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1 ania-like behaviors and hippocampal neuronal hypoactivity.
2 ronal homeostasis prevents hyperactivity and hypoactivity.
3 cloprid (neonicotinoids) were used to induce hypoactivity.
4 nto the underpinnings of insecticide-induced hypoactivity.
5  with severe mood dysregulation demonstrated hypoactivity.
6 ross imaging methods and primarily reflected hypoactivity.
7  disease (AD) has been linked to cholinergic hypoactivity.
8 ive of absence epilepsy, chronic ataxia, and hypoactivity.
9 ndritic atrophy, synaptic loss, and neuronal hypoactivity across multiple cell lines.
10 t in the medial PFC (mPFC) in vitro and PVIN hypoactivity along with reductions in gamma power during
11 mines along with losses of motoric function, hypoactivity and abbreviated life-span.
12                Treatments targeting amygdala hypoactivity and blunted salience during positive autobi
13 antagonists potentiated Delta(9)-THC-induced hypoactivity and catalepsy but failed to alter Delta(9)-
14 tions were neuroactive, eliciting dark-phase hypoactivity and fraction-specific hyperactivity pattern
15                                         Both hypoactivity and hyperactivity in the amygdala are assoc
16 and experimental PD, the GPe and STN exhibit hypoactivity and hyperactivity, respectively, and abnorm
17 MA, and deficiencies in Ox signaling lead to hypoactivity and hypophagia.
18 d short-term synaptic plasticity, behavioral hypoactivity and impaired recognition memory.
19 nd 12-14 (MA) month-old Hdc(-/-) mice showed hypoactivity and increased measures of anxiety in the op
20      Mice lacking NgR are viable but display hypoactivity and motor impairment.
21 ons, which are mostly within the MeA, caused hypoactivity and obesity in both male and female mice fe
22 aggregant Tau causes neuronal and astrocytic hypoactivity and presynaptic dysfunction instead.
23  studies have indicated left fronto-cortical hypoactivity and right parietal hypoactivity in depressi
24 eus accumbens (NAc) that results in neuronal hypoactivity and thereby enhances behavioral cocaine res
25 ange of behavioral phenotypes, in particular hypoactivity and various deficits in learning and memory
26                              Despite circuit hypoactivity and weakened functional connectivity across
27 ce have trace brain dopamine content, severe hypoactivity, and aphagia, and they die without interven
28 ayed increased sensorimotor gating, anxiety, hypoactivity, and decreased motor coordination, compared
29 kness behavior symptoms, including anorexia, hypoactivity, and hyperthermia.
30 ological symptoms, such as appetite loss and hypoactivity, and include a decline in social interactio
31 d in neurons, and this leads to hyperphagia, hypoactivity, and increased fat mass.
32    These included pronounced motor deficits, hypoactivity, and reduced stereotypic behaviors.
33 x or basal ganglia causes motor dysfunction, hypoactivity, and tremor, which are abnormalities observ
34 l testing of mice of both sexes demonstrated hypoactivity, anxiety, and impaired sensorimotor gating
35 mated open-field test, IDUA(-/-) mice showed hypoactivity as early as 2 months of age and altered anx
36 nd muscle temperatures, true hypothermia and hypoactivity as well as clearly diminished locomotor and
37 strated anxiety-like avoidance of open arms, hypoactivity, as well as unaltered within-trial and betw
38 ctivity are reliable markers for cholinergic hypoactivity associated with cognitive function deficit
39 y and rearing at 1 month of age, followed by hypoactivity at 4 months and gait anomalies at 1 year.
40 brain spreading, hyperactivity augmented and hypoactivity attenuated protein transfer.
41 tive starting at 5 months, later changing to hypoactivity before early mortality.
42                They demonstrate that area 32 hypoactivity causes behavioral generalization relevant t
43 associated with amygdala and anterior insula hypoactivity during a complex affective processing task
44 milar to the depressed group, while amygdala hypoactivity during positive autobiographical recall is
45 tion abolished muscle atonia and sympathetic hypoactivity during rapid eye movement (REM) sleep.
46           Further, the larvae exhibited mild hypoactivity during the adaptation period of the optomot
47 der animals with diabetes exhibited detrusor hypoactivity, findings consistent with clinical features
48 cute biphasic locomotor effects of morphine (hypoactivity followed by hyperactivity) were examined.
49 prefrontal cortex (VmPFC), marked by initial hypoactivity followed by increased VmPFC activation, poi
50 es to dopamine receptor stimulation, showing hypoactivity following injection of d-amphetamine or met
51  mice show features similar to RS, including hypoactivity, forelimb stereotypies, breathing irregular
52  a parallel transition from hyperactivity to hypoactivity has been found in orbitofrontal-striatal gl
53                                        NMDAR hypoactivity has been implicated in the pathophysiology
54 lic brain inhibition as the primary cause of hypoactivity, hypothermia and hyporesponsiveness.
55    The ability of CP 55,940 to produce motor hypoactivity, hypothermia and immobility was reduced 163
56 thalamus are suggestive of the NMDA receptor hypoactivity hypothesis of schizophrenia and are consist
57                         Restoring prefrontal hypoactivity, ideally in a noninvasive manner, is an int
58 ood which surprisingly is underpinned by LHb hypoactivity in acute slices, accompanied by alterations
59 for the aetiology of the posterior cingulate hypoactivity in Alzheimer's disease, but also show how d
60 nto-cortical hypoactivity and right parietal hypoactivity in depressive disorders, so aspects of late
61 present only in proximal CA3, with potential hypoactivity in distal CA3.
62 at coupled with theta phase, but exacerbated hypoactivity in exploratory behavior.
63                                    Moreover, hypoactivity in hippocampus and cortex among EL offsprin
64 pletes monoamines, and causes depression and hypoactivity in humans and rodents.
65                     Dhx9(-/-) mice exhibited hypoactivity in novel environments, tremor, and sensorin
66 ctivity is a necessary event for cholinergic hypoactivity in PC12 cells.
67 P < .05) during executive functioning tasks; hypoactivity in posterior insula (P < .005) during posit
68 ed hyperactivity in exploratory behavior and hypoactivity in QW and expanded the range of gamma that
69 ence suggests depression is characterized by hypoactivity in the dorsal anterior cingulate, whereas h
70 nterior insula and bilateral cerebellum, and hypoactivity in the dorsal medial prefrontal cortex (mPF
71 ce excessive PVS enlargement, it may lead to hypoactivity in the dorsolateral prefrontal cortex (DLPF
72                         They showed relative hypoactivity in the left occipital cortex for the low sp
73 ted that injury results in abnormal neuronal hypoactivity in the non-injured primary somatosensory co
74        Furthermore, DJ-1(-/-) mice displayed hypoactivity in the open field.
75              The pooled meta-analysis showed hypoactivity in the posterior insula, superior temporal,
76 cytes and oligodendrocytes), (2) evidence of hypoactivity in the prefrontal cortex (PFC) and hyperact
77                   RCAN1-mediated calcineurin hypoactivity in the PVN augments sympathetic outflow by
78  in association with prefrontal and striatal hypoactivity in the schizophrenia group.
79 SHR in the residential figure-eight maze and hypoactivity in the SD in the running wheels.
80 n contrast, the ASD group showed distinctive hypoactivity in the temporal pole (TP) during social dec
81                      PTSD is associated with hypoactivity in the ventromedial prefrontal cortex (vmPF
82 uitry models of these disorders propose that hypoactivity in the vmPFC engenders disinhibited activit
83 2C/H variants display both hyperactivity and hypoactivity in vitro, contradicting traditional charact
84 cessive inhibition was responsible for their hypoactivity in vivo Together with previous studies, the
85 features of RTT: tremors, motor impairments, hypoactivity, increased anxiety-related behavior, seizur
86     Yet, genetically conferred MAOA or 5-HTT hypoactivity is associated with altered aggression and i
87 , and a potential therapeutic target, as its hypoactivity is considered an important risk factor of d
88                            Thus, cholinergic hypoactivity is thought to be important in cognitive dys
89 ggest that in addition to LHb hyperactivity, hypoactivity likely also promotes an adverse phenotype.
90 a in PNKD, and suggest that indirect pathway hypoactivity may be a key mechanism for the generation o
91                            One cause of this hypoactivity may be defective corticocortical or thalamo
92    The role of Par-4 in inducing cholinergic hypoactivity may have significant implications in the un
93                                     Amygdala hypoactivity may represent an intermediate phenotype, of
94 luN2 phosphorylation, we postulated that Src hypoactivity may result from convergent alterations of v
95 eloping pentylenetetrazole-induced seizures (hypoactivity, myoclonic jerks, continuous tonic-clonic),
96 ynaptic and intrinsic plasticity, leading to hypoactivity of AgRP neurons and subsequently causing be
97                                              Hypoactivity of CB1KO mice accounts for their impaired e
98      The high-trauma-exposed group displayed hypoactivity of cerebellar regions in response to neutra
99  of explicit (more than implicit) memory and hypoactivity of cholinergic projections to the hippocamp
100 ractivity of subcortical DA transmission and hypoactivity of cortical DA in schizophrenia (SCH).
101    In mice, however, experimentally inducing hypoactivity of D1 NAcSh MSNs after cocaine withdrawal d
102 ceptor 1 (D1) medium spiny neurons (MSN) and hypoactivity of dopamine receptor 2 (D1) MSNs within the
103                                          The hypoactivity of dorsolateral prefrontal cortex in schizo
104                                              Hypoactivity of excitatory NMDAR-mediated neurotransmiss
105 observations suggest that the hypophagia and hypoactivity of mutants result not only because of the a
106 n overall permissive role of cocaine-induced hypoactivity of NAcSh MSNs in gating increased cocaine s
107 ubstantial fluid deficit and originates from hypoactivity of neurons in the circumventricular organs,
108                                              Hypoactivity of NRF2 in Krt16-/- footpad skin correlated
109 ctable models, we found that cocaine-induced hypoactivity of nucleus accumbens shell (NAcSh) medium s
110 partially and fully ameliorated the abnormal hypoactivity of postsynaptic subthalamic nucleus (STN) a
111        Finally, our data show that hyper- or hypoactivity of PP5 mutants increases Hsp90 binding to i
112                   Relative hyperactivity and hypoactivity of regional cerebral blood flow in brain re
113  the Drinking-in-the-Dark (DID) model led to hypoactivity of SST neurons in the prelimbic (PL) cortex
114 ed neurotransmission accompanying functional hypoactivity of the frontal lobes.
115          Hence, our study indicates that the hypoactivity of the hypothalamic-pituitary-adrenal (HPA)
116                  Hyperserotonergic state and hypoactivity of the hypothalamic-pituitary-adrenal axis
117                            Here we establish hypoactivity of the mTOR pathway as a clinically relevan
118  either overactivity of the arousal systems, hypoactivity of the sleep-inducing systems, or both.
119                                 Furthermore, hypoactivity of the spinal cannabinoid system results in
120                Counteracting cocaine-induced hypoactivity of these neurons selectively in sleep enhan
121 present the first direct evidence for mGluR5 hypoactivity, propose a reciprocal interplay between Glu
122 ic polymorphism rs16147 may contribute to IL hypoactivity, resulting in impaired extinction memory an
123 ed L5 activation rescues a stress-associated hypoactivity state, persists following exposure, and is
124       SSRIs induce SNr hyperactivity and SNc hypoactivity that can also be reversed by systemic 5-HT2
125                        As with the nocturnal hypoactivity, this effect was observed only during the f
126 licated neural correlates of ASB is amygdala hypoactivity to another person's fear.
127 relates of Conduct Problems (CP) is amygdala hypoactivity to another person's fear.
128 motional traits are associated with amygdala hypoactivity to consciously perceived fear, while low le
129 ical intervention), suggesting that amygdala hypoactivity to fear could be an important neural signat
130          We aimed to assess whether amygdala hypoactivity to fear in children with CPs is remediated
131           Our findings suggest that amygdala hypoactivity to fear is a marker for ASB that is resista
132                                     Amygdala hypoactivity to fear was observed only in boys with CPs
133           Oxytocin failed to reduce amygdala hypoactivity to fearful faces, but increased activation
134    Dopamine agonist-related ventral striatal hypoactivity to risk is consistent with impaired risk ev
135 l cholinergic responses such as hypothermia, hypoactivity, tremor, and salivation were enhanced in GR
136                       We additionally report hypoactivity, unrelated to anxiety or motoric function,
137 gnitive control load, however, Abeta-related hypoactivity was found in the right inferior frontal cor
138 ingulate, pre-supplementary motor and insula hypoactivity was observed for both successful NOGOs and
139            In contrast, inflammation-induced hypoactivity was unaffected, demonstrating the physiolog
140        To test genomic underpinnings for Src hypoactivity, we examined genome-wide association study
141 e mice were hyperactive and displayed neural hypoactivity with less neuron counts in the caudate puta
142 ctions (effective connectivity), rather than hypoactivity within individual brain regions, may contri

 
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