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1 osure to inescapable electric shock in rats (learned helplessness).
2 e Th17 cell function, reduced Th17-dependent learned helplessness.
3 sed feeding (NSF), social defeat stress, and learned helplessness.
4 vioral paradigms for anhedonia, despair, and learned helplessness.
5 d induction of escape deficits in a model of learned helplessness.
6 sion, chronic unpredictable stress (CUS) and learned helplessness.
7 tidepressant effects of sleep deprivation on learned helplessness.
8 ct on the landscape of the hippocampus after learned helplessness.
9 roach to be critical to induce resilience to learned helplessness.
10 Whereas synaptic potentiation was linked to learned helplessness, a depression-like behavior, synapt
11 selectively bred line of rats susceptible to learned helplessness, a model of depression, presents an
12 ng biases, anhedonia, despair-like behavior (learned helplessness) - affords unique opportunities for
13 nce of the transcription factor DeltaFosB on learned helplessness, an animal model of affective disor
14 ed increased motivation for food, heightened learned helplessness and anhedonia, and altered stress s
16 ibility to social aversion, "anhedonia," and learned helplessness and causes impaired glucocorticoid-
21 nregulated in the hippocampus after both the learned helplessness and forced swim test (FST) paradigm
22 ing to identify gut bacteria associated with learned helplessness and to quantify the level of the qu
23 digm where no vehicle-treated mice developed learned helplessness, and impaired novelty suppressed fe
29 Three groups were studied: (1) rats bred for learned helplessness (cLH); (2) rats resistant to learne
30 ed helplessness (cLH); (2) rats resistant to learned helplessness (cNLH); and (3) control Sprague Daw
32 heels showed antidepressant-like behavior in learned helplessness, forced-swim (FST) and tail suspens
33 Th17 cell production exhibited resistance to learned helplessness, identifying modulation of RORgamma
35 unsolvable anagrams have been used to induce learned helplessness in humans, this finding may provide
37 r CIS, specifically: struggling, aggression, learned helplessness, inhibitory avoidance, and escape b
39 fect in behavioral models of depression, the learned helplessness (LH) and forced swim test (FST) par
40 al consequences of uncontrollable stress, or learned helplessness (LH) behaviors, are thought to invo
41 he nucleus (DRN) are implicated in mediating learned helplessness (LH) behaviors, such as poor escape
42 e tested the response of brain FoxO3a in the learned helplessness (LH) paradigm and tested signaling
43 lase promoter, showed protection against the learned helplessness (LH) paradigm, an animal model to t
44 ST), the tail suspension test (TST), and the learned helplessness (LH) paradigm-as well as in the fem
46 g a chronic social defeat (SD) stress model, learned helplessness (LH), and a chronic corticosterone
47 r either contextual fear conditioning (CFC), learned helplessness (LH), stress enhanced fear learning
50 ens CREB-dynorphin influence behavior in the learned helplessness model and suggest that this signali
54 tidepressant-like behavioural effects in the learned helplessness paradigm and regulates molecular ev
55 th their susceptibility or resilience to the learned helplessness paradigm in a sex- and microbiota-d
57 ificance of this transcription factor in the learned helplessness paradigm, a behavioral model of dep
58 proximate mediator of escape deficits in the learned helplessness paradigm, suggesting that neuronal
64 ehavioral responses to stress induced by the learned helplessness procedure, in which animals are sub
65 hological (illness behavior, social support, learned helplessness, smoking, drinking), clinical, sero
66 d the role of ACh signaling in the mPFC in a learned helplessness task in which mice were exposed to
67 e, progressive ratio responding to food, and learned helplessness task were normal, such avolition-li
68 the Porsolt, novelty induced hypophagia, and learned helplessness tests in rats without exhibiting su
69 cientific contributions-from conceptualizing learned helplessness to uncovering the neural and immune