Final Flashcards
What is the cause of menopause? Name 5 consequences of menopause.
Menopause happens because the ovaries stop producing enough estrogen and progesterone, leading to the end of menstrual cycles. Its effects include hot flashes, bone loss, higher heart disease risk, vaginal dryness, and mood changes.
Describe the regulatory elements of the hypothalamic pituitary gonadal (HPG) axis. Include regulatory inputs on the hypothalamic neurons.
The HPG axis is regulated by GnRH, which triggers LH and FSH release from the pituitary to stimulate gonads. Sex steroids provide negative feedback, but high estradiol causes positive feedback for ovulation. GnRH is influenced by kisspeptin, stress, leptin, and circadian rhythms to align reproduction with the body’s needs.
How does estradiol exert both positive and negative feedback on the GnRH neuons?
Estradiol exerts feedback on GnRH neurons indirectly through kisspeptin neurons. Low to moderate levels suppress GnRH (negative feedback), while high levels stimulate kisspeptin to trigger a GnRH surge (positive feedback) for ovulation.
Describe the type of experimental evidence required to demonstrate that one subpopulation of neurons (e.g. kisspeptin) controls secretion of another type of neuron (e.g. GnRH)
Neuronal Pathway Mapping:
Trace connections between kisspeptin and GnRH neurons to show that kisspeptin neurons directly influence GnRH neurons.
Genetic Manipulation:
Use techniques like optogenetics or chemogenetics to activate or deactivate kisspeptin neurons and observe changes in GnRH secretion.
Hormonal Measurement:
Measure GnRH levels before and after altering kisspeptin activity to confirm its role in regulating GnRH release.
Behavioral Impact:
Assess changes in reproductive behavior or puberty timing when kisspeptin neurons are altered, indicating their role in controlling GnRH.
List the 4 basic requirements for a circadian pacemaker
A circadian pacemaker must generate self-sustained oscillations, synchronize to external cues like light, provide output signals to regulate rhythms, and maintain temperature compensation across varying temperatures.
Describe the steps whereby the light entrains the SCN
Light Detection: Photoreceptors in the retina (specifically melanopsin) detect light.
Signal Transmission: The retinal ganglion cells send signals via the retinohypothalamic tract to the SCN.
SCN Adjustment: The SCN adjusts its rhythm based on the light signal, synchronizing the circadian clock to the external light-dark cycle.
Describe the core loops of the molecular circadian clock
Transcription-Translation Feedback Loop (TTFL):
Clock genes (Per, Cry, Bmal1, Clock) are transcribed, their proteins inhibit their own transcription, creating a feedback loop.
Protein Degradation:
Per and Cry proteins degrade over time, removing inhibition and restarting the cycle.
These two steps together maintain the 24-hour circadian rhythm.
GnRH pulse amplitude is highest during…
puberty
Name two non-reproductive changes that occur in the brain during adolescence
Prefrontal Cortex Development:
The prefrontal cortex, responsible for decision-making, planning, and impulse control, continues to mature, improving cognitive abilities and self-regulation.
Increased Dopamine Sensitivity:
There is heightened sensitivity to dopamine in areas of the brain involved in reward and pleasure, contributing to increased risk-taking behavior and sensitivity to rewards during adolescence.
Of the hundreds of gut peptides, GLP-1, suppresses appetite. You would expect it to… NPY/AgRP neurons and… POMC neurons
inhibit
activate
The hypothalamic POMC and NPY/AgRP neurons communicate with a variety of neurons to regulate food intake and energy expenditure. Name 4 types of, or the location of these neurons. What physiological outputs do they control.
Paraventricular Nucleus (PVN) Neurons:
Control appetite, energy expenditure, and stress response by regulating autonomic functions and hormone release (e.g., thyroid hormone, cortisol, prolactin).
Lateral Hypothalamus (LH) Neurons:
Regulate feeding behavior, arousal, and motivate food-seeking behavior through reward pathways.
Dorsal Vagal Complex (DVC) Neurons:
Control gastric motility and insulin secretion, impacting digestion and nutrient absorption.
Ventromedial Hypothalamus (VMH) Neurons:
Regulate satiety and energy balance by influencing thermogenesis, glucose homeostasis, and fat storage.
How does leptin regulate bodyweight homeostasis? Why isn’t it commonly used as a weight loss drug?
Leptin signals the brain about fat stores. High leptin reduces appetite and increases energy expenditure; low leptin increases hunger and reduces energy use.
Why Not Used as a Weight Loss Drug:
Leptin Resistance: Obese individuals become less responsive to leptin.
Limited Efficacy: Leptin doesn’t reduce weight in obese people due to resistance.
Side Effects: Potential immune and hormonal issues make it impractical.
Describe the steps involved in a sexual differentiation of the male and female reproductive tracts. Include the important hormonal and enzymatic steps.
Male Sexual Differentiation:
SRY Gene Activation:
The SRY gene on the Y chromosome triggers the development of testes.
Testosterone Production:
The testes produce testosterone, which drives the development of the male reproductive tract.
Müllerian Inhibiting Substance (MIS):
The testes also secrete MIS (also called Anti-Müllerian Hormone), which causes the regression of the Müllerian ducts (female precursor structures).
Dihydrotestosterone (DHT) Production:
Testosterone is converted to DHT by the enzyme 5α-reductase, which is responsible for the development of male external genitalia (e.g., penis, scrotum).
Female Sexual Differentiation:
Absence of SRY Gene:
Without the SRY gene, the gonads develop into ovaries.
Estrogen Production:
The ovaries produce estrogens, which promote the development of the female reproductive tract (e.g., uterus, fallopian tubes).
Müllerian Ducts Develop:
In the absence of MIS, the Müllerian ducts develop into the female reproductive tract (e.g., uterus, cervix, upper vagina).
Wolffian Duct Regression:
The Wolffian ducts regress due to the absence of testosterone, as they are the precursors to the male reproductive tract.
If the developing fetus has a complete mutation in the androgen receptor gene, what would be the resulting phenotype of the baby’s external genitalia?
This results in a female phenotype externally but with male genetic sex (XY).
When is the critical period for sexual differentiation of the brain? what are potential mechanisms by which steroid hormones act to influence the permanent structure/ function of the brain?
The critical period for sexual differentiation of the brain is during early development, around mid-gestation in humans or postnatal days 1-5 in rodents.
Mechanisms:
Receptor Binding: Steroids bind to nuclear receptors, influencing gene expression.
Synaptic Connectivity: Steroids alter synapse growth and pruning.
Epigenetic Changes: Steroids cause DNA methylation and histone modifications.
Neurogenesis: Steroids affect neuron formation and brain region differentiation.
