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. 2026 Sep 20;21:868–873. doi: 10.1016/j.ibneur.2026.09.011

Oxytocin preserves excitatory responsiveness of VTA dopaminergic neurons in PTSD model rats

Qiuxia Chen 1,1, Zhen Liu 1,1, Haiyu Huang 1,1, Wenyi Duan 1, Qinghui Lan 1, Peiling Zhou 1,⁎, Changzheng Zhang 1,⁎
PMCID: PMC13634406  PMID: 42830945

Abstract

Dysfunction of the ventral tegmental area (VTA) dopaminergic circuits is strongly implicated in the pathological progression of post-traumatic stress disorder (PTSD). Oxytocin (OXT) exerts robust stress-buffering effects, yet its direct neuromodulatory influence on VTA dopaminergic neurons under PTSD pathological conditions remains poorly defined. Here, we performed in vivo extracellular recordings to quantify spontaneous firing and burst activity in normal control and single prolonged stress (SPS)-induced PTSD model rats. Graded intracerebroventricular OXT infusions and OXTR antagonist pretreatment were used to characterize OXT-mediated neuronal modulation. Baseline spontaneous firing and burst rates were markedly suppressed in PTSD model rats; however, OXT elevated neuronal excitability in both cohorts, an effect nearly abolished by pretreatment with the selective OXTR antagonist L-371,257. Although absolute firing values remained persistently lower in PTSD model rats at baseline and following OXT administration, the relative fold increase in response to OXT was comparable to that observed in normal controls. These electrophysiological findings demonstrate that PTSD-like traumatic stress depresses baseline VTA dopaminergic activity, whereas the excitatory responsiveness of VTA dopaminergic neurons to exogenous OXT is largely preserved in PTSD model animals.

Keywords: Oxytocin, Post-traumatic stress disorder, Ventral tegmental area, Dopaminergic neurons, In vivo electrophysiology

Highlights

  • •

    Oxytocin elicits dose-dependent excitation of VTA dopaminergic neurons.

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    PTSD reduces baseline firing and burst activities of VTA dopaminergic neurons.

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    PTSD does not alter oxytocin’s excitatory effects on VTA dopaminergic neurons.

Introduction

Post-traumatic stress disorder (PTSD) is a chronic stress-related neuropsychiatric disorder characterized by intrusive recollections, avoidance behavior and persistent affective disturbances, while existing clinical interventions exhibit limited and variable therapeutic efficacy (Ben-Zion et al., 2025, Leithner et al., 2026, Yuan et al., 2025). Convergent preclinical and clinical evidence identifies dysfunction of the ventral tegmental area (VTA) dopaminergic circuit as a critical pathogenic factor underpinning stress maladaptation (Liu et al., 2023, Wang et al., 2025). Single-nucleus RNA-sequencing data further demonstrate trauma-induced transcriptional remodeling specifically within VTA dopaminergic neurons (Zhou et al., 2025). Consistent with these molecular alterations, electrophysiological recordings reveal suppressed firing of VTA dopaminergic neurons correlated with PTSD-like behavioral deficits (Corralfrias et al., 2013, Wang et al., 2025). Our previous functional assays further confirm that selective activation of this dopaminergic population alleviates PTSD-associated anxiety and aberrant fear memory consolidation (Guan et al., 2022, Huang et al., 2024). Complementary human studies also link disrupted mesolimbic dopamine signaling to core PTSD clinical manifestations (Cisler et al., 2020, Jia et al., 2023, Zhou et al., 2021).

Oxytocin (OXT), a hypothalamic neuropeptide regulating stress resilience and mesolimbic reward processing, exerts biological actions via OXT receptors (OXTRs) widely distributed across brain regions (Menon and Neumann, 2023, Thurston et al., 2025). Optogenetic studies confirm that OXT signaling facilitates mesolimbic dopamine release (Hung et al., 2017, Sun et al., 2025, Xiao et al., 2017). Clinical and preclinical investigations further report reduced peripheral OXT concentrations and blunted peripheral physiological responses to OXT in PTSD patients and PTSD model rodents (Carmassi et al., 2021, Horn et al., 2024, Yan et al., 2025). Despite these peripheral observations, it remains unresolved whether PTSD impairs the intrinsic responsiveness of VTA dopaminergic neurons to central OXT at the single-cell level.

Here, we carried out in vivo extracellular recordings to characterize acute electrophysiological responses of VTA dopaminergic neurons to intracerebroventricular OXT administration in normal control and single prolonged stress (SPS)-induced PTSD model rats. We aimed to clarify whether central exogenous OXT produces dose-dependent excitatory modulation of VTA dopaminergic activity, and whether this OXT-evoked neuronal potentiation remains intact under PTSD pathological conditions. These findings provide a mechanistic foundation to guide future translational research exploring OXT-targeted strategies for PTSD.

Materials and methods

Animals

Healthy male Sprague-Dawley rats (2 months old, 230–260 g; total n = 62) were purchased from the Guangdong Medical Laboratory Animal Center (Foshan, China). Animals were housed at 23 ± 1 °C under a 12 h light-dark cycle with ad libitum access to food and water, and acclimated for 7 days before experimental operations. All animal manipulations complied with the NIH Guide for the Care and Use of Laboratory Animals, and the protocol was approved by the Academic and Ethics Committee of Lingnan Normal University (Approval No. LNU-2026-S050). All procedures were designed to minimize animal suffering and reduce sample size.

PTSD model induction

Thirty rats served as normal control subjects, and 29 rats underwent the SPS paradigm to establish PTSD models as described in previous reports (Guan et al., 2022, Huang et al., 2024, Yan et al., 2025). Briefly, animals were restrained individually for 2 h, followed by 20-min forced swimming in water maintained at 23 ± 1 °C. After a 15-min recovery interval, rats were exposed to ether vapor until loss of consciousness, then returned to home cages and left undisturbed for 7 days to develop PTSD-like phenotypes.

Surgical preparation

Given OXT’s limited blood-brain barrier permeability (Leng and Ludwig, 2016, Parmaksiz and Kim, 2025), intracerebroventricular delivery into the lateral ventricle (LV) was adopted for drug administration. Rats were anesthetized with isoflurane and secured on a stereotaxic frame (RWD Life Science Co. Ltd., Shenzhen, China). A cranial window was created, and a stainless-steel guide cannula (outer diameter = 0.48 mm, inner diameter = 0.34 mm, 5.0 mm projection) was implanted targeting the LV at coordinates AP −0.48 mm, ML + 1.60 mm, DV −4.20 mm (Paxinos and Watson, 2007). The cannula was temporarily fixed to the skull with dental cement. A matching microinjection needle (0.30 mm outer diameter, 5.5 mm length, extending 0.5 mm beyond the cannula tip) was inserted for subsequent intracerebroventricular infusions.

Bilateral cranial openings were then made over the VTA at AP −4.92 to −5.20 mm, ML 0.0 to ±0.6 mm, DV −8.3 to −8.8 mm (Paxinos and Watson, 2007). A bifurcated multichannel recording array (2 × 4 channels per hemisphere, impedance ~500 kΩ; KD-MWA, Kedou Brain-Machine Technology, Suzhou, China) was slowly lowered into bilateral VTA regions via a computerized stepper motor (IVM-1000; Scientifica, East Sussex, UK) for in vivo extracellular recordings.

In vivo extracellular recording and neuronal classification

To maintain intact brain circuitry and endogenous neurochemical signaling under native physiological conditions, in vivo extracellular recording was adopted for real time monitoring of VTA neuronal activity in response to OXT challenge. Electrophysiological signals were acquired using a signal collection and processing system (AlphaLab SnR, Alpha Omega Engineering, Nof HaGalil, Israel). Following a 20-min neuronal stabilization period, baseline firing activity was recorded for 5 min prior to drug delivery. All animals received intracerebroventricular infusions of either vehicle saline or graded doses of OXT (0.3, 1.0, 3.0 µg/kg, termed LD-OXT, MD-OXT, HD-OXT; Macklin Inc., Shanghai, China) at a flow rate of 1 µl/min, followed by 30 min of continuous neuronal recording post-infusion. To verify OXTR-mediated effects, a subset of rats received pretreatment with the selective OXTR antagonist L-371,257 (L371, 5 µg/kg in 2 µl; Tocris, Bristol, UK) 3 min before HD-OXT infusion (L371 +HD-OXT group). Sample sizes for each experimental group: normal controls, saline (n = 5), LD-OXT (n = 6), MD-OXT (n = 7), HD-OXT (n = 6), L371 + HD-OXT (n = 6); SPS-induced PTSD model rats, saline (n = 6), LD-OXT (n = 6), MD-OXT (n = 5), HD-OXT (n = 6), L371 + HD-OXT (n = 6).

Neuronal firing rates and burst firing events were analyzed using 300-s baseline and post-treatment epochs (corresponding to the maximal response within 15 min after OXT infusion). Offline spike sorting and quantitative neuronal analyses were performed. Detailed pharmacological procedures for neuronal subtype discrimination and electrophysiological classification criteria are provided in the Supplementary Materials.

Upon recording completion, direct current stimulation (300 µA for 5 min) was delivered through one recording electrode to mark recording sites. Brain tissues were sectioned using a freezing microtome (CM1860, Leica Instruments, Mannheim, Germany) for histological verification.

Immunofluorescence staining

Three additional normal rats were used for immunofluorescence co-labeling to detect OXTR expression in VTA dopaminergic neurons. Detailed methods are presented in Supplementary Materials.

Statistical analysis

All data are expressed as mean ± standard error of the mean (SEM). Statistical tests included paired t-tests (intra-group pre–post comparisons), unpaired Student’s t-tests (normal vs PTSD intergroup contrasts), one-way ANOVA (multiple OXT dose comparisons) and two-way ANOVA (treatment × time interactive effects). Where ANOVA yielded significant main or interactive effects, Fisher’s least significant difference post-hoc test was used for pairwise comparisons. A threshold of p < 0.05 was defined as statistically significant.

Results

OXT increased dopaminergic neuronal activity in normal control rats

A total of 113 single-unit signals from putative VTA dopaminergic neurons were obtained in normal control rats. Baseline firing rates were comparable across groups prior to drug infusion (F3,109 = 0.445, p = 0.721; Fig. 1A). One-way ANOVA revealed a significant main effect of OXT treatment on firing rate (F3,109 = 8.293, p < 0.001). Post-hoc comparisons confirmed that HD-OXT produced a 1.96-fold increase in firing rate relative to the saline group (p < 0.01). Two-way ANOVA detected significant main effects of treatment, recording time, and a significant treatment × time interaction (all p < 0.01).

Fig. 1.

Fig. 1

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OXT elevates VTA dopaminergic neuronal firing and burst activity in normal and SPS-induced PTSD model rats. A, B. Firing rate (A) and burst rate (B) of VTA dopaminergic neurons in normal control rats before and after intracerebroventricular delivery of saline, LD-OXT, MD-OXT, HD-OXT, or HD-OXT combined with prior pretreatment using the OXTR antagonist L-371,257. C, D. Firing rate (C) and burst rate (D) recorded in SPS-induced PTSD model rats following identical drug administration protocols. E. Representative brain slice verifying cannula placement targeting the lateral ventricle (LV). F. Histological confirmation of in vivo extracellular recording sites within the VTA. Inset displays representative spike traces under baseline conditions and following HD-OXT infusion. Data are presented as mean ± SEM. **p < 0.01, *p < 0.05, n.s., no significant difference.

Baseline burst rates were also comparable among all groups (F3,109 = 0.376, p = 0.771; Fig. 1B). OXT significantly elevated burst activity in a dose-dependent manner (F3,109 = 7.855, p < 0.001), with HD-OXT inducing a 10.37-fold increase compared with saline controls (p < 0.01). Two-way ANOVA confirmed significant main effects of treatment, time, and their interaction on burst firing (all p < 0.01).

Pretreatment with the OXTR antagonist L371 significantly blocked OXT-induced elevations in both firing and burst rates (p < 0.01 vs HD-OXT alone, Fig. 1A, B). The baseline firing rate of VTA GABAergic neurons averaged 13.48 ± 0.49 Hz, with no significant alterations observed following OXT or antagonist administration (Figures S1, 2).

OXT increased dopaminergic neuronal activity in PTSD model rats

A total of 151 dopaminergic single-unit recordings were acquired from SPS-induced PTSD model rats. Baseline firing rates were consistent across all groups before drug treatment (F3,147 = 0.139, p = 0.936; Fig. 1C). OXT exerted robust dose-dependent excitatory effects on neuronal firing frequency (F3,147= 6.481, p < 0.001), with HD-OXT producing a 2.63-fold elevation relative to saline treatment (p < 0.01). Two-way ANOVA revealed significant main effects of treatment and recording time, as well as a significant treatment × time interaction (all p < 0.01).

Baseline burst rates showed no significant intergroup differences prior to drug delivery (F3,147 = 0.525, p = 0.666; Fig. 1D). OXT significantly enhanced burst firing activity (F3,147 = 6.010, p < 0.001), whereby HD-OXT induced a 15.47-fold increase in burst rate (p < 0.01). Two-way ANOVA confirmed significant main and interactive effects for burst firing modulation (all p < 0.01).

Pretreatment with L371 almost nearly abrogated HD-OXT-triggered potentiation of firing and burst activity (p < 0.01 vs HD-OXT). The baseline firing frequency of VTA GABAergic neurons in PTSD model rats was 13.66 ± 0.35 Hz, which remained unaltered following OXT or antagonist application (Figure S2).

Comparison of OXT response magnitude between normal and PTSD model rats

VTA dopaminergic neurons in PTSD model rats exhibited significantly lower baseline firing and burst rates than those in normal control animals (both p < 0.01, Table 1). Notably, absolute post-treatment firing and burst values remained consistently lower in PTSD model rats across all OXT doses. However, independent t-tests revealed that the intergroup difference in firing rate failed to reach statistical significance under HD-OXT (p = 0.16), whereas differences in burst rate following MD-OXT and HD-OXT administration only approached significance (p = 0.06–0.07), indicating marginal trends.

Table 1.

Comparison of OXT-mediated neuronal activities in VTA dopaminergic neurons between normal and PTSD model rats.

Normal rats PTSD model rats
Firing rate (pre-treatment, Hz) 1.43 ± 0.07 0.82 ± 0.06**
Firing rate after LD-OXT treatment (Hz) 2.78 ± 0.27 1.83 ± 0.22**
Firing rate after MD-OXT treatment (Hz) 3.27 ± 0.32 2.22 ± 0.27*
Firing rate after HD-OXT treatment (Hz) 4.34 ± 0.59 3.06 ± 0.69n.s.
Burst rate (pre-treatment, Hz) 0.04 ± 0.01 0.02 ± 0.00**
Burst rate after LD-OXT treatment (Hz) 0.15 ± 0.03 0.08 ± 0.02*
Burst rate after MD-OXT treatment (Hz) 0.21 ± 0.04 0.12 ± 0.03#
Burst rate after HD-OXT treatment (Hz) 0.33 ± 0.06 0.18 ± 0.05#
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Note: Pre-treatment values are pooled from all groups [saline, low-dose (LD)-OXT, medium-dose (MD)-OXT, high-dose (HD)-OXT] before drug injection. Normal rats: saline (n = 5), LD-OXT (n = 6), MD-OXT (n = 7), HD-OXT (n = 6); PTSD model rats: saline (n = 6), LD-OXT (n = 6), MD-OXT (n = 5), HD-OXT (n = 6). **p < 0.01; *p < 0.05; #p = 0.06–0.07 (trend); n.s., not significant.

To further compare neuronal responsiveness between groups, post-treatment activity was normalized to individual baseline levels to calculate fold changes (Fig. 2). Two-way ANOVA revealed no significant main effect of animal group on either firing fold change (F1,196 = 2.127, p = 0.146) or burst fold change (F1,196 = 1.396, p = 0.239). A significant main effect of OXT dose was detected for firing potentiation (F2,196 = 5.968, p = 0.003), whereas burst activity exhibited a marginal dose-dependent trend (F2,196 = 3.266, p = 0.040). No significant group × dose interaction was observed for either firing or burst modulation (p > 0.05).

Fig. 2.

Fig. 2

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OXT-induced relative fold increases in VTA dopaminergic neuronal firing and burst rates in normal and PTSD model rats. A. Fold increase in firing rate; B. Fold increase in burst rate. Line plots illustrate neuronal activity responses to low-dose (LD)-OXT, medium-dose (MD)-OXT, and high-dose (HD)-OXT across the two animal cohorts. All values are quantified as fold change relative to individual baseline pre-OXT recordings. Data are expressed as mean ± SEM; n.s., no significant difference for comparison between the same OXT dose in PTSD model versus normal rats.

OXTR co-localization with TH-positive VTA neurons

Immunofluorescence co-staining results (Figure S3) confirmed co-localization of tyrosine hydroxylase (TH, a specific marker of dopaminergic neurons) and OXTR immunoreactivity within VTA neuronal somata. No specific fluorescent signals were detected in primary antibody-negative control sections.

Discussion

The present in vivo electrophysiological study characterizes OXT-mediated modulation of VTA dopaminergic neuronal activity in both control and PTSD model rats. Consistent with our previous findings (Guan et al., 2022, Huang et al., 2024), traumatic stress exerts robust inhibitory effects on VTA dopaminergic neuronal output. This stress-induced suppression of baseline firing activity provides a critical functional background for evaluating central OXT neuromodulation. Central OXT infusion dose-dependently enhanced VTA dopaminergic excitability, and this facilitatory effect was largely abolished by pretreatment with the selective OXTR antagonist L371, confirming that OXT-driven neuromodulation is strictly OXTR-dependent. Notably, the relative fold increases in firing and burst activity induced by OXT were comparable between control and PTSD groups, indicating that traumatic stress does not impair the relative excitatory responsiveness of VTA dopaminergic neurons to exogenous OXT.

The present findings refine current understanding of midbrain OXT signaling under pathological stress conditions. Phasic burst firing of VTA dopaminergic neurons drives mesolimbic dopamine release and is essential for fear extinction, stress coping and reward salience encoding (Floresco et al., 2003, Paladini et al., 2001). Impaired dopaminergic burst transmission is tightly linked to core PTSD behavioral deficits, including defective fear regulation and emotional dysregulation (Wang et al., 2025). Here, OXT-induced augmentation of dopaminergic burst activity provides a credible neurophysiological basis for its stress-buffering effects, consistent with accumulating preclinical and clinical evidence that OXT alleviates trauma-related emotional dysfunction (Baldi et al., 2021, Moshfeghinia et al., 2025, Zhang et al., 2023). These functional observations further support our previous behavioral results that specific activation of VTA dopaminergic neurons ameliorates PTSD-associated behavioral impairments (Guan et al., 2022, Huang et al., 2024).

Immunofluorescence analyses further support the anatomical substrate for OXT signaling, revealing robust OXTR expression in VTA dopaminergic neurons. Importantly, neither OXT application nor OXTR antagonism altered the firing properties of local VTA GABAergic neurons, indicating that OXT preferentially modulates dopaminergic neurons rather than engaging indirect GABAergic inhibitory circuits. These findings align with established models showing that OXT directly elevates the intrinsic excitability of VTA dopaminergic neurons to regulate stress resilience and mesolimbic reward function (Borland et al., 2019, Hung et al., 2017). Such cell-type-specific modulation avoids broad disruption of local inhibitory circuitry, further supporting the mechanistic plausibility of OXT-targeted intervention for stress-related neuropathology.

As illustrated in the schematic diagram (Fig. 3), traumatic stress induces persistent suppression of baseline VTA dopaminergic activity, diminishing both tonic and phasic dopamine output within mesolimbic circuits (Zhou et al., 2021). Despite this stress-evoked neuronal hypofunction, the OXTR-dependent excitatory signaling cascade triggered by exogenous OXT remains functionally intact in PTSD model rats (Fig. 2). Accordingly, OXT can counteract stress-related dopaminergic depression via preserved neuronal responsiveness, partially restoring mesolimbic dopaminergic transmission under pathological stress conditions. By reinstating adaptive burst firing in dopaminergic neurons, OXT may stabilize dysfunctional fear-processing circuits and mitigate stress-driven emotional maladaptation, offering a refined circuit-level mechanism accounting for OXT-mediated stress resilience.

Fig. 3.

Fig. 3

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Schematic model illustrating the neurophysiological mechanism by which OXT reverses trauma-evoked mesolimbic dopaminergic insufficiency. A. Diagram of intracerebroventricular OXT delivery. Exogenous OXT infused into the lateral ventricle (LV) acts on OXTR-expressing dopaminergic neurons within VTA. B. Temporal dynamics of mesolimbic dopamine output following traumatic stress. Under baseline conditions, neurons exhibit stable tonic firing accompanied by physiological dopamine release. Trauma triggers an acute burst-firing surge, which subsequently shifts to prolonged low-frequency discharge and persistent hypodopaminergia (Corralfrias et al., 2013). Solid black curves represent untreated PTSD model animals with sustained dopaminergic deficit; green dotted lines denote OXT-evoked restoration of tonic firing and mesolimbic dopamine output in OXT-treated PTSD model rats, counteracting trauma-induced dopaminergic suppression. The inset box summarizes three distinct firing patterns of VTA dopaminergic neurons and their corresponding magnitudes of dopamine release.

Several limitations of this study should be acknowledged. First, despite the well-validated SPS paradigm for generating PTSD-like phenotypes (Huang et al., 2024, Zhou et al., 2025), independent behavioral and endocrine validation (e.g., fear-conditioning paradigms, plasma corticosterone measurements) is absent in this study. Recorded electrophysiological signatures constitute only indirect evidence and cannot act as surrogates for full-blown PTSD-related behavioral manifestations. Second, intracerebroventricular administered OXT diffuses broadly across the brain. The observed excitation of VTA dopaminergic neurons may arise from local VTA OXTR activation or indirect modulation by OXTR-positive upstream circuits (such as amygdala, hypothalamus, prefrontal cortex). Definitive dissociation of direct versus indirect effects would require dedicated intra-VTA OXT microinjection experiments. Finally, all experiments were performed in male rats, while substantial sex differences in OXT signaling, stress susceptibility and mesolimbic circuit function have been well documented (Grieb et al., 2024, Moshfeghinia et al., 2025), highlighting the need for follow-up studies using female animal cohorts.

Conclusion

Central exogenous OXT enhances the excitability of VTA dopaminergic neurons in both normal control and PTSD model rats. Although traumatic stress persistently suppresses baseline VTA dopaminergic activity, the relative excitatory responsiveness of VTA dopaminergic neurons to exogenous OXT is largely preserved under PTSD pathological conditions. These neurophysiological findings demonstrate intact OXTR-mediated neuromodulation of mesolimbic dopaminergic circuits following traumatic stress, providing refined mechanistic insights into central OXT-dependent stress regulation and supporting the potential of OXT-targeted strategies for PTSD neuropathology intervention.

CRediT authorship contribution statement

Qiuxia Chen: Writing – original draft, Methodology, Investigation, Formal analysis, Data curation. Zhen Liu: Formal analysis, Data curation. Haiyu Huang: Formal analysis, Data curation. Wenyi Duan: Methodology, Investigation. Qinghui Lan: Writing – review & editing, Writing – original draft. Peiling Zhou: Writing – review & editing, Writing – original draft, Methodology, Conceptualization. Changzheng Zhang: Writing – review & editing, Writing – original draft, Supervision, Funding acquisition, Conceptualization.

Ethics declaration

This study was conducted in accordance with the ARRIVE (Animal Research: Reporting of In Vivo Experiments) guidelines as well as the following guidelines for animal welfare and/or reporting: Guide for the Care and Use of Laboratory Animals: Eighth Edition. (Washington, DC: The National Academies Press, 2011). This study was approved by the Academic and Ethics Committee of Lingnan Normal University. (Approval No. LNU-2026-S050)

Funding

This work was supported by grants from the National Natural Science Foundation of China (81871062), Guangdong Basic and Applied Basic Research Foundation (2024A1515012913), Key Research Foundation of Guangdong Provincial Education Bureau (2025ZDZX2041), the Special Fund of Science and Technology Innovation Cultivation of Guangdong University Students (pdjh2025ak133), and Guangdong Provincial College Students Innovation and Entrepreneurship Training Program (S202610579011).

Declaration of Competing Interest

The authors declare no conflicts of interest.

Footnotes

Appendix A

Supplementary data associated with this article can be found in the online version at doi:10.1016/j.ibneur.2026.09.011.

Contributor Information

Peiling Zhou, Email: peilingzhouvip@163.com.

Changzheng Zhang, Email: neurozhang@163.com.

Appendix A. Supplementary material

Supplementary material

mmc1.pdf (651.3KB, pdf)

Data availability

The data supporting the conclusions of this study are available from the corresponding author (Zhang C.) upon reasonable request.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Supplementary material

mmc1.pdf (651.3KB, pdf)

Data Availability Statement

The data supporting the conclusions of this study are available from the corresponding author (Zhang C.) upon reasonable request.

Articles from IBRO Neuroscience Reports are provided here courtesy of Elsevier

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