A simulation model for compensatory plasticity in the prefrontal cortex inducing a cortico-cortical dysconnection in early brain development

Abstract The glutamatergic–mediated excitatory system in the brain is vital for the regulation of sleep–wake and general anesthesia. Specifically, the paraventricular hypothalamic nucleus (PVH), which contains mainly glutamatergic neurons, has been shown to play a critical role in sleep–wake. Here, we sought to explore whether the PVH glutamatergic neurons have an important effect on the process of general anesthesia. We used c‐fos staining and in vivo calcium signal recording to observe the activity changes of the PVH glutamatergic neurons during isoflurane anesthesia and found that both c‐fos expression in the PVH and the calcium activity of PVH glutamatergic neurons decreased in isoflurane anesthesia and significantly increased during the recovery process. Chemogenetic activation of PVH glutamatergic neurons prolonged induction time and shortened emergence time from anesthesia by decreasing the depth of anesthesia. Using chemogenetic inhibition of PVH glutamatergic neurons under isoflurane anesthesia, we found that inhibition of PVH glutamatergic neurons facilitated the induction process and delayed the emergence accompanied by deepening the depth of anesthesia. Together, these results identify a crucial role for PVH glutamatergic neurons in modulating isoflurane anesthesia.

Premovement neuronal activity

10.1096/fj.202200974rr

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Citations (7)

EAT-4, a Homolog of a Mammalian Sodium-Dependent Inorganic Phosphate Cotransporter, Is Necessary for Glutamatergic Neurotransmission inCaenorhabditis elegans

Journal of Neuroscience (1999)

Raymond Lee Elizabeth R. Sawin Martin Chalfie H. Robert Horvitz Leon Avery

The Caenorhabditis elegans gene eat-4 affects multiple glutamatergic neurotransmission pathways. We find that eat-4 encodes a protein similar in sequence to a mammalian brain-specific sodium-dependent inorganic phosphate cotransporter I (BNPI). Like BNPI in the rat CNS, eat-4 is expressed predominantly in a specific subset of neurons, including several proposed to be glutamatergic. Loss-of-function mutations in eat-4 cause defective glutamatergic chemical transmission but appear to have little effect on other functions of neurons. Our data suggest that phosphate ions imported into glutamatergic neurons through transporters such as EAT-4 and BNPI are required specifically for glutamatergic neurotransmission.

10.1523/jneurosci.19-01-00159.1999

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Citations (353)

Functional Implications of Glutamatergic Projections to the Ventral Tegmental Area

Reviews in the Neurosciences (2008)

Stefanie Geisler Roy A. Wise

Glutamatergic afferents of the ventral tegmental area (VTA) play an important role in the functioning of the VTA and are involved in the pathophysiology of drug addiction. It has recently been demonstrated that the VTA is densely innervated by glutamatergic axons and that glutamatergic neurons projecting to the VTA are situated in almost all structures that project there. While the projection from the prefrontal cortex is essentially entirely glutamatergic, subcortical glutamatergic neurons innervating the VTA intermingle with non-glutamatergic, most likely GABAergic and/or peptidergic VTA-projecting neurons. The first part of this review focuses on the origins and putative functional implications of various glutamatergic projections to the VTA. In the second part we consider how different neuropeptides via different mechanisms modulate glutamatergic actions in the VTA. We conclude by developing a model of how the glutamatergic afferents might together contribute to the functions of the VTA.

10.1515/revneuro.2008.19.4-5.227

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Citations (110)

Medial septal dysfunction by Aβ-induced KCNQ channel-block in glutamatergic neurons

Neurobiology of Aging (2011)

Richardson N. Leão Luis V. Colom Lotta Borgius Ole Kiehn André Fisahn

Premovement neuronal activity

10.1016/j.neurobiolaging.2011.07.013

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Citations (32)

Glutamatergic lateral hypothalamus promotes defensive behaviors

Neuropharmacology (2020)

Li Chen Ping Cai Renfei Wang Yiping Lu Huiyun Chen

Anterograde tracing

Lateral hypothalamus

Periaqueductal gray

Basolateral amygdala

10.1016/j.neuropharm.2020.108239

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Citations (17)

Glutamatergic abnormalities in schizophrenia: A review of proton MRS findings

Schizophrenia Research (2014)

Eline M. P. Poels Lawrence S. Kegeles Joshua T. Kantrowitz Daniel C. Javitt Jeffrey A. Lieberman

10.1016/j.schres.2013.12.013

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Citations (151)

Transcranial photobiomodulation changes neuronal morphology in the cerebral cortex of rats

Neuroscience Letters (2022)

Fabrízio dos Santos Cardoso Fernando Tadeu Serra Norberto Cysne Coimbra F. Gonzalez‐Lima Sérgio Gomes da Silva

10.1016/j.neulet.2022.136681

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Citations (4)

[Development and the developmental disorders of human brain. I. Early development of the cerebrum].

PubMed (2001)

Hans J. ten Donkelaar Pieter Wesseling Martin Lammens W. O. Renier R.A. Mullaart

The recent discovery of many genes that regulate brain development is revolutionizing our knowledge of neuroembryology and, moreover, our understanding of how gene defects cause human birth defects. The first 8 weeks of the development of the cerebrum can be subdivided into 23 stages, with early development of mostly the spinal cord and the brain stem. Regionalization of the brain has been related to genes that play a part in it. A characteristic developmental disorder for this early phase in the development of the forebrain is holoprosencephaly, a brain patterning disorder. Numerous genes play a part in its occurrence; abnormal function of signal factors as well as of transcription factors may lead to holoprosencephaly.

Forebrain

Brain Development

Human brain

Corticogenesis

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Citations (1)