ライフサイエンスコーパス: neurosteroid

1 ol treatment exaggerated sensitivity to this neurosteroid.

2 e in the cognitive effects of this sulphated neurosteroid.

3 onse of GABA(A) receptors in adult cortex to neurosteroid.

4 ant adrenal androgen and also functions as a neurosteroid.

5 nits is required for binding of potentiating neurosteroids.

6 maximum effects similar to barbiturates and neurosteroids.

7 The activity of NMDARs can be modulated by neurosteroids.

8 anization of GABA(A)Rs through the action of neurosteroids.

9 icated in mediating the analgesic actions of neurosteroids.

10 olecular target for the analgesic actions of neurosteroids.

11 ons for the physiological role of endogenous neurosteroids.

12 inhibition of GABA(A) receptors by sulfated neurosteroids.

13 otentiating and direct activation effects of neurosteroids.

14 ey can override the endogenous production of neurosteroids.

15 nd metabolism to GABA(A) receptor-modulating neurosteroids.

16 acids, 24(S)-hydroxycholesterol, and various neurosteroids.

17 effect on GABAA receptors via the action of neurosteroids.

18 ding zinc, polyamines, protons, and sulfated neurosteroids.

19 ors, which respond sensitively to endogenous neurosteroids.

20 ctly act on neuronal excitability, acting as neurosteroids.

21 nism indistinguishable from that of sulfated neurosteroids.

22 lving neuronal aromatase, which produces the neurosteroid 17beta-estradiol (E2).

23 Here we describe the mechanism by which the neurosteroid 3alpha, 21-dihydroxy-5alpha-pregnan-20-one

24 EC50 values for GABA in the presence of the neurosteroid 3alpha, 21-dihydroxy-5alpha-pregnan-20-one

25 ro after a short (30 min) treatment with the neurosteroid 3alpha,5alpha-tetrahydrodeoxycorticosterone

26 Cortical levels of the GABAergic neurosteroid 3alpha-hydroxy-5alpha-pregnan-20-one (3alph

27 entiated by pentobarbital, diazepam, and the neurosteroid (3alpha,5alpha)-3-hydroxypregnan-20-one (3a

28 ring coapplication of GABA and an endogenous neurosteroid (3alpha,5alpha)-3-hydroxypregnan-20-one (3a

29 n by GABA or macroscopic potentiation by the neurosteroid 3alpha5alphaP.

30 The neurosteroid 5alpha-pregnan-3alpha-ol-20-one (5alpha3alp

31 arallel effects on DHEAS, suggesting the two neurosteroids act through similar mechanisms.

32 hydroxy-5beta-pregnan-20-one), the principal neurosteroid acting via gamma-aminobutyric acid (GABA).

33 8), the mIPSC duration is prolonged by local neurosteroids acting in a paracrine or autocrine manner

34 8), the mIPSC duration is prolonged by local neurosteroids acting in a paracrine or autocrine manner

35 his proposal comes from the observation that neurosteroid action is region and neuron selective.

36 Due to the increasing evidence for neurosteroid action on multiple cell traits, it may be t

37 pite their importance, fundamental issues of neurosteroid actions remain unresolved.

38 Neurosteroids activate extrasynaptic deltaGABAA receptor

39 and neither of the amino acids identified as neurosteroid activation determinants are located at the

40 hole-cell currents were also enhanced by the neurosteroid allopregnanolone (10 nM).

41 We show that the neurosteroid allopregnanolone (ALLO) and T0901317, a syn

42 The neurosteroid allopregnanolone acts as a positive alloste

43 ork has shown that a single injection of the neurosteroid allopregnanolone at postnatal day 7 signifi

44 The neurosteroid allopregnanolone is a potent allosteric mod

45 Importantly, the acute addition of the neurosteroid allopregnanolone mitigated functional impai

46 The neurosteroid allopregnanolone partially mediates the ane

47 functional GABA site are potentiated by the neurosteroid allopregnanolone regardless of whether the

48 e in the conversion of progesterone into the neurosteroid allopregnanolone.

49 ed the therapeutic potential of a neurogenic neurosteroid, allopregnanolone, in the restoration of th

50 that acetazolamide, chlorthalidone, and the neurosteroid, allopregnanolone, which inhibits chloride

51 ptor properties including sensitivity to the neurosteroid, allopregnanolone.

52 receptors can be modulated by the endogenous neurosteroids, allopregnanolone and tetrahydro-deoxycort

53 f mutations that remove potentiation by most neurosteroids (alpha1 Q241L, alpha1 Q241W).

54 Injection of the neurosteroid also significantly reduced astrocyte prolif

55 Because sulfated neurosteroids also modulate NMDARs, here we examined the

56 previously shown to abolish potentiation by neurosteroids, also diminish potentiation by BI-2.

57 a fluorescently tagged analog of a sulfated neurosteroid altered membrane capacitance similar to the

58 these neurosteroid binding sites directly, a neurosteroid-analog photolabeling reagent, (3alpha,5beta

59 ,3-benzoxadiazol-4-yl amino (NBD)-conjugated neurosteroid analogs photopotentiate GABA(A) receptor fu

60 In this study, we describe a new class of neurosteroid analogues which possess structural modifica

61 stricted distribution, confers resistance to neurosteroid and anesthetic modulation, and causes spont

62 nic inhibition and the actions of endogenous neurosteroids and alcohol.

63 ted by a variety of compounds, including the neurosteroids and barbiturates.

64 this enzyme may participate in metabolism of neurosteroids and drugs that can cross the blood-brain b

65 A model of the alignment of neurosteroids and ent-neurosteroids at the same binding

66 Neurosteroids and some anxiolytics share an important si

67 Endogenous neurosteroids and their synthetic analogs (neuroactive s

68 gets for anesthetics, sleep-promoting drugs, neurosteroids, and alcohol.

69 tes, and activation by GABA, potentiation by neurosteroids, and the agonist activity of piperidine-4-

70 These data suggest that the neurosteroid androsterone contributes to the regulation

71 ted steroids, which bind a presumed external neurosteroid antagonist site, and hydroxysteroids, which

72 azepine site antagonists, the development of neurosteroid antagonists may help clarify the role of GA

73 at this tonic inhibition will be enhanced by neurosteroids, antiepileptics, and sedative/hypnotic dru

74 Although neurosteroids are accepted allosteric modulators of GABA

75 Neurosteroids are allosteric modulators of both synaptic

76 Endogenous neurosteroids are among the most potent and efficacious

77 osteroid exposure and suggest that GABAergic neurosteroids are critical for normal development of GAB

78 Neurosteroids are endogenous allosteric modulators of GA

79 Neurosteroids are endogenous neuromodulators that bind a

80 Neurosteroids are endogenous regulators of neuronal exci

81 Neurosteroids are potent modulators of GABA-A receptors.

82 Neurosteroids are potent neuromodulators which act in pa

83 Neurosteroids are powerful modulators of brain function

84 Neurosteroids are produced de novo in neuronal and glial

85 Although neurosteroids are relatively promiscuous toward differen

86 Furthermore, endogenous neurosteroids are shown to be important regulators of py

87 Neurosteroids are synthesized de novo in the brain durin

88 Neurosteroids are synthesized within the brain and act a

89 In brain, these neurosteroids are transformed predominantly into 7alpha-

90 The analgesic activities of neurosteroids are well known; however, here we describe

91 ion of CRF-releasing neurons, and identifies neurosteroids as putative early regulators of the stress

92 el of the alignment of neurosteroids and ent-neurosteroids at the same binding site on gamma-aminobut

93 nstrating that extracellular Zn(2+) prevents neurosteroid augmentation of tonic current and protectio

94 nity for the development of new therapeutic, neurosteroid-based ligands and transgenic disease models

95 unity for the development of new therapeutic neurosteroid-based ligands to treat diseases associated

96 This study identifies a novel neurosteroid binding site and demonstrates the feasibili

97 To identify these neurosteroid binding sites directly, a neurosteroid-anal

98 act with the benzodiazepine, barbiturate, or neurosteroid binding sites in the GABAAR.

99 ther recent studies have identified putative neurosteroid binding sites on GABA(A) receptors.

100 a pattern consistent with a single class of neurosteroid binding sites.

101 ABA at GABA(A) receptors expressing specific neurosteroid binding sites.

102 Here we show that neither neurosteroid binds to the S1S2 domain of the NMDA NR1-1b

103 sive behavior is the result of a TP-mediated neurosteroid biosynthesis down-regulation that can be re

104 correlates with the down-regulation of brain neurosteroid biosynthesis.

105 Neurosteroids can alter GABA(A)R expression on a rapid t

106 Neurosteroids can reduce HPA axis responses, so allopreg

107 Brain-derived steroids (neurosteroids) can act as fast signaling molecules in th

108 Ethanol-induced increases in neurosteroids could be pertinent to the etiology of slee

109 The adrenal androgen and neurosteroid dehydroepiandrosterone (DHEA) is available

110 A previous study showed that the neurosteroid dehydroepiandrosterone (DHEA), when adminis

111 the UNC-49 GABA receptor by another sulfated neurosteroid, dehydroepiandrosterone sulfate (DHEAS).

112 To assess the neurosteroids' direct effects on mtPTP activity at the s

113 ing establishes that the GABA(A)R-modulating neurosteroids do not inhibit photolabeling of GABA(A)R a

114 ationic channel blockers but unlike sulfated neurosteroids, DPA antagonism was voltage dependent.

115 ors in response to fluctuations in GABAergic neurosteroids during ethanol withdrawal.

116 The large increase in progesterone-derived neurosteroids during pregnancy and their precipitous dec

117 sed ligands and transgenic disease models of neurosteroid dysfunction.

118 n of inhibition provide a mechanism by which neurosteroid E2 could modulate hippocampus-dependent beh

119 One likely function of neurosteroid E2 is to acutely potentiate excitatory syna

120 dependence suggest that locally synthesized neurosteroid E2 may activate this effect in vivo.

121 tradiol (E2), the physiological role of this neurosteroid E2, as distinct from ovarian E2, is unknown

122 otential future directions for research into neurosteroid effects on emotion regulation neurocircuitr

123 ha,5alpha)-androst-16-en-3-ol], a blocker of neurosteroid effects on GABA(A) receptors.

124 lar, brain imaging has not been used to link neurosteroid effects to emotion neurocircuitry.

125 lar, brain imaging has not been used to link neurosteroid effects to emotion regulation neurocircuitr

126 urther investigation into the brain basis of neurosteroid emotion regulatory effects.

127 pyramidal neurons has demonstrated that this neurosteroid engages specific mechanisms in different ar

128 Biologically active neurosteroids enhance rather than inhibit azietomidate p

129 als (fEPSPs) to investigate the mechanism of neurosteroid enhancement of short-term synaptic facilita

130 In contrast, our data suggest that neurosteroid enhancement of tonic inhibition will be gre

131 The neurosteroid estradiol potently augments depolarizing GA

132 These results reveal neurosteroid estrogen synthesis as a previously unknown

133 n of a subset of interneurons in response to neurosteroid exposure and suggest that GABAergic neurost

134 , NCEH-1 also stimulates cholesterol-derived neurosteroid formation and lowers cellular reactive oxyg

135 imilarly mitigated the effects of a clinical neurosteroid general anesthetic, allopregnanolone, belie

136 y also represent functional targets for some neurosteroid general anesthetics.

137 hat these adverse effects may be mediated by neurosteroids, given their well-documented role in stres

138 analyses of direct activation of GABA(A)R by neurosteroids have each led to the proposal that these s

139 Although neurosteroids have rapid effects on GABA(A) receptors, s

140 Neurosteroid homeostasis is critical for normal cognitiv

141 l traits, it may be that locally synthesized neurosteroids impact cells along the proliferative zone

142 y help clarify the role of GABA-potentiating neurosteroids in health and disease.

143 ed in regions that would indicate a role for neurosteroids in neural organization.

144 r the modification of dehydroepiandrosterone neurosteroids in the brain.

145 ate (PS), one of the most commonly occurring neurosteroids in the central nervous system, influences

146 of GABA-enhancing neurosteroids, the role of neurosteroids in the clinical effects of BDZs is unknown

147 upport for the pathophysiologic relevance of neurosteroids in this condition.

148 We conclude that, in very young rats, (i) neurosteroids induce oxytocin release from the supraopti

149 rom rats of 3-4 weeks old or less, all three neurosteroids induced oxytocin release from the isolated

150 The neurosteroid-induced augmentation of this tonic conducta

151 These findings highlight the neurosteroid inhibitory site on NMDA receptors as a valu

152 This neurosteroid insensitivity did not primarily result from

153 le diversity in the way different classes of neurosteroids interact with GABA(A) receptors.

154 Determining how neurosteroids interact with the GABA(A) receptor is a pr

155 ity is interesting because current models of neurosteroid interactions with GABA(A) receptors, based

156 h alpha1beta2gamma2L channel potentiation by neurosteroids, into one of the two concatemeric construc

157 g indicates that a pregnenolone sulfate-like neurosteroid is a previously unrecognized retrograde mes

158 acy of P4S is increased, and potentiation by neurosteroids is diminished.

159 to higher concentration and potentiation by neurosteroids is diminished.

160 and medial dorsal thalamus, indicating that neurosteroid levels are important for proper development

161 To test this hypothesis, we stabilized neurosteroid levels by administering the 5alpha-reductas

162 In the face of the highly elevated neurosteroid levels during pregnancy, which can act on d

163 Changes in neurosteroid levels during the luteal phase of the menst

164 rations of dopamine metabolism, and abnormal neurosteroid levels in brain, potentially implicating th

165 Midazolam, but not clonazepam, increased neurosteroid levels in CA1 pyramidal neurons without cha

166 determined whether specific manipulation of neurosteroid levels in the hippocampus would alter seizu

167 al conditions characterized by elevations in neurosteroid levels induce a reorganization of GABA(A)Rs

168 therapy, raising the possibility that brain neurosteroid levels may be modulated therapeutically.

169 Fluctuating neurosteroid levels over the ovarian cycle modulate neur

170 Serum neurosteroid levels were assessed at baseline and week 1

171 Large baseline-to-exit changes in neurosteroid levels were observed in the pregnenolone gr

172 Alcohol increases GABA release, raises neurosteroid levels, and may potently enhance the functi

173 of ADHD with regard to STS polymorphisms and neurosteroid levels.

174 ological scenarios associated with perturbed neurosteroid levels.

175 u73 as the site of photoincorporation of our neurosteroid ligand in the IMP, mouse voltage-dependent

176 Our results support the hypothesis that neurosteroids may act to influence brain organization an

177 tone in the face of shifting levels of these neurosteroids may induce HPA axis dysfunction, thereby i

178 Studies suggest that neurosteroids may play important roles in neuronal circu

179 evaluate the contribution of a key enzyme in neurosteroid metabolism [i.e., 3alpha-hydroxysteroidoxid

180 Here, we investigate the role of neurosteroid metabolism by using electrophysiological te

181 ults support the theory that an imbalance in neurosteroid metabolism could be a major cause of the ne

182 receptor isoforms, the contribution of local neurosteroid metabolism has been relatively unexplored.

183 e to block conversion of progesterone to its neurosteroid metabolite allopregnanolone in women with p

184 ersion of progesterone to its 5alpha-reduced neurosteroid metabolite mitigates symptoms in PMDD.

185 tion in the brainstem is allopregnanolone, a neurosteroid metabolite of progesterone.

186 of reorganizing GABA(A)Rs by actions through neurosteroid metabolites.

187 Accumulated evidence suggests that neurosteroids modulate GABA(A) receptors through binding

188 Certain neurosteroids modulate NMDARs experimentally but their l

189 Many hormones act as neurosteroids, modulating brain excitability via direct

190 ies demonstrate that, in epileptic DGCs, the neurosteroid modulation of synaptic currents is diminish

191 ivity of alphabetadelta receptor channels to neurosteroid modulation prompted investigation of whethe

192 n NMDA-treated cultures was reduced, and its neurosteroid modulation was also diminished.

193 eceptors previously associated with positive neurosteroid modulation.

194 (A) receptor subunits that are important for neurosteroid modulation.

195 Inhibitory neurosteroids, molecules generated in glia from circulat

196 or pathophysiological conditions may trigger neurosteroid neosynthesis, thereby providing a local mec

197 In addition, effects of this neurosteroid on symptomatic disease, as well as the rece

198 and voltage-independent inhibitory effect of neurosteroids on NMDAR responses.

199 ects of fluctuations in progesterone-derived neurosteroids on the brain.

200 e data demonstrate that positive feedback of neurosteroids onto CRH neurons is required to mount the

201 ed the normal development of brain levels of neurosteroids or altered steroid action at GABA(A) recep

202 ulators of GABA function (e.g., anesthetics, neurosteroids or ethanol).

203 FLI tag was coupled to an alkyne-containing neurosteroid photolabeling reagent and used to identify

204 demonstrates the feasibility of identifying neurosteroid photolabeling sites by using mass spectrome

205 We demonstrate that neurosteroids potentiate the protein kinase C-dependent

206 ntiation does not require a known ligand for neurosteroid potentiating sites on the GABAA receptor.

207 onsistent with previous work indicating that neurosteroid potentiation is mediated by an action that

208 en-3-ol (17PA), that selectively antagonized neurosteroid potentiation of GABA responses.

209 Using an antibody against 5alpha-reduced neurosteroids, predominantly allopregnanolone, we found

210 We suggest that neurosteroids preferentially enhance low-efficacy GABA(A

211 Here, we show that an endogenous neurosteroid pregnanolone sulfate is more potent at inhi

212 by numerous compounds, including endogenous neurosteroid pregnanolone sulfate.

213 enous anesthetic propofol and the endogenous neurosteroid pregnanolone using whole cell macroscopic r

214 R-induced currents than the known endogenous neurosteroid, pregnanolone sulfate (IC50 = 24.6 muM).

215 90 nM to 5.4 muM) than the known endogeneous neurosteroid-pregnanolone sulfate (IC50 = 24.6 muM).

216 The neurosteroid pregnenolone (PREG) and its metabolites pre

217 In the current report, the effect of the neurosteroid pregnenolone on depressive symptoms in BPD

218 TRPM3 can be activated by the neurosteroid pregnenolone sulfate (PregS) and heat.

219 pondences with models of the GABA-inhibitory neurosteroid pregnenolone sulfate (PREGS), suggesting co

220 The endogenous neurosteroid pregnenolone sulfate (PS) is known to enhan

221 ot alter basal CatSper currents, whereas the neurosteroid pregnenolone sulfate exerted similar effect

222 We report here that the excitatory neurosteroid pregnenolone sulfate induces a long-lasting

223 such as the one mediating the effects of the neurosteroid pregnenolone sulfate, or the allosteric reg

224 ory site first postulated for the inhibitory neurosteroid pregnenolone sulfate.

225 We have previously shown that the sulfated neurosteroids pregnenolone sulfate and 3alpha-hydroxy-5b

226 One of these neurosteroid, pregnenolone sulfate (PS), depends on six

227 onsistent with a novel biologic role for the neurosteroid PregS that acts at picomolar concentrations

228 and second by rapidly up-regulating an acute neurosteroid-producing gene, StARD1, which requires the

229 Furthermore, the effects of ethanol on neurosteroid production and LTP were mimicked by a low c

230 hat ethanol paradoxically enhances GABAergic neurosteroid production by activation of unblocked NMDAR

231 Thus, downregulation of neurosteroid production in the brain may underlie HPA ax

232 Deficits in central neurosteroid production were indicated by reduced 5alpha

233 In summary, endogenous neurosteroids profoundly influence GABAergic neurotransm

234 ody provide evidence for a role for aberrant neurosteroid regulation of the GABA(A) receptor subunit

235 bclass that shows high affinity for GABA and neurosteroids, relative insensitivity to benzodiazepines

236 Thus, significant receptor activation by neurosteroids relies on occupancy of both the activation

237 In this Opinion, we argue that neurosteroids require a membranous route of access to tr

238 fluctuations in ovarian hormones and derived neurosteroids result in alterations in regulation of the

239 reflecting a reduction in the extrasynaptic, neurosteroid-sensitive alpha4/delta containing receptor

240 may be beneficial to decrease the number of neurosteroid-sensitive receptors to maintain a steady-st

241 report a novel inhibitory role of Zn(2+) at neurosteroid-sensitive, extrasynaptic deltaGABAA recepto

242 Thus, Zn(2+) inhibition of neurosteroid-sensitive, extrasynaptic GABAA receptors in

243 e selective functional blockade by Zn(2+) of neurosteroid-sensitive, extrasynaptic GABAA receptors in

244 receptors that mediate tonic inhibition and neurosteroid sensitivity in the dentate gyrus.

245 ileptic animals are modified such that their neurosteroid sensitivity is reduced and delta subunit ex

246 imal models of temporal lobe epilepsy (TLE), neurosteroid sensitivity of GABA(A) receptors on dentate

247 based compensation mechanism for the reduced neurosteroid sensitivity of inhibition measured in femal

248 t study investigated a mechanism for loss of neurosteroid sensitivity of synaptic GABA(A) receptors i

249 The neurosteroid sensitivity of these extrasynaptic GABA(A)R

250 olecular mechanisms underlying such enhanced neurosteroid sensitivity remain unclear.

251 SW-induced seizures, confirming delta-linked neurosteroid sensitivity.

252 This neurosteroid staining was increased following 15 min adm

253 bility of NMDA to inhibit LTP and to enhance neurosteroid staining was reversed by finasteride and du

254 Neurosteroids, steroids made in the brain, affect neuron

255 Analgesic neurosteroids such as 5alpha-pregnan-3alpha-ol-20-one (5

256 the formation of 24(S)-hydroxycholesterol or neurosteroids such as CYP46A1, 3alphaHSD, and CYP11A1.

257 Endogenous neurosteroids, such as allopregnanolone (AP), regulate n

258 Neurosteroids, such as allopregnanolone (AP; 3alpha-hydr

259 Neurosteroids, such as pregnenolone sulfate, were previo

260 rgic transmission and consequently a blunted neurosteroid suppression of neuronal firing.

261 nyl)estra-4,9-dien-3- one)], suggesting that neurosteroid synthesis and not progesterone receptor act

262 e found that the genes necessary for de novo neurosteroid synthesis at posthatch day 1 (P1) and P5 sh

263 be blocked by finasteride, an antagonist of neurosteroid synthesis from progesterone.

264 re prevented by finasteride, an inhibitor of neurosteroid synthesis, or 17PA [17-phenyl-(3alpha,5alph

265 not substantially affected by inhibition of neurosteroid synthesis.

266 , rather than glia, are the major sources of neurosteroid synthesis.

267 An insensitivity of the tonic current to the neurosteroid tetrahydrodeoxy-corticosterone was consiste

268 ted that physiological concentrations of the neurosteroid tetrahydrodeoxycorticosterone were less eff

269 neurons are modulated by the stress-derived neurosteroid, tetrahydrodeoxycorticosterone (THDOC), act

270 NP-C mouse brain contains substantially less neurosteroid than wild-type brain and has an age-related

271 f both males and females synthesizes E2 as a neurosteroid that could acutely modulate synaptic functi

272 -beta-pregnan-20-one hemisuccinate (ABHS), a neurosteroid that inhibits excitatory amino acid recepto

273 Pregnanolone sulfate (PAS) is an endogenous neurosteroid that inhibits NMDA receptors and is neuropr

274 We found that an endogenous neurosteroid that is selective for high-affinity delta s

275 to release dehydroepiandrosterone (DHEA), a neurosteroid that promotes neurogenesis and neuron survi

276 y to identify the structural features in ent-neurosteroids that enhance their activity as positive al

277 gents such as anesthetics, barbiturates, and neurosteroids, the cellular mechanisms neurons use to re

278 and promote the synthesis of GABA-enhancing neurosteroids, the role of neurosteroids in the clinical

279 ings may represent a molecular rationale for neurosteroid therapy of catamenial epilepsy.

280 Given the wide availability of this neurosteroid, this finding has important implications fo

281 s of high-affinity GABAA receptors including neurosteroids, this phenomenon provides a potentially im

282 pression is increased by 48h exposure to the neurosteroid THP (3alpha-OH-5alpha[beta]-pregnan-20-one)

283 e thalamus retains the ability to synthesise neurosteroids, thus preserving the capacity to enhance b

284 Therefore, the ability of neurosteroids to modulate the phosphorylation and membra

285 However, by P10, this neurosteroid 'tone' rapidly dissipates, thereby producin

286 contributes to the pathology of NP-C; thus, neurosteroid treatment may be useful in ameliorating pro

287 Neurosteroids typified by 5alpha-pregnan-3alpha-ol-20-on

288 S is derived from PREG, the precursor of all neurosteroids, via a single sulfation step and is presen

289 ition in the female gamma2(Y356/367F) +/- to neurosteroids was markedly reduced compared with WT.

290 t, synaptic inhibition and its modulation by neurosteroids were preserved in these neurons.

291 ism of modulation of NMDARs by an endogenous neurosteroid, which has implications for identifying sta

292 It has been suggested that neurosteroids, which act as negative modulators of excit

293 m a precisely timed loss of locally produced neurosteroids, which act as positive allosteric modulato

294 ts that the brain is capable of synthesizing neurosteroids, which in developing zebra finches may be

295 variety of allosteric modulators, including neurosteroids, which in turn makes them promising therap

296 unsaturated fatty acids (PUFAs), 2) sulfated neurosteroids, which play a role in brain development, 3

297 ial for growth and development; low sulfated neurosteroids, which play a role in brain development; l

298 Dehydroepiandrosterone (DHEA) is a neurosteroid with anxiolytic, antidepressant, and antigl

299 Dehydroepiandrosterone (DHEA) is a neurosteroid with potential effects on neurogenesis and

300 around the menstrual period associated with neurosteroid withdrawal (NSW).