Motivation of Sexual Behaviours Flashcards

1
Q

How is the urogenital system differentiated?

A

Based on the Sry gene (either on Y, on X, or absent/ dysfunctional)

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2
Q

What steroids are higher in females?

A

Estrogens such as estradiol, estrone, estriol, and estetrol

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3
Q

What steroids are higher in males?

A

Androgens such as testosterone and dihydrotestosterone

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4
Q

How do steroids work?

A

Steroids are hormones which are lipophilic, meaning they can enter cells or neurons through the cell membrane. They were primarily thought to exert their effects slowly by way of gene expression

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5
Q

What are the two pathways for steroids to exert effects?

A

The genomic pathway and the non-genomic pathway (through steroid receptors on the cell membrane)

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6
Q

Which brain regions are sexually dimorphic?

A

The preoptic area (POA) (in the anterior hypothalamus), Ventromedial hypothalamus (VMH), Medial amygdala (MeA), and Spinal nucleus of the bulbocavernosus (SNB)

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7
Q

What are the organizational effects of steroids?

A

To guide the organization of the brain, endocrine glands, and behavior during hormone-sensitive “critical periods” or epochs of fetal and postnatal life

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8
Q

What are the activational effects of steroids?

A

At puberty and afterward, to generate the growth of secondary sex characteristics, to activate endocrine systems involved in sperm and egg production, to mature neuroendocrine systems required for pregnancy, and to stimulate sexual behaviors

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9
Q

What is masculinization?

A

An active process of acquiring “male-typical” anatomy, physiology, and behavioural functions. The process involves testosterone being converted to estradiol

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10
Q

What is feminization?

A

Default or “passive” process in mammals of acquiring “female-typical” anatomy, physiology, and behavioural functions

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11
Q

How can masculinization be disrupted and restored?

A

Cyclooxygenase-2 (COX-2) inhibitors disrupt SDN formation and the display of masculine sexual behaviour after puberty. However, the replacement of Prostaglandin E2 (PGE2) in perinatally castrated males can restore those processes

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12
Q

Why does the female brain not masculinize if estradiol is the masculinizing hormone?

A

Alpha-fetoprotein is secreted by the liver and was thought to either facilitate or inhibit estrogen from reaching neural tissue. α-fetoprotein gene loss results in partial masculinization of the brain

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13
Q

What is the role of Gonadotropin-releasing hormones (GnRH)?

A

When GnRH is released from the hypothalamus, it induces the release of gonadotropins (Luteinizing hormone, Follicle-stimulating hormone) from the pituitary gland

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14
Q

How does progesterone relate to ovulation?

A

Progesterone peaks just prior to ovulation, it is a critical hormone for signalling the upcoming time of ovulation

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15
Q

What is the Dual Control Model?

A

Sexual behaviours are regulated through the balance of inhibitory neuromodulators (opioids, serotonin) and excitatory neuromodulators (dopamine, norepinephrine, melanocortins). Neuromodulators play a large role in regulating mating behaviours

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16
Q

What are the two sequences of sexual behaviour for male rats?

A

Appetitive (sexual excitement, arousal, preparatory behaviours) & Consummatory (mounting, ejaculation)

17
Q

What happens when the medial preoptic area (mPOA) is lesioned?

A

Copulation is abolished, but not 2nd order responding

18
Q

What happens when the medial amygdala is lesioned?

A

2nd order responding is abolished, but not copulation. This is because the medial amygdala is involved in motivated behaviour

19
Q

How is Dopamine increased in Nac and mPOA?

A

Motivationally-relevant stimuli increase dopamine. NAc is responsive to novelty but more to a sexually receptive partner. mPOA is responsive to estrous secretions and sexually receptive partner

20
Q

What melanocortins have an effect on sexual behaviour?

A

POMC peptides, Beta-endorphin, ACTH, alpha-MSH (facilitates lordosis and erections)