Transport activities and expression patterns of glycine transporters 1 and 2 in the developing murine brain stem and spinal cord

Lall, Deepti; Armbruster, Anja; Ruffert, K; Betz, Heinrich; Eulenburg, Volker

doi:10.1016/j.bbrc.2012.06.007

Cited by 7 publications

(6 citation statements)

References 28 publications

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“…On the other hand, GlyT2 displays weak expression in the brain cortex and hippocampus, but is more abundant in the cerebellum (Jursky et al, 1994; Jursky and Nelson, 1996). Remarkably, the progressive development observed in the spinal cord where GlyT2 increases in expression to regulate the level of glycine in combination with GlyT1 (Lall et al, 2012) does not seem to occur in the developing brain. In contrast, later during postnatal development glycine level is exclusively controlled by GlyT1 independently of GlyT2 in the cortex (Gomeza et al, 2003; Kunz et al, 2012).…”

Section: Glycine Receptors Endogenous Agonists During Developmentmentioning

confidence: 99%

Glycine receptors and brain development

Ávila

Nguyen

Rigo

2013

Front. Cell. Neurosci.

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Glycine receptors (GlyRs) are ligand-gated chloride ion channels that mediate fast inhibitory neurotransmission in the spinal cord and the brainstem. There, they are mainly involved in motor control and pain perception in the adult. However, these receptors are also expressed in upper regions of the central nervous system, where they participate in different processes including synaptic neurotransmission. Moreover, GlyRs are present since early stages of brain development and might influence this process. Here, we discuss the current state of the art regarding GlyRs during embryonic and postnatal brain development in light of recent findings about the cellular and molecular mechanisms that control brain development.

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Section: Glycine Receptors Endogenous Agonists During Developmentmentioning

confidence: 99%

Glycine receptors and brain development

Ávila

Nguyen

Rigo

2013

Front. Cell. Neurosci.

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“…Manipulation of the excitatory-inhibitory input balance alters the onset and closure of the critical period in the developing visual cortex 21 . Inhibitory neural activity increases with development in the spinal cord 22 23 24 . Glycinergic inhibition predominates over GABAergic inhibition in the ventral spinal cord 27 , where the density of glycine receptors increases during development 22 23 .…”

Section: Resultsmentioning

confidence: 99%

“…Inhibitory neural activity increases with development in the spinal cord 22 23 24 . Glycinergic inhibition predominates over GABAergic inhibition in the ventral spinal cord 27 , where the density of glycine receptors increases during development 22 23 . To test whether termination of the critical period can be affected by development of inhibitory neural activity in the spinal cord, we partially blocked glycinergic receptors by adding a low dose (0.2 μM) of strychnine to co-cultures for a period that extended beyond the end of the critical period (9–15 DIV) 28 29 .…”

Section: Resultsmentioning

confidence: 99%

“…Manipulation of the balance of excitatory-inhibitory neural activity has also been shown to alter the onset and closure of the critical period in the developing visual cortex 21 . Given that the numbers of glycine receptors in the ventral spinal cord increase progressively toward adulthood 22 23 24 , it is possible that the development of inhibitory activity is also involved in closing critical periods. Here we tested these two possibilities using our model system of developmental CS synapse elimination.…”

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confidence: 99%

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The decline in synaptic GluN2B and rise in inhibitory neurotransmission determine the end of a critical period

Isoo

Ohno

Isowaki

et al. 2016

Sci Rep

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Neuronal plasticity is especially active in the young, during short windows of time termed critical periods, and loss of a critical period leads to functional limitations in the adults. The mechanism that governs the length of critical periods remains unknown. Here we show that levels of the NMDA receptor GluN2B subunit, which functions as a Ca2+ channel, declines in spinal cord synapses toward the end of the critical period for activity-dependent corticospinal synapse elimination. This period could be prolonged by blocking the decline of GluN2B, and after its termination the critical period could be reopened through upregulation of GluN2B. It is known that inhibitory neural activity increases with development in the CNS including the spinal cord. Suppression of the increasing inhibitory activity using low-dose strychnine also prolonged this critical period. During the strychnine-widened time window, Ca2+ influx through GluN2B channels returned to a level comparable to that seen during the critical period, though the level of GluN2B was slightly reduced. These findings indicate that loss of GluN2B subunits and the associated reduction in Ca2+ influx determines the end of the critical period in our in vitro CS system.

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“…However, several reports provide evidence that this is not the case. Lall et al (2012) have reported that the expression levels of both GlyT1 and GlyA differ by 20% in the brain stems of 10-day-old mouse Fig. 6.…”

Section: Discussionmentioning

confidence: 98%