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Hypothalamus Lecture Notes 2016 525 1012
Hypothalamus Lecture Notes 2016 525 1012
Dr. Salm
Lecture Notes
Hypothalamus
Dr. Salm
asalm@hsc.wvu.edu
These are your objectives for this lecture. Under point # 5 (Understand
the data...) this includes data from rodent studies that led to the
experiments on humans that have provided emerging data for a
biological basis for sexual preference, performance and gender
identity. An understanding of the animal work on what the other
hypothalamic nuclei are doing is also recommended. Many of these
studies would not be ethically feasible in humans but have
nevertheless provided valuable insight into the human condition.
Exposing students to translational studies (i.e., preclinical rodent
experiments) is an objective listed in the AAMC guidelines for medical
education and, thus, is included in this lecture.
Because of the tight packing of the nuclei, closed head injuries, brain
surgery, meningitis, encephalitis, strokes, subarachnoid hemorrhages
and neoplasms can all present as a constellation of disturbances,
depending on which nuclei are affected.
You do not need to memorize which nuclei are included in each area.
Slide 16. The medial preoptic nucleus (MPOA) is located in the most
anterior part of the hypothalamus (anterior to the anterior nucleus, in
fact). There is a medial and lateral component to it as well as other
subparts with non-reproductive functions.
I have posted an addendum in the lecture folder on SOLE with many
links and references.
Adult sexual behavior in the rat depends on whether the brain was
organized by gonadal hormones during the first few days after birth.
Sexual behaviors and preferences are highly correlated with the size of
the POA.
The Interstitial Nucleus of the Anterior Hypothalamus is the human
analog of the POA in rodents and similar data have been gained in
humans at this time.
The developing brain is, by default, female with respect to the POA. In
male rats, exposure to testosterone in the perinatal period (G18-21)
changes a female POA to a male POA. Males ultimately develop larger
POAs due to more neurons and larger dendritic arbors, than do
females.
Slide 21. In this study from Oomura et al., (1983), the role of the
preoptic area in sexual functioning was amply demonstrated. Male
primates were restrained in apparatus that nevertheless let them be
sexually active. They were able to bar press in order to draw a
receptive female in a suitably flexible restraining apparatus towards
them. Firing rates of neurons in the medial POA are recorded as the
male monkey mounts, mates and ejaculates.
Slide 22. In this experimental set-up, male primates are able to bar
press in order to draw a receptive female in a flexible restraining
apparatus towards them. Neurons in the medial POA are recorded as
the male monkey mounts, mates and ejaculates.
Slide 23. Soooo what about humans?? The third interstitial nucleus of
the anterior hypothalamus appears to be the human homolog to the
sexually dimorphic preoptic area in rodents.
Slide 26. These are high magnification images taken from the 1991
LeVay paper.
Slide 27. There are many non-sexual behaviors that also have a
distinctive female vs. male expression. Since most all-biological
variables are distributed normally, this explains the Bell-curve of many
gender related human behaviors.
Slide 28-29. More interesting data, from humans this time, that
demonstrates the role of the POA (called anterior hypothalamus here)
in sexual responsiveness and perhaps sexual identity as well. In this
study, 18 healthy, self-professed heterosexual males were given a
drawing test to determine the strength (Hetero)sexual Identity. Then
their brains were imaged with fMRI while watching hard core erotic
video clips interspersed with clips of the 2011 Mountaineer bowl game
to determine which they found more arousing oops just joking- they
were really generic sports clips which served as controls.
They also wore a penile tumescence-measuring device (also
affectionately known as the peter meter in the sexual research
community) to provide another measure of sexual arousal
(interestingly quantified as mm Hg; similar to a thermometer).
Slide 35 This is the basic plan for control of all the anterior lobe
hormones: releasing factors or inhibitory factors are released to the
portal system for transport to anterior lobe. There they act on
secretory cells.
Slide 36. This slide illustrates the functions of the hormones that are
released from the anterior and posterior pituitary glands.
Slide 37. The suprachiasmatic nucleus is the clock of the body. It
gets information about luminance and this acts on clock genes that
are in these cells alone. Activation of these genes sets up cyclic
molecular events (for example, neurotransmitter synthesis, firing
rates) within the SCN cells. Such rhythms have been demonstrated to
persist for long periods of time, even in in tissue slices where the SCN
has been isolated from all other inputs.
SCN Afferents: peripheral retinal ganglion cells concerned with
luminance.
Efferents: SCN projects to the IML cell column to SCG to finally arrive
at the pineal (also see slide 39 however). Here it regulates the
production and synthesis of melatonin from the pineal gland.
Functions: entrains circadian rhythms of sleeping, eating, melatonin
synthesis and release from the pineal gland.
Slide 38 There are pacemaker type cells in different glands and tissues
of the body. It is beleived that the SCN is the main clock, and that the
other centers are entrained to it.
Slide 38.This shows the best known route of SCN regulation of the
pineal. It projects either by itself or via a relay through the
paraventricular nucleus to autonomic brainstem enters or the IMLCC to
stimulate sympathetic apparatus carried by the superior cervical
ganglion which crawls up vasculature to reach the pineal. . From there
it goes superior cervical ganglion to regulate synthesis and release of
melatonin from the pineal. Melatonin is a common jet lag remedy for
those traveling to different time zones. About 3 mgs is recommended
on the first several days after arriving-to be taken at the local bedtime.
It appears to work by helping to rapidly reset the circadian clock.
Slide 39.Figure 23.5 Nolte (page 585). Left side. Hamsters kept in
constant light will slightly deviate each day from an entrained activity
cycle until their SCNs are lesioned. Likewise when humans are placed
in a situation of only artificial light and allowed to naturally wake-up
and go to sleep, the free-running cycle drifts to about 25.3 hours.
This is perhaps why we feel sleep deprived so much of the time.
Slide 45 Dr. Haut will cover the types of memory loss associated with
pathology of the mammillary bodies.
Slide 46-48. Control of the ANS and Horners syndrome. Here for your
review.
Slide 55. This is an admittedly not great picture of the fornix and
mammillothalamic tract as seen in a single sagittal myelin stained
section. The fornix should be an easy ID for you at this time. However,
please see Haines atlas pages 173 and 175 (plates7-2 and 7-4, 8th
edition) for better images of the mammillothalamic tract if you are
not sure about its location from this figure.
Slide 56. The median forebrain bundle is a fiber system that runs in the
lateral hypothalamus from rostral to caudal and vice versa. It is not
identifiable in sections prepared by conventional means. It connects
forebrain structures with brainstem structures and with the
hypothalamus in between. You dont need to memorize the list of
structures.
Slides 57 and 58
The DLF ascending tract has its origins in nuclei of the reticular
formation and nucleus solitarius. These fibers carry visceral sensory
information to the periventricular, paraventricular, and posterior
hypothalamus.
Hypothalamic efferents in DLF arise from the PVN, SON and
periventricular area and go to the
1) midbrain central gray for pain modulation,
2) the medullary autonomic centers for heart rate, blood pressure, and
respiration,
3) brainstem parasympathetic nuclei (dorsal motor nucleus of the
Vagus),
5) IMLCC, and
6) lumbo-sacral preganglionic parasympathetic neurons.