Biology Reference
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(
Bozdagi et al., 2008
). LTD and LTP are activity-dependent changes in syn-
aptic efficacy resulting from synaptic plasticity—actual changes in the syn-
aptic structure. LTDweakens synaptic strength, while LTP enhances it. The
absence of
VGF
resulted in the inability to weaken synaptic strength,
suggesting that
VGF
could be important for the reduction of synaptic con-
nectivity seen in the song control system after the breeding season in song-
birds, and also in torpor bouts of hibernating mammals.
Hibernation is characterized by changes in energy metabolism and ther-
moregulation and also involves coordinated synaptic plasticity, making
VGF
a candidate for involvement in the control of this phenotype. In the
thirteen-lined ground squirrel brain,
VGF
expression is increased in Octo-
ber in both the cerebral cortex and the hypothalamus (
Schwartz et al., 2013
).
This time point is characterized by decreased food consumption, increased
white adipose stores, and onset of shallow torpor bouts.
VGF
in the hypo-
thalamus could be playing a role in the seasonal switch from the hyperphagic
behavior of summer and early fall to the hypophagic behavior seen in hiber-
nation. The fact that the same expression pattern is seen in the cerebral cor-
tex suggests that it could also be playing a role in synaptic plasticity.
5.3. Modulation of neuronal cilia
The primary cilium is a cellular organelle found in almost all eukaryotic cells,
including neurons (
Louvi & Grove, 2011
). Each cell has only one primary
cilium, a protrusion of the cell membrane covering a cytoskeletal axoneme
core consisting of nine microtubule pairs, which provides structural support
to the cilium (
Fig. 9.6
). The axoneme is anchored by a ciliary basal body,
which is a modified centriole. There is a transition zone at the base of the
primary cilium for selected protein entry via intraflagellar transport. The
exact function of neuronal primary cilia is unclear, but these organelles sense
and receive signals from the environment and relay that information to the
cell (
Adams, 2010
).
Deficits in primary cilia are the cause of several disorders, deemed
ciliopathies, includingBardet-Biedl syndrome (BBS) andAlstromsyndrome,
both characterized by obesity (
Badano, Mitsuma, Beales, & Katsanis, 2006
).
BBS is associated with mutations in at least 11 genes (
BBS1
-
11
)(
Mutch &
Cl´ment, 2006
).
BBS1
has been implicated in fat storage in
C. elegans
(
Mak, Nelson, Basson, Johnson, & Ruvkun, 2006
). Loss of primary cilia in
the brain using conditional alleles of two ciliogenic genes (
Tg737
and
Kif3a
)
induced hyperphagia and obesity in adult mice (
Davenport et al., 2007
). This
