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 s modulation of the rho1 GABA(A) receptor by neurosteroids.

5 tor modulation by combinations of endogenous neurosteroids.

6 nism indistinguishable from that of sulfated neurosteroids.

7 it site that mediates receptor activation by neurosteroids.

8 nits is required for binding of potentiating neurosteroids.

9 subunit promoting effects that vary between neurosteroids.

10 maximum effects similar to barbiturates and neurosteroids.

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

12 icated in mediating the analgesic actions of neurosteroids.

13 olecular target for the analgesic actions of neurosteroids.

14 ons for the physiological role of endogenous neurosteroids.

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

16 otentiating and direct activation effects of neurosteroids.

17 ey can override the endogenous production of neurosteroids.

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

19 The activity of NMDARs can be modulated by neurosteroids.

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

21 ors, which respond sensitively to endogenous neurosteroids.

22 ctly act on neuronal excitability, acting as neurosteroids.

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

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

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

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

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 The endogenous neurosteroid (3alpha,5alpha)3-hydroxypregnan-20-one (3al

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

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

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

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

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

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

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

37 ceptors are the primary molecular targets of neurosteroid action, the structural details of neuroster

38 3-alpha1 intersubunit sites are critical for neurosteroid action.

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

40 Neurosteroids activate extrasynaptic deltaGABAA receptor

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

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

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

44 The neurosteroid allopregnanolone acts as a positive alloste

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

46 The neurosteroid allopregnanolone is a potent allosteric mod

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

48 The neurosteroid allopregnanolone partially mediates the ane

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

50 e to GABA or the combination of GABA and the neurosteroid allopregnanolone, which was intended to des

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

52 We found that the potentiating neurosteroid, allopregnanolone, but not its inhibitory 3

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

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

55 ptor properties including sensitivity to the neurosteroid, allopregnanolone.

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

57 ) GABA(A) receptor (GABA(A)R) contributes to neurosteroid allosteric modulation.

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

59 Injection of the neurosteroid also significantly reduced astrocyte prolif

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

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

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

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

64 ,3-benzoxadiazol-4-yl amino (NBD)-conjugated neurosteroid analogs photopotentiate GABA(A) receptor fu

65 We synthesized neurosteroid analogue photolabeling reagents in which th

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

67 Two neurosteroid analogues with diazirine moieties replacing

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

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

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

71 Neurosteroids and some anxiolytics share an important si

72 Endogenous neurosteroids and their synthetic analogs (neuroactive s

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

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

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

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

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

78 nds provide potential chemical scaffolds for neurosteroid antagonists.

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

80 Although neurosteroids are accepted allosteric modulators of GABA

81 Neurosteroids are allosteric modulators of both synaptic

82 Endogenous neurosteroids are among the most potent and efficacious

83 Neurosteroids are endogenous allosteric modulators of GA

84 Neurosteroids are endogenous modulators of neuronal exci

85 Neurosteroids are endogenous neuromodulators that bind a

86 Neurosteroids are endogenous regulators of neuronal exci

87 Neurosteroids are potent modulators of GABA-A receptors.

88 Neurosteroids are potent neuromodulators which act in pa

89 Neurosteroids are powerful modulators of brain function

90 Neurosteroids are produced de novo in neuronal and glial

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

92 Neurosteroids are synthesized de novo in the brain durin

93 Neurosteroids are synthesized within the brain and act a

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

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

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

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

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

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

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

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

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

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

104 labeled residues representing three distinct neurosteroid binding sites in the human alpha1beta3 GABA

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

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

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

108 urosteroid action, the structural details of neurosteroid binding to these proteins remain ill define

109 ial occupancy and efficacy at three discrete neurosteroid-binding sites determine whether a neuroster

110 ow site-specific binding to three identified neurosteroid-binding sites in the alpha(1)beta(3) GABA(A

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

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

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

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

115 Neurosteroids can reduce HPA axis responses, so allopreg

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

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

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

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

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

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

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

123 dition consists of administering a synthetic neurosteroid during the postpartum period to alleviate t

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

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

126 sed ligands and transgenic disease models of neurosteroid dysfunction.

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

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

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

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

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

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

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

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

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

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

137 Biologically active neurosteroids enhance rather than inhibit azietomidate p

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

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

140 -alpha deletion, PPAR-alpha antagonists, and neurosteroid-enzyme inhibitors.

141 The neurosteroid estradiol potently augments depolarizing GA

142 These results reveal neurosteroid estrogen synthesis as a previously unknown

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

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

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

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

147 urosteroid-binding sites determine whether a neurosteroid has potentiating, inhibitory, or competitiv

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

149 Neurosteroid homeostasis is critical for normal cognitiv

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

151 pregnanolone, a gamma-aminobutyric acidergic neurosteroid implicated in mood disorders.

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

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

154 r the modification of dehydroepiandrosterone neurosteroids in the brain.

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

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

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

158 f the human rho1 GABA(A) receptor by several neurosteroids, individually and in combination, in the f

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

160 This neurosteroid insensitivity did not primarily result from

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

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

163 predicted critical residues contributing to neurosteroid interaction with the GABAA receptors.

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

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

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

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

168 to higher concentration and potentiation by neurosteroids is diminished.

169 Neurosteroid levels before and after PEA treatment were

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

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

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

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

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

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

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

177 Fluctuating neurosteroid levels over the ovarian cycle modulate neur

178 Serum neurosteroid levels were assessed at baseline and week 1

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

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

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

182 ological scenarios associated with perturbed neurosteroid levels.

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

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

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

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

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

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

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

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

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

192 Certain neurosteroids modulate NMDARs experimentally but their l

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

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

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

196 eceptors previously associated with positive neurosteroid modulation.

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

198 Inhibitory neurosteroids, molecules generated in glia from circulat

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

200 Neurosteroids (NS) are the main modulators of gamma-amin

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

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

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

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

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

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

207 entification of binding sites and mapping of neurosteroid orientation within these sites.

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

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

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

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

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

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

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

215 by numerous compounds, including endogenous neurosteroid pregnanolone sulfate.

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

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

218 90 nM to 5.4 muM) than the known endogeneous neurosteroid-pregnanolone sulfate (IC50 = 24.6 muM).

219 The neurosteroid pregnenolone (PREG) and its metabolites pre

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

221 c modulators of NMDARs include an endogenous neurosteroid pregnenolone sulfate (PES), but the binding

222 ndogenous compounds, such as cholesterol and neurosteroid pregnenolone sulfate (PES).

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

224 sensitivity to stimulation by the endogenous neurosteroid pregnenolone sulfate (PS) and heat, and alt

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

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

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

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

229 The neurosteroid pregnenolone, a US Food and Drug Administra

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

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

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

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

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

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

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

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

238 In summary, endogenous neurosteroids profoundly influence GABAergic neurotransm

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

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

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

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

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

244 ps were placed at three positions around the neurosteroid ring structure, enabling identification of

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

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

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

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

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

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

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

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

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

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

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

256 olecular mechanisms underlying such enhanced neurosteroid sensitivity remain unclear.

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

258 This neurosteroid staining was increased following 15 min adm

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

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

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

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

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

264 Neurosteroids, such as pregnenolone sulfate, were previo

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

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

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

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

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

270 not substantially affected by inhibition of neurosteroid synthesis.

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

272 The endocannabinoid and neurosteroid systems regulate emotions and stress respon

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

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

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

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

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

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

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

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

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

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

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

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

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

286 Computational docking studies of neurosteroid to the three sites predicted critical resid

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

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

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

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

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

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

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

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

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).