Rise of the Animal Kingdom and Epigenetic Mechanisms of Evolution - Building the Most Complex Structure on Earth - page 279

Neural mechanisms involved in the increased thermogenesis are constrictions of
skin vessels for reducing heat loss, shivering, and migration toward warmer places.
When the environmental temperature is elevated, the CNS activates mechanisms
that intend to maintain the organism's temperature within a species-specific set point
of the CNS.
Certainly, in determining the activation and the level of activation of the ther-
mogenesis, the hypothalamus processes information about the brain and core tem-
perature and it will continue to stimulate or inhibit thermogenesis until the body
temperature comes within the normal range. The hypothalamic temperature set point
is found experimentally ( Hammel et al. (1963) ). It is neither arbitrary nor inalterable.
Set points are adjustable not only in evolution but also during individual develop-
ment. Modification of the temperature set points is induced experimentally in chick-
ens and rabbits. Rearing rabbits in cold temperatures lowers their temperature set
points ( Tzschenke and Nichelmann, 1997 ). Changes in the incubation temperatures
also alter the set point in chickens ( Gallus domesticus ). Warm-blooded animals mod-
ify their temperature set points to adapt their physiology to various stress conditions.
They also modify their temperature set points in response to cyclic changes in estro-
gen levels.
Neural responses are normally adaptive, as they tend to avert possible negative
effects of stimuli or utilize their possible positive effects. In a generalized case, the
processing output in the CNS starts a signal cascade, which ends with the activation
of one or more genes in a specific cell, tissue, or organ ( Figure 5.16 ). For exam-
ple, the output of the processing in a bird's brain of the changes in the photoper-
iod (lengthening of the day) or in social stimuli (e.g. song of conspecifics) leads to
the activation of gonadotropin-releasing hormone (GnRH)-secreting hypothalamic
neurons. In turn, the secreted GnRH starts the well-known hypothalamic-pituitary-
gonadal cascade, which induces its reproductive activity.
While neural electrical signals are encoded in the form of variations in intensity,
frequency, duration, and patterns of electrical spikes, chemical signals released by
the CNS for starting signal cascades are often encoded in amplitudes or pulses of the
release of neurohormones.
An interesting example of encoded hypothalamic epigenetic information is
offered by the pulsatile patterns of GnRH secretion. GnRH is secreted by a few hun-
dred hypothalamic neurons in humans. It is secreted in brief pulses that vary from
about 1 h during the follicular phase to about 6 h during the luteal phase. The pulse
frequency is the form in which the hypothalamus instructs the pituitary cells on
which of the two alternative forms of gonadotropic hormones, luteinizing hormone
(LH) or follicle-stimulating hormone (FSH), to be produced ( Walker et al., 2010 ).
Slower pulses of the GnRH secretion stimulate the pituitary cells to produce LH,
whereas higher pulses stimulate the secretion of FSH, with all the consequences in
the reproductive organs and functions ( Krakauer et al., 2002 ) .
Now we know of a potential mechanism used by the pituitary cells to decode the
epigenetic information about which of the two alternative pituitary gonadotropins to
secrete. A slower pulse frequency activates the secretion of the immediate Egr1 and