Ontogeny of neurotransmitter amino acids in human fetal brains

Das, Sutapa; Ray, Pradip Kumar

doi:10.1080/15216549700202581

Cited by 3 publications

(5 citation statements)

References 10 publications

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“…However, in rat and human fetal brains taurine is the most abundant neurotransmitter (Das and Ray, 1997; Benitez-Diaz et al, 2003). It has been suggested that taurine can be released from immature neurons after electrical stimulation or by hypoosmolar solution (Flint et al, 1998; Kilb et al, 2008) by non-synaptic processes, e.g., by volume-sensitive organic osmolyte channels or reversal of taurine transport (Ando et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Taurine activates GABAergic networks in the neocortex of immature mice

Sava¹,

Chen²,

Sun³

et al. 2014

Front. Cell. Neurosci.

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Although it has been suggested that taurine is the main endogenous neurotransmitter acting on glycine receptors, the implications of glycine receptor-mediated taurine actions on immature neocortical networks have not been addressed yet. To investigate the influence of taurine on the excitability of neuronal networks in the immature neocortex, we performed whole-cell patch-clamp recordings from visually identified pyramidal neurons and interneurons in coronal slices from C57Bl/6 and GAD67-green fluorescent protein (GFP) transgenic mice (postnatal days 2–4). In 46% of the pyramidal neurons bath-application of taurine at concentrations ≥ 300 μM significantly enhanced the frequency of postsynaptic currents (PSCs) by 744.3 ± 93.8% (n = 120 cells). This taurine-induced increase of PSC frequency was abolished by 0.2 μM tetrodotoxin (TTX), 1 μM strychnine or 3 μM gabazine, but was unaffected by the glutamatergic antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and (±) R(-)-3-(2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid (CPP), suggesting that taurine specifically activates GABAergic network activity projecting to pyramidal neurons. Cell-attached recordings revealed that taurine enhanced the frequency of action potentials (APs) in pyramidal neurons, indicating an excitatory action of the GABAergic PSCs. In order to identify the presynaptic targets of taurine we demonstrate that bath application of taurine induced in GAD67-GFP labeled interneurons an inward current that is mainly mediated by glycine receptors and can generate APs in these cells. We conclude from these results that taurine can enhance network excitability in the immature neocortex by selectively activating GABAergic interneurons via interactions with glycine receptors.

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Section: Discussionmentioning

confidence: 99%

Taurine activates GABAergic networks in the neocortex of immature mice

Sava¹,

Chen²,

Sun³

et al. 2014

Front. Cell. Neurosci.

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“…In the hippocampus both GAD-65 and GAD-67 protein could be detected at E18, with both isoforms expressed mainly at somatic locations during prenatal development (Dupuy and Houser, 1996). Expression of GAD has also been found in fetal human brain before gestational week 15 (Das and Ray, 1997), when GAD-67 is the prominent isoform (Chan et al, 1997). Thus in particular a somatic generation of GABA can appear during early stages of corticogenesis.…”

Section: Development Of Extrasynaptic and Synaptic Gabaergic Transmismentioning

confidence: 99%

“…One intriguing candidate for such a substance is taurine, which is an agonist of GABA A , GABA B , and glycine receptors (Albrecht and Schousboe, 2005). In rat and human fetal brain taurine is the most abundant neurotransmitter (Das and Ray, 1997; Benitez-Diaz et al, 2003). In early postnatal cortex a glycinergic agonist, presumably taurine, is released upon electrical stimulation in a Ca 2+ and action potential independent manner (Flint et al, 1998) and in the presence of a hypoosmolar solution (Flint et al, 1998; Kilb et al, 2008), indicating that taurine can be release in the immature central nervous system (CNS) mainly by non-synaptic processes.…”

Section: Origin and Nature Of Endogenous Gabaergic Agonistsmentioning

confidence: 99%

Role of tonic GABAergic currents during pre- and early postnatal rodent development

Kilb¹,

Kirischuk²,

Luhmann³

2013

Front. Neural Circuits

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In the last three decades it became evident that the GABAergic system plays an essential role for the development of the central nervous system, by influencing the proliferation of neuronal precursors, neuronal migration and differentiation, as well as by controlling early activity patterns and thus formation of neuronal networks. GABA controls neuronal development via depolarizing membrane responses upon activation of ionotropic GABA receptors. However, many of these effects occur before the onset of synaptic GABAergic activity and thus require the presence of extrasynaptic tonic currents in neuronal precursors and immature neurons. This review summarizes our current knowledge about the role of tonic GABAergic currents during early brain development. In this review we compare the temporal sequence of the expression and functional relevance of different GABA receptor subunits, GABA synthesizing enzymes and GABA transporters. We also refer to other possible endogenous agonists of GABAA receptors. In addition, we describe functional consequences mediated by the GABAergic system during early developmental periods and discuss current models about the origin of extrasynaptic GABA and/or other endogenous GABAergic agonists during early developmental states. Finally, we present evidence that tonic GABAergic activity is also critically involved in the generation of physiological as well as pathophysiological activity patterns before and after the establishment of functional GABAergic synaptic connections.

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“…Although there is a large amount of literature on Gly receptors and transporters in the embryonic brain, its concentration in the embryonic brain remains underexplored. The highly elevated Gly concentration during the period of this study provides in vivo evidence that Gly is in high demand for numerous cellular and metabolic processes in embryonic development . In addition, NAA, a putative neuronal marker, increased substantially at E17.5–18 (unpaired t ‐test, p < 0.05).…”

Section: Discussionmentioning

confidence: 64%

“…The highly elevated Gly concentration during the period of this study provides in vivo evidence that Gly is in high demand for numerous cellular and metabolic processes in embryonic development. 31,40,41 In addition, NAA, a putative neuronal marker, 42 increased substantially at E17.5-18 (unpaired t-test, p < 0.05). Tau, another abundant metabolite in neurons, exhibited a high content FIGURE 2 Typical 1 H MR spectra of one of each embryonic brain at E12.5-13 (A) and E17.…”

Section: Neurochemical Evolution Of Embryonic Brain From E125-13 Tmentioning

confidence: 96%

Feasibility of neurochemically profiling mouse embryonic brain and its development in utero using ¹H MRS at 14.1 T

et al. 2019

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We aimed to evaluate the feasibility of neurochemical profiling of embryonic mouse brain developments in utero and to seek potential in vivo evidence of an energy shift in a mitochondrial pyruvate carrier 1 (MPC1) deficient mouse model. C57BL/6 embryonic mouse brains were studied in utero by anatomical MRI and short echo localized proton (1H) MRS at 14.1 T. Two embryonic stages were studied, the energy shift (e.g., embryonic day 12.5–13, E12.5–13) and close to the birth (E17.5–18). In addition, embryonic brains devoid of MPC1 were studied at E12.5–13. The MRI provided sufficient anatomical contrasts for visualization of embryonic brain. Localized 1H MRS offered abundant metabolites through the embryonic development from E12.5 and close to the birth, e.g., E17.5 and beyond. The abundant neurochemical information at E12.5 provided metabolic status and processes relating to cellular development at this stage, i.e., the energy shift from glycolysis to oxidative phosphorylation, evidenced by accumulation of lactate in E12.5–13 embryonic brain devoid of MPC1. The further evolution of the neurochemical profile of embryonic brains at E17.5–18 is consistent with cellular and metabolic processes towards the birth. Localized 1H MRS study of embryonic brain development in utero is feasible, and longitudinal neurochemical profiling of embryonic brains offers valuable insight into early brain development.

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Ontogeny of neurotransmitter amino acids in human fetal brains

Cited by 3 publications

References 10 publications

Taurine activates GABAergic networks in the neocortex of immature mice

Taurine activates GABAergic networks in the neocortex of immature mice

Role of tonic GABAergic currents during pre- and early postnatal rodent development

Feasibility of neurochemically profiling mouse embryonic brain and its development in utero using ¹H MRS at 14.1 T

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Ontogeny of neurotransmitter amino acids in human fetal brains

Cited by 3 publications

References 10 publications

Taurine activates GABAergic networks in the neocortex of immature mice

Taurine activates GABAergic networks in the neocortex of immature mice

Role of tonic GABAergic currents during pre- and early postnatal rodent development

Feasibility of neurochemically profiling mouse embryonic brain and its development in utero using 1H MRS at 14.1 T

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Product

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Feasibility of neurochemically profiling mouse embryonic brain and its development in utero using ¹H MRS at 14.1 T