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1    Striatal (123)I-FP-CIT binding to DAT and hypothalamic (123)I-FP-CIT binding to SERT are significa
2 n: Striatal (123)I-FP-CIT binding to DAT and hypothalamic (123)I-FP-CIT binding to SERT are significa
3 r corticospinal, cerebello-rubro-spinal, and hypothalamic A11 dopaminergic systems in the development
4 ntranasal oxytocin administration suppressed hypothalamic activation to images of high-calorie compar
5  medial part of the central amygdala and the hypothalamic 'aggression area', suggest that the ACo can
6                                              Hypothalamic Agouti-related peptide (AgRP) neurons are c
7                                              Hypothalamic agouti-related peptide (AgRP) neurons poten
8                                              Hypothalamic Agrp and Npy remained elevated following re
9                                              Hypothalamic agrp mRNA levels were also higher in gravid
10 elements of the brain's feeding circuits-the hypothalamic Agrp neurons that are normally activated by
11                                              Hypothalamic and diencephalic groups were detected and,
12 ricular resistin infusion downregulated both hypothalamic and hepatic APPL1, a key protein in adipone
13 HFD on energy homeostasis, inflammation, and hypothalamic and liver gene expression and that restorat
14 us, amygdala, lateral septal nuclei, certain hypothalamic and midbrain nuclei, and several regions of
15                                  Analysis of hypothalamic and neuroendocrine responses to HFS through
16 lin in association with reductions in islet, hypothalamic, and stomach PC1 content.
17 e that tau knockout mice exhibit an impaired hypothalamic anorexigenic effect of insulin that is asso
18 ially mediated by aberrant expression of the hypothalamic anorexigenic neuropeptide proopiomelanocort
19 gative feedback effects of oestradiol in the hypothalamic anteroventral periventricular (AVPV) and ar
20                    Kisspeptin neurons in the hypothalamic arcuate nucleus (Kiss1(ARH)) co-express Kis
21                               Neurons in the hypothalamic arcuate nucleus relay and translate importa
22 in and particularly strong expression in the hypothalamic arcuate nucleus.
23  insulin receptor substrate-1 (IRS-1) in the hypothalamic arcuate was determined.
24                                          The hypothalamic arcuate-median eminence complex (Arc-ME) co
25 moting orexin neurons located in the lateral hypothalamic area (LHA) by impairing glucose and lactate
26                   Here, we show that lateral hypothalamic area (LHA) glutamatergic neurons, and their
27 mone, acts on neurons located in the lateral hypothalamic area (LHA) to maintain energy homeostasis a
28 ic states.SIGNIFICANCE STATEMENT The lateral hypothalamic area (LHA) to ventral tegmental area (VTA)
29 nts conducted over 60 years ago, the lateral hypothalamic area (LHA) was identified as a critical neu
30  in unanesthetized rats and found the dorsal hypothalamic area to be its main representation site.
31 xpression was also detected in the posterior hypothalamic area, trochlear nucleus, dorsal raphe nucle
32  the entopeduncular nucleus, and the lateral hypothalamic area.
33 had the highest representation in the dorsal hypothalamic area.
34 area; bed nuclei of terminal stria; anterior hypothalamic area; arcuate, paraventricular, and dorsome
35 and dorsomedial hypothalamic nuclei; lateral hypothalamic area; central amygdalar nucleus; parasubtha
36 and dorsomedial hypothalamic nuclei; lateral hypothalamic area; parasubthalamic nucleus; central amyg
37 e thalamus was primarily contacted by medial hypothalamic areas as well as the zona incerta and proje
38 tricular region, tuberal and retromammillary hypothalamic areas, posterior tubercle, prethalamic and
39 d by its receptor in the kisspeptin enriched hypothalamic AVPV and ARC respectively, which are essent
40 at additionally showed a significantly lower hypothalamic binding in PSP and MSA-P than PD.
41  of BDNF resulted in the reduction of global hypothalamic cell.
42                                  Presumptive hypothalamic cells derive from the rostral diencephalic
43 ice started with a substantial loss of these hypothalamic cells.
44 e peptide 1 (GLP-1)-mediated paraventricular hypothalamic circuit coordinating the global stress resp
45 t control of appetite, arcuate nucleus-based hypothalamic circuits linking energy state to the motiva
46 tanding of its effects on the development of hypothalamic circuits remains elusive.
47  suprachiasmatic nucleus (SCN) (an important hypothalamic control center).
48 ta suggest L-cells are active players in the hypothalamic control of intestinal fluid homeostasis, pr
49 olfactory cortical areas transmit signals to hypothalamic corticotropin-releasing hormone (CRH) neuro
50         A long-standing paradigm posits that hypothalamic corticotropin-releasing hormone (CRH) regul
51 that targeted interference specifically with hypothalamic Crh expression results in anxiolysis.
52 drenal glucocorticoid release, whereas extra-hypothalamic CRH has a key role in stressor-triggered be
53 k of TH immunoreactivity in this region, the hypothalamic CSF-c cells have been thought to take up DA
54 tal transcription factor orthopedia (Otp) on hypothalamic development and function.
55 iption factor POU3F2, which is important for hypothalamic development and function.
56                                     Abnormal hypothalamic development is associated with dysfunctiona
57          Maternal high-fat diet (HFD) alters hypothalamic developmental programming and disrupts offs
58 ogenesis, suggesting that obesity-associated hypothalamic dysfunction can be repaired.
59 s-related pathologies associated with limbic-hypothalamic dysfunction.
60 e, neuroestradiol is an integral part of the hypothalamic engagement in response to elevated circulat
61 entrally administered thapsigargin displayed hypothalamic ER stress, whereas genetic overexpression o
62                                         This hypothalamic excitatory projection predominates over LHb
63 h zebrafish and mouse show highly correlated hypothalamic expression in marmosets and humans, suggest
64 nal ex vivo studies in mice revealed reduced hypothalamic expression of Ctbp2 and Nbeal1 after fastin
65                                              Hypothalamic expression of Ctbp2 was increased in diet-i
66            In addition, the detected altered hypothalamic expression patterns of Ctbp2 and Nbeal1 as
67 ther observation using proteomic analysis of hypothalamic extracts that high-intensity exercise in re
68                                              Hypothalamic fatty-acid synthase activity is also elevat
69 operating on distinct timescales converge on hypothalamic feeding circuits to generate a central repr
70  a loss of Magel2 leads to the disruption of hypothalamic feeding circuits, an effect that appears to
71 ssion specifically in two GLP-1RA-responsive hypothalamic feeding nuclei/cell types, the paraventricu
72                        Likewise, compromised hypothalamic function and subsequent defects in maintain
73 arcuate nucleus to regulate other aspects of hypothalamic function.
74 ecifically involved in the regulation of the hypothalamic functions.
75 Consistent with this, microarray analysis of hypothalamic gene expression revealed a significant alte
76                        Kcnq1 is expressed in hypothalamic GHRH neurons and pituitary somatotropes.
77 -affected rats show decreased mRNA levels of hypothalamic GHS-R1a, neuropeptide Y (NPY), and agouti-r
78                   This demonstrates that the hypothalamic GLP-1R is sufficient but does not show whet
79            Pharmacological activation of the hypothalamic glucagon-like peptide 1 (GLP-1) receptor (G
80 ical type 3 (TRPC3) channels are involved in hypothalamic glucose detection and the control of energy
81                                              Hypothalamic glucose detection was studied in vivo by me
82     However, although reproduction relies on hypothalamic gonadotrophin-releasing hormone output, and
83  estrogen and androgen receptors, and by the hypothalamic gonadotropin-releasing hormone through acti
84                                              Hypothalamic growth hormone-releasing hormone (GHRH) neu
85   This evidence indicates that modulation of hypothalamic GRP78 activity may be a potential strategy
86          This study investigated the role of hypothalamic GRP78 on energy balance, with particular in
87 tudied the effect of genetic manipulation of hypothalamic GRP78.
88                           Silencing WDR47 in hypothalamic GT1-7 neuronal cells and yeast models indep
89 ntestinal uroguanylin secretion silences the hypothalamic GUCY2C endocrine axis, creating a feed-forw
90               Overall, our data suggest that hypothalamic HDAC5 activity is a regulator of leptin sig
91            One such circuit is the posterior hypothalamic histamine (HA) system, implicated in suppor
92 n insular cortex, chemogenetic activation of hypothalamic 'hunger neurons' (expressing agouti-related
93                                              Hypothalamic hypocretin (orexin) peptides mediate arousa
94                                  The lateral hypothalamic hypocretin/orexin (HCRT) system has been im
95 amus (lateral torus, lateral recess nucleus, hypothalamic inferior lobe diffuse nucleus) and an inter
96                   Obesity is associated with hypothalamic inflammation (HI) in animal models.
97                         Over the last years, hypothalamic inflammation has been linked to the develop
98  engineered to survive in the ageing-related hypothalamic inflammatory microenvironment.
99                           This activation of hypothalamic inflammatory pathways results in the uncoup
100 rent neuronal and non-neuronal cell types to hypothalamic inflammatory processes, and delineation of
101 although obesity promotes hyperlipidemia and hypothalamic injury, MC4R agonists are nevertheless more
102  nucleus (PVT) neurons receive hindbrain and hypothalamic inputs, and project to forebrain sites invo
103                      Moreover, MANF triggers hypothalamic insulin resistance by enhancing the ER loca
104 in the hypothalamus, which may contribute to hypothalamic insulin resistance.
105 es food intake and body weight by modulating hypothalamic insulin signaling.MANF is a neurotrophic fa
106 g (SOCS-3) proteins that are associated with hypothalamic leptin resistance.
107 uclear factor-kappaB pathway while restoring hypothalamic leptin sensitivity.
108  signalling adjusts specific features of the hypothalamic light response, indicating that the genicul
109 st the magnitude of circadian and more acute hypothalamic light responses according to time-of-day an
110                             We conclude that hypothalamic LPL functions in astrocytes to ensure appro
111 (2+) levels (NMDAR-DeltaCa(2+) ) occurred in hypothalamic magnocellular neurosecretory cells (MNCs) i
112 rent (IA ) influences the firing activity of hypothalamic magnocellular neurosecretory neurons (MNCs)
113 brain is influenced by nutritional cues, and hypothalamic MANF influences food intake and systemic en
114                     Increasing or decreasing hypothalamic MANF protein levels causes hyperphagia or h
115 eurons activated by water deprivation in the hypothalamic median preoptic nucleus (MnPO).
116 stems from the discoveries of leptin and the hypothalamic melanocortin system.
117 shed that the ARC is a primary residence for hypothalamic melanocortinergic neurons.
118 ale Cx3cr1 knockout mice develop 'male-like' hypothalamic microglial accumulation and activation, acc
119 Here we identify sex-specific differences in hypothalamic microglial activation via the CX3CL1-CX3CR1
120  bactericidal capacity, as well as serum and hypothalamic mRNA responses of certain proinflammatory c
121 ence-dependent component to the formation of hypothalamic neural assemblies controlling innate social
122 ostatic conditions, animals use well-defined hypothalamic neural circuits to help maintain stable bod
123   Postdieting hyperphagia along with altered hypothalamic neuro-architecture appears to be one direct
124  In zebrafish, a high level of postembryonic hypothalamic neurogenesis has been observed, but the rol
125 pothalamus, PUFAs were capable of increasing hypothalamic neurogenesis to levels similar or superior
126 behavioral, endocrine and gender traits with hypothalamic neuron identity.
127 ake and hepatic glucose production and alter hypothalamic neuronal activity in a manner that depends
128  of T1R2 and Galpha14 expression in cultured hypothalamic neuronal cells, leptin caused a transient d
129 imuli depends on orchestrated development of hypothalamic neuronal circuits.
130                                   Within the hypothalamic neuronal populations, the arcuate melanocor
131 glutamatergic synapses onto stress-sensitive hypothalamic neurons and repressed expression of the str
132  is a trophic peptide hormone synthesized by hypothalamic neurons and the biliary epithelium and exer
133 tly in Science, Paul et al. (2017) show that hypothalamic neurons control activation of a subset of N
134 ving appetite-stimulating fasting-responsive hypothalamic neurons expressing agouti-related peptide (
135                                A few hundred hypothalamic neurons form a complex network that control
136 sparse population of a few hundred primarily hypothalamic neurons forms the hub of a complex neurogli
137 ordinated differential modulation of the key hypothalamic neurons in control of energy homeostasis as
138 all shift toward excitation in liver-related hypothalamic neurons in the diabetic condition.
139 quired for the differentiation of anxiolytic hypothalamic neurons in zebrafish and mice, although the
140                                              Hypothalamic neurons producing orexins (also called hypo
141  axons of retinal ganglion cells converge on hypothalamic neurons that project directly to nuclei in
142 STRACT: In addition to peptide transmitters, hypothalamic neurons, including proopiomelanocortin (POM
143         In addition to peptide transmitters, hypothalamic neurons, including proopiomelanocortin (POM
144              We found that multiple types of hypothalamic neurons, including those that oppositely re
145 dependent re-programming of stress-sensitive hypothalamic neurons, which takes place through modifica
146 ated by inputs from serotonergic neurons and hypothalamic neurons.
147 em cell-derived foregut epithelial cells and hypothalamic neurons.
148                      We further examined the hypothalamic neuropeptide expressions in the mutant pedi
149           Recent research indicates that the hypothalamic neuropeptide hormone oxytocin is a key cent
150 s pivotal role in psychosocial behavior, the hypothalamic neuropeptide oxytocin contributes to metabo
151 r-growing body of evidence suggests that the hypothalamic neuropeptide oxytocin plays a central role
152  psychology rest on and are modulated by the hypothalamic neuropeptide oxytocin.
153 Growth hormone-releasing hormone (GHRH) is a hypothalamic neuropeptide that has been shown to act as
154 eased body weight with associated changes in hypothalamic neuropeptides involved in growth and feedin
155 ly in 1998, we and others described the same hypothalamic neuropeptides, respectively called the hypo
156 gnalling plays a critical role in modulating hypothalamic neurosecretory function.
157                               How such rapid hypothalamic neurotransmission leads to slowly evolving
158 lines revealed that, like GnRH neurons, most hypothalamic nNOS neurons have a glutamatergic phenotype
159                                      Several hypothalamic nuclei and neuronal circuits have been the
160 gulation in regions rostral of the canonical hypothalamic nuclei involved in controlling body tempera
161 oducing neurons that supply serotonin to the hypothalamic nuclei.
162 t likely from reduced oxytocin expression in hypothalamic nuclei.
163 s; paraventricular, arcuate, and dorsomedial hypothalamic nuclei; lateral hypothalamic area; central
164 a; arcuate, paraventricular, and dorsomedial hypothalamic nuclei; lateral hypothalamic area; parasubt
165                                The posterior hypothalamic nucleus (PH) stimulates autonomic stress re
166                          The paraventricular hypothalamic nucleus (PVH) receives direct melanocortin
167  preoptic nucleus (POM) and the ventromedial hypothalamic nucleus (VMH) mediating control of male and
168 ose signaling in neurons of the ventromedial hypothalamic nucleus (VMN), a brain nucleus involved in
169 n of the hypothalamus, the rostral posterior hypothalamic nucleus, targets multiple premotor regions
170                     We hypothesized that the hypothalamic opioid system might also control energy met
171 42) and noradrenergic (203,686) neurons, and hypothalamic orexinergic neurons (277,604), are markedly
172 78) and noradrenergic (127,752) neurons, and hypothalamic orexinergic neurons (68,398) are markedly h
173 nal subclasses provides new understanding of hypothalamic organization and function.
174 We also developed protocols for midbrain and hypothalamic organoids.
175 euroendocrine axes, predominantly of central/hypothalamic origin, which contributes to the low (or in
176 energy balance, and mediates the majority of hypothalamic output to control both feeding and energy e
177 cological administration or virally mediated hypothalamic overexpression converts them to a 'female-l
178                                 Importantly, hypothalamic oxytocin (OT) signaling increased coinciden
179                                        Since hypothalamic oxytocinergic projections also target the s
180 cin (OT) is a neuropeptide elaborated by the hypothalamic paraventricular (PVN) and supraoptic (SON)
181  evidence that the effects of NPS within the hypothalamic paraventricular nucleus (PVN) are mediated
182                        NMDAR activity in the hypothalamic paraventricular nucleus (PVN) is increased
183 rating NADPH oxidase (NOX) in AVP-expressing hypothalamic paraventricular nucleus (PVN) neurons in "m
184              Tmem18 expression in the murine hypothalamic paraventricular nucleus (PVN) was altered b
185 nal projections from oxytocin neurons in the hypothalamic paraventricular nucleus to midbrain DA regi
186 sponses and impaired c-fos activation in the hypothalamic paraventricular nucleus.
187                In conclusion, studies of the hypothalamic parvafox nucleus will reveal whether this e
188                          Small assemblies of hypothalamic "parvocellular" neurons release their neuro
189 ter expressing many neuropeptides, including hypothalamic peptide orthologs and their receptors.
190 ociality highlight a fundamental role of the hypothalamic peptide oxytocin (OXT) in the formation and
191 epts by highlighting the pivotal role of the hypothalamic peptide oxytocin in augmenting the salience
192  investigated how genes coding for different hypothalamic peptides involved in the central control of
193 amic (STN), premammillary (PM) and posterior hypothalamic (PH) populations.
194 to the membrane mediate reproductive-related hypothalamic physiology, via second messenger systems wi
195                           Salivary cortisol (hypothalamic pituitary axis), heart rate variability (sy
196 e production independent of their effects on hypothalamic pituitary-adrenal (HPA) axis activation, av
197                 He was offered screening for hypothalamic-pituitary axis (HPA) dysfunction because of
198 ffects of stress are largely mediated by the hypothalamic-pituitary axis, a highly conserved neurohor
199                                  The risk of hypothalamic-pituitary dysfunction (n = 138) was associa
200  comparisons and competition may involve the hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pi
201 xamined downstream molecular consequences of hypothalamic-pituitary-adrenal (HPA) axis activation by
202 nhibition holiday" so that the potential for hypothalamic-pituitary-adrenal (HPA) axis activation mig
203 emotional behaviors as well as regulation of hypothalamic-pituitary-adrenal (HPA) axis activity.
204 e risk for affective disturbance and promote hypothalamic-pituitary-adrenal (HPA) axis dysregulation,
205 e memory deficits, by reestablishment of the hypothalamic-pituitary-adrenal (HPA) axis feedback and c
206                                          The hypothalamic-pituitary-adrenal (HPA) axis has been impli
207                 Genetic variation within the hypothalamic-pituitary-adrenal (HPA) axis has been linke
208 ed to constitute CIRCI: dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, altered corti
209 tory processes, leading to activation of the hypothalamic-pituitary-adrenal (HPA) axis, the sympathet
210 mmune system-derived cytokines stimulate the hypothalamic-pituitary-adrenal (HPA) axis, triggering en
211 HSC mobilization via hormonal priming of the hypothalamic-pituitary-adrenal (HPA) axis.
212 renal (HPI) axis, the fish equivalent of the hypothalamic-pituitary-adrenal (HPA) axis.
213 ulates the mammalian stress response via the hypothalamic-pituitary-adrenal (HPA) axis.
214 otection of the newborn decreases the limbic-hypothalamic-pituitary-adrenal (LHPA) axis activity in t
215 these neurons promotes the activation of the hypothalamic-pituitary-adrenal and hypothalamic-pituitar
216 ght benefit subpopulations with demonstrable hypothalamic-pituitary-adrenal axis abnormalities.
217 e critically related to anxiety behavior and hypothalamic-pituitary-adrenal axis activity, likely thr
218 ases in chronic inflammation, or exacerbated hypothalamic-pituitary-adrenal axis activity.
219 coid receptor (GR) expression, and increased hypothalamic-pituitary-adrenal axis activity.
220  the hypothesis that PVN Sirt1 activates the hypothalamic-pituitary-adrenal axis and basal GC levels
221   This was likely mediated by inhibiting the hypothalamic-pituitary-adrenal axis and inflammatory res
222           Our data reveal that impairment of hypothalamic-pituitary-adrenal axis during depression ca
223 erted anxiolytic actions without influencing hypothalamic-pituitary-adrenal axis function.
224 ergic, but not in GABAergic, neurons induced hypothalamic-pituitary-adrenal axis hyperactivity and re
225 yte infiltration, microglial activation, and hypothalamic-pituitary-adrenal axis hyperactivity in str
226                                          The hypothalamic-pituitary-adrenal axis is a dynamic system
227                                          The hypothalamic-pituitary-adrenal axis is a pivotal compone
228      The activation of catecholaminergic and hypothalamic-pituitary-adrenal axis leads to splenic atr
229 docrine model of depression to study whether hypothalamic-pituitary-adrenal axis perturbation could b
230 halamus is an important central component of hypothalamic-pituitary-adrenal axis regulation that prep
231      FK506-binding protein 51 is involved in hypothalamic-pituitary-adrenal axis regulation.
232                            Evaluation of the hypothalamic-pituitary-adrenal axis response in these an
233 inded 1-mediated Glp1r knockdown had reduced hypothalamic-pituitary-adrenal axis responses to both ac
234  deficiency showed a significantly increased hypothalamic-pituitary-adrenal axis stress response and
235 naling (e.g., sympathetic nervous system and hypothalamic-pituitary-adrenal axis) transcription facto
236  clinical data indicate abnormalities in the hypothalamic-pituitary-adrenal axis, including signaling
237 e prefrontal cortex (PFC), the amygdala, and hypothalamic-pituitary-adrenal axis, the precise genetic
238  effects, including on the regulation of the hypothalamic-pituitary-adrenal axis, thereby affecting a
239 eased linear growth, and inactivation of the hypothalamic-pituitary-adrenal axis, without affecting e
240 olateral hippocampus-a region modulating the hypothalamic-pituitary-adrenal axis-and somatosensory, v
241 ulating the activity of the amygdala and the hypothalamic-pituitary-adrenal axis.
242 ese psychiatric conditions, by affecting the hypothalamic-pituitary-adrenal axis.
243 enesis and neurotrophic factors, normalizing hypothalamic-pituitary-adrenal reactivity, and the reduc
244 epeated restraint abolished their heightened hypothalamic-pituitary-adrenal responsivity and reduced
245  CNS controls embryonic HSPC numbers via the hypothalamic-pituitary-adrenal/interrenal (HPA/I) stress
246 rk, change in the expression of genes in the hypothalamic-pituitary-adrenal/stress system (e.g., Crhr
247 he main effects hypothesis and indicate that hypothalamic-pituitary-adrenocortical (HPA) axis regulat
248 the hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) axes in underlying
249                                          The hypothalamic-pituitary-gonadal (HPG) axis is a key biolo
250 sential for normal pituitary development and hypothalamic-pituitary-gonadal (HPG) function in adultho
251                                          The hypothalamic-pituitary-gonadal axis controls puberty and
252 e complicated by affective comorbidities and hypothalamic-pituitary-gonadal dysregulation.
253 y parameters and transcriptional analysis of hypothalamic-pituitary-gonadal-liver axis revealed negli
254 nvestigated behaviour and functioning of the hypothalamic-pituitary-interrenal (HPI) axis, the fish e
255 may interrupt menstrual patterns by altering hypothalamic-pituitary-ovarian axis function.
256 uences of concussion and the function of the hypothalamic-pituitary-ovarian axis.
257 on of the hypothalamic-pituitary-adrenal and hypothalamic-pituitary-thyroid axes, as well as a rise i
258 -defective TRbeta leads to disruption of the hypothalamic-pituitary-thyroid axis with resistance to T
259 putational models for the following: (a) the hypothalamic-pitutitary-gonadal axis in female FHMs, whe
260 esynaptic and postsynaptic NMDAR activity of hypothalamic presympathetic neurons in hypertension.
261 sm involved in potentiated NMDAR activity of hypothalamic presympathetic neurons remains unclear.
262             Together, our studies identify a hypothalamic progenitor population defined by Fgf10 and
263 t rx3 is required to select tuberal/anterior hypothalamic progenitors and to orchestrate their anisot
264  In disc1 mutant embryos, proliferating rx3+ hypothalamic progenitors are not maintained normally and
265        17beta-estradiol (E2) also influences hypothalamic programming through estrogen receptor (ER)
266 nt studies focused on MOR desensitization in hypothalamic proopiomelanocortin (POMC) neurons as these
267 ion of somatic mu-opioid receptors (MORs) in hypothalamic proopiomelanocortin (POMC) neurons leads to
268                                  KEY POINTS: Hypothalamic proopiomelanocortin (POMC) neurons release
269             Glucose is the primary driver of hypothalamic proopiomelanocortin (POMC) neurons.
270                                              Hypothalamic proopiomelanocortin neurons selectively inn
271 ling was associated with decreased levels of hypothalamic proopiomelanocortin, leading to increased f
272 per in Science, Paul et al. (2017) show that hypothalamic propiomelanocortin (POMC) neurons innervate
273 te the ARN(KISS) neurons as the long-elusive hypothalamic pulse generator driving fertility.
274 T) occur in the periventricular zones of the hypothalamic region of most vertebrates except for place
275 S revealed the number of neurons in the left hypothalamic region to be similar in obese versus contro
276 ignal transduction pathway contribute to the hypothalamic regulation of energy and glucose homeostasi
277 and has a particularly important role in the hypothalamic regulation of energy homeostasis.
278 .1(+ve) neurons are sufficient to coordinate hypothalamic response and expression of compulsive behav
279  the light-dark cycle suggests uncoupling of hypothalamic responses involving appetite-stimulating fa
280 +ve) neurons is sufficient to restore normal hypothalamic responses to negative energy balance.
281 leep, and here we report that the vertebrate hypothalamic RFamide neuropeptide VF (NPVF) regulates sl
282 ression during sexual differentiation of the hypothalamic sexually dimorphic nucleus.
283  conditions, the transcriptional activity of hypothalamic SF-1 was activated by SUMO, but this was at
284                              Interactions of hypothalamic signaling pathways that control body temper
285 halamus to maintain normal expression of the hypothalamic signals involved in the induction and subse
286  and induces expression of galanin (galn), a hypothalamic sleep-inducing peptide.
287       Using whole cell recordings in coronal hypothalamic slices from adult female rats, we demonstra
288             Compared to controls, superfused hypothalamic slices of fasted birds treated with CART-pe
289                   Patch clamp experiments on hypothalamic slices showed that the mean amplitude of th
290  ageing speed is substantially controlled by hypothalamic stem cells, partially through the release o
291 eing, whereas central treatment with healthy hypothalamic stem/progenitor cell-secreted exosomes led
292                             Mechanistically, hypothalamic stem/progenitor cells contributed greatly t
293 ere we develop several mouse models in which hypothalamic stem/progenitor cells that co-express Sox2
294 ice that were locally implanted with healthy hypothalamic stem/progenitor cells that had been genetic
295 eying information about ambient light to the hypothalamic suprachiasmatic nucleus, the site of the ma
296 asopressin (VP) magnocellular neurons in the hypothalamic supraoptic (SON) and paraventricular nuclei
297 specific labeling in the ventral wall of the hypothalamic third ventricle, which is formed by special
298 inergic (HA) neurons, found in the posterior hypothalamic tuberomammillary nucleus (TMN), extend fibe
299 rogenesis by modulating the activity of this hypothalamic-V-SVZ connection.
300                        Thus, we targeted the hypothalamic ventromedial nucleus (VMH) to selectively o

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