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Query: UNIPROT:Q86TM3 (
cage
)
29,987
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The purpose of the review is to highlight the influences of ambient temperature (T(a)) and caloric restriction (CR) on metabolism, cardiovascular function and behavior in mice. Standard vivarium ambient temperatures (T(a)?23 degrees C) are a mild cold stress for mice requiring elevated metabolic rate and food intake. Increasing T(a) into the zone of thermoneutrality (TMN?29-33 degrees C) markedly reduces food intake, metabolic rate, heart rate (HR) and blood pressure in mice. Mice are members of a diverse, yet unique group of homeothermic animals that respond to thermal and energetic challenges by allowing body temperature (T(b)) to fall to less than 31 degrees C, a condition known as torpor. In mice housed at standard T(a), torpor is induced by a single night of fasting or a few days of CR. The mechanisms responsible for initiating torpor are related to reduced caloric availability, but do not require leptin. Mice housed at
TMN
and subjected to CR exhibit physiologic reductions in metabolic rate and HR, but do not appear to enter torpor. Finally, mice exhibit differential locomotor activity responses during CR that depends on T(a). At standard T(a), mice display increased light-phase home-
cage
activity with CR. This response is virtually eliminated when CR is performed at
TMN
. We suggest that researchers using mice to investigate energy homeostasis and cardiovascular physiology carefully consider the influence of T(a) on physiology and behavior.
...
PMID:Behavioral and physiologic responses to caloric restriction in mice. 1523 80
The biological responses to caloric restriction (CR) are generally examined in rats with elevated metabolic rates due to being housed at ambient temperatures (T(a)) below the zone of thermoneutrality. We determined the physiological and behavioral responses to 2 wk of 30-40% CR in male FBNF1 rats housed in cool (T(a) = 12 degrees C) or thermoneutral (
TMN
; T(a) = 30 degrees C) conditions. Rats were instrumented with telemetry devices and housed continuously in home-
cage
calorimeters for the entire experiment. At baseline, rats housed in cool T(a) had reduced rate of weight gain; thus a mild CR (5%) group at thermoneutrality for weight maintenance was also studied. Rats housed in cool T(a) exhibited elevated caloric intake (cool = 77 +/- 1;
TMN
= 54 +/- 2 kcal), oxygen consumption (Vo(2); cool = 9.9 +/- 0.1;
TMN
= 5.5 +/- 0.1 ml/min), mean arterial pressure (cool = 103 +/- 1;
TMN
= 80 +/- 2 mmHg), and heart rate (cool = 374 +/- 3;
TMN
= 275 +/- 4 beats/min). Cool-CR rats exhibited greater CR-induced weight loss (cool = -62 +/- 3;
TMN
= -42 +/- 3 g) and reductions in Vo(2) (cool = -2.6 +/- 0.1;
TMN
= -1.5 +/- 0.1 ml/min) but similar CR-induced reductions in heart rate (cool = -59 +/- 1; TMN= -51 +/- 7 beats/min). CR had no effect on arterial blood pressure or locomotor activity in either group. Unexpectedly, weight maintenance produced significant reductions in Vo(2) and heart rate. At thermoneutrality, a single day of refeeding effectively abolished CR-induced reductions in Vo(2) and heart rate. The results reveal that rats with low or high baseline metabolic rate exhibit comparable compensatory reductions in Vo(2) and heart rate and suggest that T(a) can be used to modulate the metabolic background on which the more prolonged effects of CR can be studied.
...
PMID:Homeostatic responses to caloric restriction: influence of background metabolic rate. 1593 59
The histaminergic neurons of the tuberomammillary nucleus (
TMN
HDC
) of the posterior hypothalamus have long been implicated in promoting arousal. More recently, a role for GABAergic signaling by the
TMN
HDC
neurons in arousal control has been proposed. Here, we investigated the effects of selective chronic disruption of GABA synthesis (via genetic deletion of the GABA synthesis enzyme, glutamic acid decarboxylase 67) or GABAergic transmission (via genetic deletion of the vesicular GABA transporter (VGAT)) in the
TMN
HDC
neurons on sleep-wake in male mice. We also examined the effects of acute chemogenetic activation and optogenetic inhibition of
TMN
HDC
neurons upon arousal in male mice. Unexpectedly, we found that neither disruption of GABA synthesis nor GABAergic transmission altered hourly sleep-wake quantities, perhaps because very few
TMN
HDC
neurons coexpressed VGAT. Acute chemogenetic activation of
TMN
HDC
neurons did not increase arousal levels above baseline but did enhance vigilance when the mice were exposed to a behavioral
cage
change challenge. Similarly, acute optogenetic inhibition had little effect upon baseline levels of arousal. In conclusion, we could not identify a role for GABA release by
TMN
HDC
neurons in arousal control. Further, if
TMN
HDC
neurons do release GABA, the mechanism by which they do so remains unclear. Our findings support the view that
TMN
HDC
neurons may be important for enhancing arousal under certain conditions, such as exposure to a novel environment, but play only a minor role in behavioral and EEG arousal under baseline conditions.
SIGNIFICANCE STATEMENT
The histaminergic neurons of the tuberomammillary nucleus of the hypothalamus (
TMN
HDC
) have long been thought to promote arousal. Additionally,
TMN
HDC
neurons may counter-regulate the wake-promoting effects of histamine through co-release of the inhibitory neurotransmitter, GABA. Here, we show that impairing GABA signaling from
TMN
HDC
neurons does not impact sleep-wake amounts and that few
TMN
HDC
neurons contain the vesicular GABA transporter, which is presumably required to release GABA. We further show that acute activation or inhibition of
TMN
HDC
neurons has limited effects upon baseline arousal levels and that activation enhances vigilance during a behavioral challenge. Counter to general belief, our findings support the view that
TMN
HDC
neurons are neither necessary nor sufficient for the initiation and maintenance of arousal under baseline conditions.
...
PMID:Reassessing the Role of Histaminergic Tuberomammillary Neurons in Arousal Control. 3154 32
