
  • most run via thalamus to cortex
  • most pathways run through the thalamus, which is near the center of the brain, out to the sensory cortices on the surface of the cerebrum
199
Q

What sense is the exception to running through the thalamus?

A
  • Olfactory (smell), they don’t project straight to the cortex via the thalamus
  • Equilibrium pathways project mainly to the cerebellum
200
Q

What is sensory processing largely composed of?

A

Inference
- our brain is a detective and has to infer and fill in the gaps
- the inference is very unconscious and fast (we can identify things visually in 160 ms without conscious effort
- however the brain can be fooled
- the brain mistrust coincindences

201
Q

What are the two chambers of the eye and how are they divided?

A
  1. Anterior chamber filled with aqueous humor, a plasma like fluid
  2. Lens, a transparent disk that focuses light and is suspended by ligaments called zonules
  3. Vitreous chamber filled with the vitreous body, a clear jelly that helps maintain the eyeball’s shape
202
Q

What is the cornea?

A

A transparent bulge at the front of the eye, cont. with the white of the eye (sclera)

203
Q

What do the cornea and lens do?

A
  • focus light on the retina, the inner lining of the eye with photoreceptors
  • light passes from the cornea to the lens through a hole in the iris called the pupil
204
Q

What is pupil size controlled by?

A
  • in bright light, parasympathetic signals from the brain contract the ring-shaped pupillary constrictor muscle, shrinking the pupil
  • in the dark, sympathetic signals contract the radial pupillary dilator muscle of the iris, dilating the pupil (radial streak, fibers of muscle)
204
Q

What are the features of the pupil?

A
  • in bright light the pupil constricts reducing the amount of light reaching the lens
  • in the dark they dilate (enlarge) by 20 times more to let in more light
  • the eye operates over a huge range of illumination (a sunny afternoon is 100 million times brighter than a moonless night)
205
Q

What does the pupil do?

A

Helps to focus light
- a small pupil ensure that each point on the retina receives light from just one direction in space
- one area of retina getting light from only one outside thing

206
Q

How do pupils control depth of field?

A
  • when the pupil is tightly constricted, we have full depth of field, everything is equally in focus
  • when the pupil is dilated, we have a shallow depth of field, only objects near one specific distance are in focus
207
Q

What is refraction and how does it work?

A
  • refraction helps solve the pinhole focus paradox
  • light bends when it enters a medium with a different refractive index
  • Our corneas are made of clear collagen. They bend light strongly because there is a big difference between the refractive indices of air and collagen. This is refraction
  • In water, refraction is weaker because the refractive indices of collagen and water are similar
207
Q

What is the problem with using the pupil alone to focus light?

A
  • with pinhole focusing, the retinal image is dim because the pinhole doesn’t admit much light
  • enlarging the hole makes the image brighter, but also blurrier
208
Q

What is responsible for refracting light?

A
  • both the cornea and the lens
  • the cornea is responsible for about 2/3 of the eye’s refraction
  • the lens is responsible for about 1/3
208
Q

What is the lens made of?

A
  • clear cells without nuclei called crystallins and they are zippered together in concentric layers for flexibility
  • has no blood supply, but absorbs nutrients from the aqueous humor
209
Q

Why is the lens convex? what is concave?

A
  • a convex lens is fatter in the middle and thinner at the edges. It makes light rays converge to a focal point, like a magnifying glass
  • CONCAVE lenses are thinner in the middle and fatter around the edges. They disperse light and are used in some glasses
210
Q

What is the angle of incidence and what does it do?

A
  • The angle at which the light rays hit the interface between the media. THe angle at which it hits the lens surface
  • at a right degree angle of incidence the light doesn’t bend at all, there is no refraction regardless of difference in refractive indicies
  • The angle depends on the shape of the lens and the direction of the light ray
  • by changing the shape of the lens we can alter these angles and bend the light more or less
211
Q

How does one change the focal point?

A
  • by rounding the lens, light is bent more and has a CLOSER focal point
  • round=closer focal point
212
Q

What allows for clear vision

A
  • the focal point falling on the retina
213
Q

What happens if the object draws closer, but the lens stays flat?

A

The focal point falls behind the retina

214
Q

How do objects come into focus?

A
  • round the lens
215
Q

How does the body round the lens?

A
  • parasympathetic nerve signals contract the ring-shaped, smooth CILIARY muscle reducing tension in the zonules, making the lens rounder, so light rays bend more and the focal point moves forward
  • sympathetic signals relax the ciliary muscle, making the lens flatter for far vision
216
Q

What is accomadation?

A

Rounding the lens for near vision, making it fatter

217
Q

What is the near point of accommodation? How does it change with age? What is this called?

A

the closest point a person can focys on
- With advancing age, the lens stiffens, hindering accommodation this is called presbyopia

218
Q

What is hyperopia? How is it fixed?

A
  • far sightedness, you can see far away, but not up close
  • the focal point is falling behind the retina
  • This is fixed with a CONVEX lens in front of the eye
  • the eye isn’t bending light rays enough to look at up close objects so the lens helps out
219
Q

What is myopia?

A
  • the focal point falls in front of the retina
  • you can see near, but not far away
  • near-sightedness
  • can be caused by too much focus/refraction or the eyeball is too long
220
Q

How is myopia fixed?

A
  • a CONCAVE lens causes light rays to spread out more
  • the lens of the eye is bending the light rays too much, the concave lens counteracts this by spreading out the rays
221
Q

Where are photoreceptors found? and what are they?

A
  • the retina
  • Light-sensitive neurons that convert light energy into electrical energy in cells
  • This process is called phototransduction
222
Q

What are the two main types of photoreceptors our retinas have?

A
  • cones and rods
  • each retina contains 6 mil cones and 120 mil rods
  • Rods and cones are neurons, thought they do not fire action potentials, instead they respond to stimuli with graded membrane potentials
223
Q

What is the structure of rods and cones?

A
  • in the outer segment (closer to the back of the eye) the membrane folds into disk-like layers which contain visual pigments that respond to light
  • the inner segment are the nucleus and organelles for protein synthesis, and in a basal layer, a synapse that releases glutamate
  • both receptors points toward the back of the eye
224
Q

How do photoreceptors detect light?

A
  • using membrane bound visual pigments
  • When light hits them, pigment molecules change shape, starting a chemical cascade that hyperpolarizes the cell, reducing its release of glutamate
  • photoreceptors are more active in darkness
  • Each photoreceptor contains millions of molecules of its pigment, but each type of photoreceptor has just one type of pigment
  • rhodopsin in rods
  • 3 other pigments in 3 types of cones
225
Q

How are photoreceptors distributed?

A
  • they are most densely packed in the macula, a central disk, and ESPECIALLY in its central pit called the FOVEA
  • this has a 2 degree visual angle (about as wide as two fingers viewed at arms length)
  • We use the fovea for detailed vision
  • 5 degrees away from its center, acuity is quartered, at 20 degrees it falls below the standard for legal blindness
226
Q

What is the blind spot?

A
  • the hole where axons carrying visual information exit the eyeball to form the optic nerve
  • it has no receptors
227
Q

What are the differences between rods and cones?

A
  • cones are for bright lights, rods are for dim
  • Cones are less sensitive than rods, they are responsible for vision in bright light and for distinguishing colors, but they don’t operate in dim conditions
  • Rods can detect single photons, but they operate only in low light
  • in daylight rods are “bleached out”
  • their rhodopsin is broken down so they can’t sense light
  • when the lights go dim the rods dark adapt, they have to build their stores of rhodopsin over 30 min
228
Q

How are rods and cones distributed?

A
  • the blind spot has neither
  • the fovea has almost exclusively cones
  • more peripheral retina contain many rods
  • your peripheral retina is more sensitive to light than your fovea (see dim star better looking slightly away)
229
Q

What are the 3 layers in the retina?

A

(from the back of the eye forward) photoreceptors–>bipolar cells–>ganglion cells
- up to 45 photoreceptors can converge on a single bipoar cell
- bipolar in turn converge on ganglion cells, so in each eye the signal from 126 million receptors in condensed into 1 million ganglion cells (important info conserved)
- convergence is greatest in the peripheral retina and least in the fovea where some receptors project 1:1 to bipolar

230
Q

What are the bipolar cells receptive fields like?

A
  • bipolar cells receive input from several photoreceptors
  • every neuron in the visual system has a receptive field also called a visual field
  • the receptive field is the region of the retina where light affects the cell’s activity (the set of photoreceptors which affect the cell)
  • bipolar cells have center-surround fields with a round center region and a doughnut-shaped surround
  • for every one neuron there will be a region of your retina where their getting their input from
231
Q

Describe on-center receptive fields for bipolar cells

A
  • On-center cells are excited by light in the center their of their field, and inhibited by light in the surround
  • so these cells respond most when a light fills their center and the surround is dark
  • if the surround is partially lit the cells are mildly excited and depolarized
232
Q

Describe off-center receptive fields for bipolar cells

A
  • off-center cells are inhibited by light in the center, and excited by the light in the surround. they respond best when a dark spot fills the center and the surround is light
233
Q

What does contrast have to do with bipolar cells?

A
  • When the lighting is uniform neither bipolar cell responds, becasue the effects of the center and surround cancel out, leaving the cell at its resting activity (only weakly active)
  • bipolar cells react strongly only when lighting is not uniform (respond to contrast)
  • They respond with graded membrane potentials; they do not fire action potentials
  • they are neurons but don’t fire action potentials
234
Q

How are bipolar cells and retinal ganglion cells related?

A
  • both types of bipolar cells synapse onto the next processing layer, the retinal ganglion cells, which unlike photoreceptors and bipolar cells, do fire action potentials
  • but like bipolar cells most retinal ganglion cells also have center-surround receptive fields, and these fields can also be on-center or off-center
  • so like bipolar cells, ganglion cells detect contrast
235
Q

What explains the Chevreul illusion?

A
  • the emphasis on contrast
  • the bands are all a uniform shade of grey, but they look darker to the right and lighter to the left
  • the contrast at the edges of where the bands meet is accentuated because bipolar and ganglion cells sense contrast
  • it may also explain the hermann grid (dots appearing in the middle of the black squares)
236
Q

How do receptive fields differ depending on the area of the retina?

A
  • ganglion cell’s receptive fields are different sizes depending on retina area
  • A ganglion cell near the fovea gets input (via bipolars) from only a few photoreceptors, mostly cones. Farther out, each ganglion cell gets input from many receptors, mostly rods
  • in the periphery each ganglion cell is very sensitive to light, but poor at reporting spatial detail because it blends information from a wide swathe of receptors
  • near the fovea, ganglion cells are less sensitive to light but have better spatial resolution because each one gets input from just a few densely packed cones
237
Q

What are M cells?

A

Large, magnocellular ganglion cells, provide information that is used by the brain to infer the movements of objects. These cells are phasic. 10% of retinal ganglion cells are M

238
Q

What are P cells?

A
  • small, parvocellular ganglion cells, or P cells, provide information that is used to infer form and fine detail, such as texture. 70% of retinal ganglion cells are P cells
239
Q

What are the cells that are at the center for circadian rhythms?

A
  • 1% of retinal ganglion cells are melanopsin ganglion cells, which are photoreceptors, with their own visual pigment, melanopsin. They project to the suprachiasmatic nucleus, a center for circadian rhythms
240
Q

How does visual information leave the retinas?

A
  • the optic nerves
  • each of the million ganglion cells in each retina sends its axon out the back of the eye through the blind spot
  • these million fibers from each eye form its optic nerve known as cranial nerve 2
241
Q

Where do the optic nerve fibers cross?

A
  • only half the optic-nerve fibers cross at the optic chiasm
  • when each optic nerve reaches the optic chiasm, half its fibers cross to the other side of the brain
  • fibers from the nasal half of each retina cross, those from the temporal retinas do not
242
Q

Why do the fibers cross?

A
  1. in the eye, the right side of the scene, the right visual hemifield, projects onto the left side of each retina
    - onto the nasal side of the right retina and the temporal side of the left retina
  2. because the nasal fibers cross, all the information from the right hemifield comes together in the left cerebral hemisphere, and vice versa
243
Q

How does information move from the eyes to the brain?

A
  • the nerve bundles emerging from the chiasm are called the optic tracts.
  • the name of the fibers bundles changes from optic nerve to optic tracts
  • They end in the 2 lateral geniculate nuclei (LGN) in the thalamus, which project via the optic radiations to primary visual cortex, V1
  • Together the 2 LGN have 2 million neurons the same as the number of ganglion cells in the 2 retina-whereas V1 has far more neurons
244
Q

Where is V1 found

A

Occipital lobe?

245
Q

How are visual areas of the brain organized?

A
  • neurons close to each other in the brain get information from close-together parts of the retina
  • this arrangement is found in the lateral geniculate nuclei, V1, and many higher visual processing areas
  • when light hits the retina in one area, that area in the visual processing parts of the brain also is active
246
Q

What does the retinotopic not preserve?

A
  • areas
  • the fovea, which covers only a small area of the retina, projects to large areas in the V1 (and in other cortical regions and LGN
  • a large proportion of visual cells in the brain receive and process data from foveal photoreceptors
  • the fovea gets a lot of space because it has many photoreceptors, bipolars, and ganglion cells, and so carries a lot of information
247
Q

What does color depend on and what makes it up?

A
  • it depends on light
  • light is made up of wavelengths
248
Q

What is a wavelength? What can we see?

A
  • the distance from one wave peak to the next, different wavelengths correspond to different colors
  • we normally see a range from 400 nm for violet to 700nm for red
  • we can also see extremely powerful infrared lights and people who have had their lenses removed can see some ultraviolet.
249
Q

Why did evolution give us eyes that see 400-700

A
  • the power in sunlight peaks there
  • Earth atmosphere is most transparent to these wavelengths
  • the seawater, where eyes first evolved is most transparents at 500 nm
250
Q

How do humans sense color?

A
  • 3 types of cones: red, green, blue
  • In most people 63% of cones are red, 31% are green, and 6% are blue
  • Each type of cone has its own type of visual pigment
  • All these pigments are similar to rhodopsin but not identical to it, and so all prefer different wavelengths of light
  • because we sense color with 3 types of cone we are called trichromats
251
Q

How does the brain infer color?

A
  • comparing data from the 3 types of cones
  • yellow light affects red and green cones, but not blue ones, so if your red and green cones are hyperpolarized, but not blue, then you perceive yellow
  • You can be fooled though
  • a red and green light with no yellow can produce the same cone activities as a yellow light would so the brain sees yellow both times
252
Q

Describe how different pigments prefer different wavelengths

A
  • blue: 420, blue-green: 498, green: 533, green-yellow: 564
  • the chart shows how much light the visual pigments absorb (as a percentage of the maximum for that pigment) at each wavelength
  • red and green cone pigments prefer yellow and yellow-green light. Blue cone pigment prefer blue
  • Rhodopsin (and rods) prefer blue-green
  • melanopsin prefers blue
253
Q

How can we produce any color perception?

A
  • by mixing the three wavelengths
  • any color we can experience corresponds to a pattern of activity in our 3 types of cones
  • the primary colors red, green, blue can produce any other colors
  • TVs, computer screen, etc show full color with just those three lights
254
Q

What are spectral colors?

A
  • spectral colors are those that can be evoked by light of a single wavelength
  • they are the rainbow colors, from violet through blue, green, yellow, orange, and red
255
Q

What are extra spectral colors?

A
  • colors such as purple or white that are evoked only by a mix of wavelengths
  • we see purple when 2 or more wavelengths affect red and blue cones more than green
256
Q

Describe the process of ganglion cells deciphering color…

A
  • there are 3 different classes of cones so there are 3 different channels
  • Some ganglion cells are excited by red light and by green light they are R+G cells or the yellow channel
  • Some are EXCITED by red light but INHIBITED by green R-G, others are INHIBITED by red and EXCITED by green G-R. These are the red green opponent channel
  • Some are EXCITED by blue and inhibited by red and green (B-R-G), which is the same as B-(R+G), blue minus yellow. Others are yellow minus blue. These two types for the blue-yellow opponent channel
257
Q

What are opponent channels thought to explain?

A
  • after images
  • when you stare at something green, your G-R cells gradually fatigue
  • when you look away, those cells are less active than your R-G and so you see red (same for blue vs. yellow)
  • We aren’t sure the responsible cells in the retina, as there are color-opponent cells in the LGN and visual cortex as well
258
Q

What is the most common variant of color blindness?

A
  • red-green color blindness
  • also called Daltonism where people have trouble distinguishing those colors
259
Q

What was special about color blindness?

A
  • it was the first trait to be linked to a chromosome
  • inheritance pattern= color blind father have normal daughters who have colorblind sons
  • the genes for red and green cone visual pigments lie of the X-chromosome
  • problems at these loci underlie 95% of all variations in color vision (the “blue” gene on chromosome 7 is more stable)
  • women are seldom color blind because the other X compensates for the other defective one
  • If two X-chromosome code for 2 different functional red cone pigments, a woman may be a tetrachromat
260
Q

What is reflectance?

A
  • the intrinsic color of a surface
  • its tendency to reflect certain wavelengths of light and absorb others
  • a yellow banana reflects more yellow light than other wavelengths
  • the reflectance of an object carries info about it (ex. ripeness)
261
Q

What does the light an object sends to our eyes depend on?

A
  • reflectance and illumination
  • ex. if you put a ripe yellow banana in greenish light then the bananas reflectance doesn’t change, but now it send mainly green light to our eyes
  • nonetheless, our brains can usually infer the reflectance so we see the ripe banana as yellow even in green light
  • this crucial ability is called color constancy
262
Q

What is a demonstration of color constancy?

A
  • the 2 Rubik’s cubes show in yellow and blue light, however, you can tell which parts of the rubiks cube are which color in both
  • However the color you perceive is not the light being shown on your eyes
  • the light is the same on both pictures and appears as grey when you hide everything except one square
  • in the yellowish light, blue squares reflect a lot of yellow and only a little blue (not much blue light), and so they send a grayish mix of wavelengths to the eye
  • in the original photo, your brain sees a lot of yellow and correctly infers the lighting is yellow and the squares are blue without context you can’t deduce lighting or reflectance
263
Q

Comparisons that underlie constancy cause what?

A
  • Illusions
  • The center squares are identical in color, but the surrounding colors affect our perception of brightness, hue, and saturation
264
Q
A

PSL300 (1 decks)

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