Intranasal oxytocin in the treatment of autism spectrum disorders: A multilevel meta-analysis

Huang, Yi; Huang, Xin; Ebstein, Richard P.; Yu, Rongjun

doi:10.1016/j.neubiorev.2020.12.028

Cited by 73 publications

(47 citation statements)

References 69 publications

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“…A very large proportion of individuals with ASD also are hypo- or hypersensitive to sensory inputs (Marco et al, 2011 ; Suarez, 2012 ), consistent with the function of oxytocin in regulating cortical neural circuit wiring. However, clinical trials investigating the effectiveness of oxytocin as a treatment for ASD reported mixed results (Guastella and Hickie, 2016 ; Ooi et al, 2017 ; Keech et al, 2018 ; Huang et al, 2021 ). The dynamic developmental effects of oxytocin likely add to the difficulty of obtaining consistent results.…”

Section: Discussionmentioning

confidence: 99%

Oxytocin Regulates Synaptic Transmission in the Sensory Cortices in a Developmentally Dynamic Manner

Zhang

Miao

et al. 2021

Front. Cell. Neurosci.

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The development and stabilization of neuronal circuits are critical to proper brain function. Synapses are the building blocks of neural circuits. Here we examine the effects of the neuropeptide oxytocin on synaptic transmission in L2/3 pyramidal neurons of the barrel field of the primary somatosensory cortex (S1BF). We find that perfusion of oxytocin onto acute brain slices significantly increases the frequency of miniature excitatory postsynaptic currents (mEPSC) of S1BF L2/3 pyramidal neurons at P10 and P14, but reduces it at the later ages of P22 and P28; the transition occurs at around P18. Since oxytocin expression is itself regulated by sensory experience, we also examine whether the effects of oxytocin on excitatory synaptic transmission correlate with that of sensory experience. We find that, indeed, the effects of sensory experience and oxytocin on excitatory synaptic transmission of L2/3 pyramidal neurons both peak at around P14 and plateau around P18, suggesting that they regulate a specific form of synaptic plasticity in L2/3 pyramidal neurons, with a sensitive/critical period ending around P18. Consistently, oxytocin receptor (Oxtr) expression in glutamatergic neurons of the upper layers of the cerebral cortex peaks around P14. By P28, however, Oxtr expression becomes more prominent in GABAergic neurons, especially somatostatin (SST) neurons. At P28, oxytocin perfusion increases inhibitory synaptic transmission and reduces excitatory synaptic transmission, effects that result in a net reduction of neuronal excitation, in contrast to increased excitation at P14. Using oxytocin knockout mice and Oxtr conditional knockout mice, we show that loss-of-function of oxytocin affects baseline excitatory synaptic transmission, while Oxtr is required for oxytocin-induced changes in excitatory synaptic transmission, at both P14 and P28. Together, these results demonstrate that oxytocin has complex and dynamic functions in regulating synaptic transmission in cortical L2/3 pyramidal neurons. These findings add to existing knowledge of the function of oxytocin in regulating neural circuit development and plasticity.

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Section: Discussionmentioning

confidence: 99%

Oxytocin Regulates Synaptic Transmission in the Sensory Cortices in a Developmentally Dynamic Manner

Zhang

Miao

et al. 2021

Front. Cell. Neurosci.

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“…The role of OXT thus far has been limited to its immediate effect after administration and hence is not a single treatment option for ASD. Nonetheless, as illustrated by a recent meta-analysis, there does seem to be overall beneficial effects of OXT on social symptoms of ASD, although this review included both children and adults [90]. There is also some promising research looking at the role of OXT in combination with other treatment modalities including behavior therapy and probiotics, with clinical trials in this area ongoing [91,92].…”

Section: Oxytocinmentioning

confidence: 99%

An Update on Psychopharmacological Treatment of Autism Spectrum Disorder

et al. 2022

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While behavioral interventions remain the mainstay of treatment of autism spectrum disorder (ASD), several potential targeted treatments addressing the underlying neurophysiology of ASD have emerged in the last few years. These are promising for the potential to, in future, become part of the mainstay treatment in addressing the core symptoms of ASD. Although it is likely that the development of future targeted treatments will be influenced by the underlying heterogeneity in etiology, associated genetic mechanisms influencing ASD are likely to be the first targets of treatments and even gene therapy in the future for ASD. In this article, we provide a review of current psychopharmacological treatment in ASD including those used to address common comorbidities of the condition and upcoming new targeted approaches in autism management. Medications including metformin, arbaclofen, cannabidiol, oxytocin, bumetanide, lovastatin, trofinetide, and dietary supplements including sulforophane and N-acetylcysteine are discussed. Commonly used medications to address the comorbidities associated with ASD including atypical antipsychotics, serotoninergic agents, alpha-2 agonists, and stimulant medications are also reviewed. Targeted treatments in Fragile X syndrome (FXS), the most common genetic disorder leading to ASD, provide a model for new treatments that may be helpful for other forms of ASD.

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“…The causality between OXT and ASD has been extensively discussed in the last two decades [172][173][174][175][176][177] and has been tested in several animal models for ASD and NDDs. 178 This has led to increased interest in using the OXT peptide as a therapeutic to treat social behavior deficits in these disorders, [179][180][181] with little attention being given to whether the OXT system is impacted by NDDs or ASD-associated mutations. To date, there has been no genetic evidence that directly implicates the OXT or OXT receptor coding genes in NDDs.…”

Section: Con Clus Ionsmentioning

confidence: 99%

The interplay between glutamatergic circuits and oxytocin neurons in the hypothalamus and its relevance to neurodevelopmental disorders

Leithead

Tasker

Harony‐Nicolas

2021

J Neuroendocrinology

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Oxytocin (OXT) neurons of the hypothalamus are at the center of several physiological functions, including behavior. 1,2 These neurons are classified as magnocellular and parvocellular neurons, mainly based on their shape, size and intranuclear localization. They also differ in their projection targets and implications in distinct brain circuits. [3][4][5][6][7][8][9][10][11] Magnocellular OXT neurons are located in three hypothalamic nuclei: the paraventricular nucleus (PVN), the supraoptic nucleus (SON) and the accessory nuclei, whereas parvocellular OXT neurons are mainly located in the PVN. 7 Early immunohistochemical studies in mammalian species have demonstrated that axonal projections of OXT neurons are spread throughout the central nervous system and that magnocellular and parvocellular neurons each have a specific pattern of distribution. 6 Magnocellular OXT neurons project to the posterior pituitary where OXT is released into

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Intranasal oxytocin in the treatment of autism spectrum disorders: A multilevel meta-analysis

Cited by 73 publications

References 69 publications

Oxytocin Regulates Synaptic Transmission in the Sensory Cortices in a Developmentally Dynamic Manner

Oxytocin Regulates Synaptic Transmission in the Sensory Cortices in a Developmentally Dynamic Manner

An Update on Psychopharmacological Treatment of Autism Spectrum Disorder

The interplay between glutamatergic circuits and oxytocin neurons in the hypothalamus and its relevance to neurodevelopmental disorders

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