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1 5%) and feeding (47%) responses to focal PFH glucoprivation.
2 in modulate the CRR and feeding responses to glucoprivation.
3 ympathetic nerve activity (ASNA) to systemic glucoprivation.
4 rdiorespiratory activity and the response to glucoprivation.
5 o regulate adrenaline release in response to glucoprivation.
6 ry peptide enkephalin in responses evoked by glucoprivation.
7 cholaminergic A1-C1m neurons is activated by glucoprivation.
8 counter-regulatory neurohumoral responses to glucoprivation.
9 mic responses to both systemic and hindbrain glucoprivation.
10 -glucose (2DG; 200 mg/kg) was used to induce glucoprivation.
11  of these CRRs following repeated antecedent glucoprivation.
12 Fos-ir was diminished or unaffected by prior glucoprivation.
13 in the feeding and hyperglycemic response to glucoprivation.
14 tors in mediating the hyperphagic effects of glucoprivation.
15 olamine neurons in mediation of responses to glucoprivation.
16  catecholamine neurons that are activated by glucoprivation.
17 pulations activated by 2-deoxyglucose evoked glucoprivation.
18 ng) response to focal PFH (69%) and systemic glucoprivation (39%), while increasing PFH 5-HT levels a
19 eprivation (24 h), 2-deoxy-D-glucose-induced glucoprivation (500 mg/kg) or mercaptoacetate-induced li
20                                              Glucoprivation activates neurons in the perifornical hyp
21 response to insulin-induced hypoglycemia and glucoprivation and replicated hypoglycemia-associated au
22 roanatomical sites that are altered by prior glucoprivation and that mediate some of the physiologica
23 rgeted ODN induced weight loss, counteracted glucoprivation, and improved glucose clearance in rats.
24 , neuroendocrine, and autonomic responses to glucoprivation are impaired after a glucoprivic episode.
25               These neurons are activated by glucoprivation, but unlike the C1 cell group, not by hyp
26 %) projecting to celiac ganglia activated by glucoprivation could direct pancreatic and hepatic or ot
27                 Thirdly, in vivo or in vitro glucoprivation did not affect the activity of RVLM adren
28                      In these animals, prior glucoprivation did not attenuate 2DG-induced feeding in
29  Marked deficits in glucose availability, or glucoprivation, elicit organism-wide counter-regulatory
30               Consequently, glucose deficit (glucoprivation) elicits a variety of physiological and b
31       Glucocorticoids, which are elevated by glucoprivation, have been implicated in the pathogenesis
32 ke elicited by such regulatory challenges as glucoprivation induced by 2-deoxy-D-glucose (2DG) or foo
33 ce, DD mice fail to eat in response to acute glucoprivation induced by insulin or 2-DG.
34 untary overconsumption of palatable food, or glucoprivation induced by systemic 2-deoxy-D-glucose.
35 n, their hyperglycemic response to hindbrain glucoprivation induced with 5-thio-glucose was impaired,
36 tic preganglionic neurons (SPN) activated by glucoprivation, induced by 2-deoxy-D-glucose (2DG).
37 A)-pPVT communication significantly impaired glucoprivation-induced feeding while leaving other major
38 e signaling in the CPu is not sufficient for glucoprivation-induced feeding, we propose that this fee
39 hanisms by which VLM(CA) neurons orchestrate glucoprivation-induced food seeking behavior.
40 ously-neglected node selectively controlling glucoprivation-induced food seeking.
41                   These results suggest that glucoprivation-induced increases in gastric motility are
42   We investigated the hypothesis that during glucoprivation, lactate regulates neuronal monocarboxyla
43 entially alter feeding responses elicited by glucoprivation, lipoprivation and by different opioid pe
44 f A1/C1 CA neurons resulting from antecedent glucoprivation may account, at least in part, for impair
45                                    Secondly, glucoprivation of neurons in the PeH increased ASNA.
46 fuel attenuates transactivational effects of glucoprivation on PVN and SON AVP neurons.
47  of repeated 2-deoxy-D-glucose (2DG)-induced glucoprivation on subsequent 2DG-induced feeding and hyp
48 cated in mediating the suppressive effect of glucoprivation on the reproductive neuroendocrine axis,
49                                              Glucoprivation or hypoglycemia induces a range of counte
50  in vivo and 2) whether direct activation by glucoprivation or orexin release in the RVLM modulates t
51         These results indicate that cerebral glucoprivation produced by pharmacological doses of 2DG
52                               Prior repeated glucoprivation reduced subsequent feeding and hyperglyce
53                Severe or repeated antecedent glucoprivation results in attenuation of these CRRs and
54                                 Furthermore, glucoprivation suppressed PVN(MC4R) activity, which was
55  model, we compared the effect of antecedent glucoprivation targeting hindbrain or hypothalamic gluco
56  modulate feeding elicited by deprivation or glucoprivation, there has been no systematic examination
57 trating that glycogen depletion from morning glucoprivation was not responsible for the absence of th
58 the hyperphagic response elicited by central glucoprivation was suppressed by an ODN agonist.
59 o 2-deoxy-D-glucose (2DG; 200 mg/kg)-induced glucoprivation were tested 3-7 d later.
60       In awake, behaving rats, bilateral PFH glucoprivation with 5-thioglucose stimulated adrenal med
61  neuroendocrine, and behavioral responses to glucoprivation, yet the functions of the individual grou