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No LGI1-null mice survived beyond postnatal day 21 (Fig. 5A),
while no LGI1
+/
or wild-type littermates had died at this age.
We noted at postnatal day 14 that the body weight of LGI1
/
mice was significantly less than that of LGI1
+/
(P = 0.0012) or
wild-type (P = 0.027) mice, whereas the body weight at postnatal
day 10 was similar for LGI1
/
, LGI1
+/
or wild-type mice
(Fig. 5B). The failure to thrive between postnatal days 10 and
14 was associated with a smaller size (LGI1
/
mice were up to
50% smaller that wild-type littermates) and an apparently slower
development in some pups (Fig. 5C). Postmortem examination
of LGI1
/
mice at postnatal day 14 revealed an absence of
stomach contents (Fig. 5D) and a lack of body fat. While early
mortality might result from dehydration and/or starvation due to
a failure to feed, we observed that death occurred during
prolonged hypertonic episodes in 28% of LGI1
/
mice (at
age postnatal days 14, 16 and 17). It may occur even more
frequently in unobserved mice. Some pups of smaller litters
were moderately malnourished but still died prematurely, sug-
gesting that seizures may have caused their death. One animal
died at postnatal day 15 during a prolonged video–EEG recording
of more than 4 h with no seizure. Brain activity was progressively
reduced during the recording.
Adult heterozygous LGI1
+/
mice
have lowered threshold to
audiogenic seizures
Heterozygous LGI1
+/
mice genetically mimic patients with
ADLTE. The mice are fertile, behaviourally similar to wild-type
animals and live for at least 18 months. Spontaneous clinical seiz-
ures have never been observed either in pups or adult mice. Since
seizures in patients with ADLTE can be triggered by sound,
we examined the susceptibility of LGI1
+/
mice to a single
sound stimulus at frequency 11 kHz and intensity 93 dB. This
stimulus did not induce seizures in LGI1
/
, LGI1
+/
or wild-type
mice at postnatal day 10 (data not shown). At postnatal day 21,
some mice exhibited sound-induced seizures, but seizure thresh-
olds of LGI1
+/
(seizures induced in 13% of animals) and
wild-type mice (seizures induced in 5% of animals tested) were
not significantly different (Fig. 6A). In contrast, at age postnatal
day 28, auditory stimulation induced seizures in a significantly
higher percentage of LGI1
+/
than wild-type littermates (52%
versus 18%, P50.03) (Fig. 6A). Typically, audiogenic seizures
began suddenly at 5–20 s after the onset of the tone, with
wild running, followed by a tonic phase and sudden death
in 23% of mice. We examined the cortical EEG of postnatal
day 28 LGI1
+/
mice (n = 8) and wild-type mice (n = 3) dur-
ing auditory stimuli. Cortical electrodes detected no epileptic
activity during the wild running or tonic phase (Fig. 6B).
Possibly audiogenic seizures are initiated in the brainstem
rather than the cortex as previously suggested (Seyfried et al.,
1999). The neuronal network of audiogenic seizures remain
to be investigated with additional recordings of midbrain
structures.
C
LGI1-/-
LGI1+/-LGI1-/-Wild-type
LGI1+/-
P14 P9
D
B
A
Figure 5 Premature death and reduced body weight in
homozygous LGI1
/
mice. (A) Kaplan–Meier survival curves of
LGI1
/
(n = 25), LGI1
+/
(n = 52) and wild-type (n = 23) mice
from postnatal day 0 until postnatal day 20. Of the LGI1
/
mice 50% had died at postnatal day 17. (B) Body weight was
comparable for LGI1
/
(n = 21), LGI1
+/
(n = 27) and wild-type
(n = 20) animals between postnatal days 8 and 10. Between
postnatal days 8 and 14, the body-weight ratio of LGI1
/
mice
was reduced with respect to LGI1
+/
and wild-type mice.
*P50.05. (C) LGI1
/
mice were smaller than LGI1
+/
and
wild-type littermates at postnatal day 14. (D) Stomach content
of LGI1
/
mice (empty) and LGI1
+/
mice (full) at postnatal
day 14. At P9, stomach sizes and contents of LGI1
/
and
LGI1
+/
mice were similar.
2756 | Brain 2010: 133; 2749–2762 E. Chabrol et al.
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