Analysis Tools
cardiovascular system
|
• surprisingly, homozygotes display a significant increase in basal mean HR relative to wild-type mice (714.0 11.5 bpm vs 625.4 20.0 bpm, respectively)
• in response to omega-CTX, homozygotes fail to exhibit a significant reduction in mean HR relative to wild-type mice (10.3 7.0 bpm vs 158.4 41 bpm, respectively)
|
hypertension
(
J:76458
)
|
• surprisingly, homozygotes display a significant elevation in basal mAP relative to wild-type mice (102.0 4.3 mmHg vs 77.0 3.9 mmHg, respectively), in the absence of cardiac structural abnormalities
• in response to omega-CTX, homozygotes fail to exhibit a significant reduction in mAP relative to wild-type mice (2.4 1.0 mmHg vs 22.6 2.6 mmHg, respectively), suggesting cardiovascular dysfunction
|
nervous system
|
• homozygotes are viable and behaviorally normal but exhibit a complete and selective loss of the omega-CTX-sensitive N-type Ca2+ currents in neurons of the superior cervical ganglion and sympathetic nerve terminals, with no significant changes in the activity of other voltage-dependent Ca2+ channel types
• in isolated left atria prepared from mutant mice, the positive inotropic responses to electrical sympathetic neuronal stimulation are significantly reduced relative to of wild-type mice; in contrast, parasympathetic nervous activity remains unaffected
|
|
• in response to bilateral carotid artery occlusion, wild-type mice exhibit a marked increase in mean arterial pressure (mAP; 21.7 5.2 mmHg) which is significantly suppressed by 30 g/kg of omega-CTX (5.8 1.2 mmHg); in contrast, homozygotes show only a slight increase in mAP (7.6 2.1 mmHg), that is insensitive to omega-CTX administartion, suggesting impaired carotid baroreflex function
|
|
• in dorsal root ganglion (DRG) neurons from mutant mice, the profile of calcium channel currents supported by Ba2+ as the charge carrier was characterized; the total current density is reduced in mutant mice, and successive applications of specific blockers for L, N, P and Q type channels indicates that the N-type calcium channels are specifically reduced and the other channel types are unaffected
|
behavior/neurological
| N |
• thresholds for mechanical stimuli in the tail pinch test are not significantly different in mutant and control mice
• no significant differences in general behavior is noted between mutant and control mice
|
hyperactivity
(
J:84684
)
|
• under novel conditions and under habituated conditions in the dark phase, mutant mice exhibit more total activity (ambulation, repetitive behavior, and rearing) than control mice
|
|
• mutant mice exhibit a trend toward increased wakefulness at the expense of sleep states
|
|
• REM sleep latency is increased and the mean inter-REM sleep interval is increased compared to controls
• EEG power spectral analysis shows that mutant mice have greater spectral power density during wakefulness and during REM sleep than controls; however, mutant mice have reduced EEG spectral power density during non-REM sleep episodes than controls
|
|
• in mutant mice, mean REM sleep episode duration is increased with a decrease in the number of REM sleep episodes compared to controls
|
|
• increase in the average interval of occurrence of NREM sleep and wakefulness episodes in mutant mice compared to controls
• decreased vigilance state fragmentation during the light phase
|
|
• the biphasic pain response of mutant mice exhibit significantly attenuated response in Phase 2, and slightly attenuated pain behaviors in Phase 1 when hindpaws are injected with 2% formalin
|
|
• mutant mice exhibit longer latencies in the hot plate test compared to controls
|
growth/size/body
| N |
• no significant differences in body weight is noted between mutant and control mice
|
|
• after 10 weeks on a high fat diet, 18 week old mutant mice weigh significantly less than controls despite no notable differences in food consumption between mutant and control mice
|
homeostasis/metabolism
| N |
• no significant differences in feeding behavior or body weight is seen between mutant and control mice
(J:84684)
• mutant mice at 16 weeks of age exhibit normal insulin homeostasis; insulin levels are similar to controls under fasting conditions and after glucose administration
(J:105212)
• glucose clearance rates in mutant mice at 17 weeks of age are similar to controls in an insulin tolerance test; these rates are also similar in mutant mice fed a high-fat diet compared to identically-fed controls
(J:105212)
• after 10 weeks on a high fat diet, 18 week old fasted mutant mice exhibit no significant differences in the plasma levels of adiponectin, total cholesterol, urea nitrogen and creatinine
(J:105212)
|
|
• after 10 weeks on a high fat diet, 18 week old mutant mice weigh significantly less than controls despite no notable differences in food consumption between mutant and control mice
|
|
• after 10 weeks on a high fat diet, 18 week old fasted mutant mice exhibit reduced plasma concentrations of glucagon
|
|
• after 8 weeks on a high fat diet, 16 week old mutant mice exhibit decreased blood insulin levels in the fasting state compared to identically fed controls; at 30, 60 and 90 minutes after oral glucose administration, these high-fat fed mutant mice exhibit lower insulin release levels than controls
|
|
• after 10 weeks on a high fat diet, 18 week old fasted mutant mice exhibit reduced plasma concentrations of leptin
|
|
• mutant mice at 16 weeks of age, starved for 16 hours and then treated with oral administration of glucose, exhibit significantly lower blood glucose levels than control mice, and the glucose disposal is faster than in controls
• after 8 weeks on a high fat diet, 16 week old mutant mice exhibit hyperglycemia at a level similar to controls and compared to normal diet- fed mice; however, in a fasting condition, mutant mice that had been fed a high fat diet for 8 weeks exhibit a lower blood glucose level than control mice that had been fed a high fat diet for 8 weeks
• after 8 weeks on a high fat diet, 16 week old mutant mice exhibit lower glucose levels in a glucose tolerance test at 60 and 120 minutes after oral glucose administration than identically -treated controls
|
|
• after 10 weeks on a high fat diet, 18 week old mutant mice exhibit less lipid deposition in the liver than identically treated controls
|
|
• after 10 weeks on a high fat diet, 18 week old fasted mutant mice exhibit reduced plasma levels of triglycerides
|
endocrine/exocrine glands
| N |
• after 10 weeks on a high fat diet, 18 week old mutant mice exhibit no significant differences in the number, size and distribution of islets of Langerhans in the pancreas compared to controls; in addition, distribution of the alpha and beta cells within the islets is indistinguishable between high fat-fed control and mutant mice
|
