444 Neuroanatomy: Draw It to Know It
Suprachiasmatic Circuitry
Here, we will draw the circuitry for the suprachiasmatic
control of melatonin production and release. As a
byproduct of 3.5 billion years of the Earth’s daily rota-
tion around its axis, all of us have a circadian rhythm of
approximately 24 hours. Because of this internal clock,
we maintain a 24-hour cycle of behavioral activities even
when we are placed in non-24-hour environments.
Importantly, the timing of our internal clock is aff ected
by certain environmental cues, called zeitgebers, of which
light is commonly considered the most potent. In this
diagram, we will see how through the retinohypotha-
lamic pathway, light acts on the suprachiasmatic nucleus
(the master timekeeper) to adjust the production and
release of melatonin and, in turn, the timing of our inter-
nal clock.
First, draw an outline of the hypothalamus — include
the pituitary gland and mammillary bodies. Next, add
the optic chiasm. Th en, label the suprachiasmatic nucleus
just above the optic chiasm in the anterior hypothalamus.
Next, label the paraventricular nucleus. Now, add a cross-
section through the cervical spinal cord. Th en, show the
superior cervical ganglion and the pineal gland.
Next, show that during the dark phase, descending
hypothalamospinal projections from the paraventricular
nucleus excite the cervical spinal cord, which, in turn,
excites the superior cervical ganglion, which activates
the production of melatonin from within the pineal
body, causing its release into circulation, which helps
promote sleep.
Now, show that during the light phase, light passes
along the retinohypothalamic pathway to excite the
suprachiasmatic nucleus. Th en, indicate that the supra-
chiasmatic nucleus inhibits the paraventricular nucleus,
which causes inhibition of the production and release of
melatonin, thus promoting wakefulness.^11
In addition to melatonin, several other substances
have been shown to play an important role in sleep
induction. At the beginning of the 20th century,
Kuniomi Ishimori in Japan and Henri Piéron in France,
independently but concurrently, performed experiments
wherein they transferred brain matter (cerebrospinal
fl uid or brain tissue) from sleep-deprived dogs to well-
rested dogs and observed that the well-rested dogs went
to sleep. From this evidence, they both concluded that
certain agents within the body must accumulate to pro-
mote sleep. Experiments over the past 30 years have
identifi ed several sleep-promoting substances. Tumor
necrosis factor-alpha and interleukin-1 are two well-
studied substances with sleep-promoting properties.
Th ey have been shown to cause sleepiness and fatigue as
well as other somatic symptoms commonly associated
with sleepiness: cognitive dysfunction, sensitivity to
pain, impaired glucose tolerance, and chronic infl amma-
tion. Another sleep-promoting substance of particular
interest is adenosine because caff eine, which is second
only to oil in its importance as a global commodity, is
believed to produce its wake-promoting eff ects through
its actions on adenosine receptors.^12