The Activation of Excitatory Glutamate Receptors Evokes a Long-Lasting Increase in the Release of GABA from Cerebellar Stellate Cells

Liu, Siqiong June; Lachamp, Philippe

doi:10.1523/jneurosci.2929-06.2006

Cited by 55 publications

(73 citation statements)

References 39 publications

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“…In rodent cerebellar cortex, glutamate released from parallel fibers induces a long-lasting increase of GABA release from stellate cells, presumably by activating preNMDARs on their terminals (Liu and Lachamp 2006). This heterosynaptic form of LTP also requires cAMP/PKA signaling (Lachamp et al 2009).…”

Section: Presynaptic Nmdar-dependent Plasticitymentioning

confidence: 99%

Presynaptic LTP and LTD of Excitatory and Inhibitory Synapses

Castillo

2011

Cold Spring Harbor Perspectives in Biology

145

134

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Ubiquitous forms of long-term potentiation (LTP) and depression (LTD) are caused by enduring increases or decreases in neurotransmitter release. Such forms or presynaptic plasticity are equally observed at excitatory and inhibitory synapses and the list of locations expressing presynaptic LTP and LTD continues to grow. In addition to the mechanistically distinct forms of postsynaptic plasticity, presynaptic plasticity offers a powerful means to modify neural circuits. A wide range of induction mechanisms has been identified, some of which occur entirely in the presynaptic terminal, whereas others require retrograde signaling from the postsynaptic to presynaptic terminals. In spite of this diversity of induction mechanisms, some common induction rules can be identified across synapses. Although the precise molecular mechanism underlying long-term changes in transmitter release in most cases remains unclear, increasing evidence indicates that presynaptic LTP and LTD can occur in vivo and likely mediate some forms of learning.A t several excitatory and inhibitory synapses, neuronal activity can trigger enduring increases or decreases in neurotransmitter release, thereby producing long-term potentiation (LTP) or long-term depression (LTD) of synaptic strength, respectively. In the last decade, many studies have revealed that these forms of plasticity are ubiquitously expressed in the mammalian brain, and accumulating evidence indicates that they may underlie behavioral adaptations occurring in vivo. These studies have also uncovered a wide range of induction mechanisms, which converge on the presynaptic terminal where an enduring modification in the neurotransmitter release process takes place. Interestingly, presynaptic forms of LTP/ LTD can coexist with classical forms of postsynaptic plasticity. Such diversity expands the dynamic range and repertoire by which neurons modify their synaptic connections. This review discusses mechanistic aspects of presynaptic LTP and LTD at both excitatory and inhibitory synapses in the mammalian brain, with an emphasis on recent findings. INDUCTION MECHANISMSAs illustrated in Figure 1, presynaptic LTP/LTD at both excitatory and inhibitory synapses can be induced in a homosynaptic or heterosynaptic manner, with induction occurring either entirely at the presynaptic terminal or requiring a retrograde messenger arising from the postsynaptic neuron. Each of these four induction

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Section: Presynaptic Nmdar-dependent Plasticitymentioning

confidence: 99%

Presynaptic LTP and LTD of Excitatory and Inhibitory Synapses

Castillo

2011

Cold Spring Harbor Perspectives in Biology

145

134

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“…However, GluNs also express in the presynaptic terminal of GABAergic interneuron in the retinotectal system and Cerebellar cortex[77, 78]. Presynaptic NRG1 type I or type II precursor interacts with postsynaptic ErbB4 in a trans-synaptic manner [79].…”

Section: Discussionmentioning

confidence: 99%

Glutamate-dependent ectodomain shedding of neuregulin-1 type II precursors in rat forebrain neurons

et al. 2017

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The neurotrophic factor neuregulin 1 (NRG1) regulates neuronal development, glial differentiation, and excitatory synapse maturation. NRG1 is synthesized as a membrane-anchored precursor and is then liberated by proteolytic processing or exocytosis. Mature NRG1 then binds to its receptors expressed by neighboring neurons or glial cells. However, the molecular mechanisms that govern this process in the nervous system are not defined in detail. Here we prepared neuron-enriched and glia-enriched cultures from embryonic rat neocortex to investigate the role of neurotransmitters that regulate the liberation/release of NRG1 from the membrane of neurons or glial cells. Using a two-site enzyme immunoassay to detect soluble NRG1, we show that, of various neurotransmitters, glutamate was the most potent inducer of NRG1 release in neuron-enriched cultures. NRG1 release in glia-enriched cultures was relatively limited. Furthermore, among glutamate receptor agonists, N-Methyl-D-Aspartate (NMDA) and kainate (KA), but not AMPA or tACPD, mimicked the effects of glutamate. Similar findings were acquired from analysis of the hippocampus of rats with KA-induced seizures. To evaluate the contribution of members of a disintegrin and metalloproteinase (ADAM) families to NRG1 release, we transfected primary cultures of neurons with cDNA vectors encoding NRG1 types I, II, or III precursors, each tagged with the alkaline phosphatase reporter. Analysis of alkaline phosphatase activity revealed that the NRG1 type II precursor was subjected to tumor necrosis factor-α-converting enzyme (TACE) / a Disintegrin And Metalloproteinase 17 (ADAM17) -dependent ectodomain shedding in a protein kinase C-dependent manner. These results suggest that glutamatergic neurotransmission positively regulates the ectodomain shedding of NRG1 type II precursors and liberates the active NRG1 domain in an activity-dependent manner.

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“…Enhanced inhibitory transmission suppresses the rate of stellate cell spiking and alters the firing pattern such that it becomes highly irregular ( Fig. 33.3c) (Liu and Lachamp 2006;Lachamp et al 2009). Application of noradrenaline also induces a long-lasting increase in GABA (Lachamp et al 2009) release through activation of b 2 -adrenoceptors (Llano and Gerschenfeld 1993a;Mitoma and Konishi 1999;.…”

Section: Activity-dependent Changes In Gaba Releasementioning

confidence: 99%

Stellate Cells: Synaptic Processing and Plasticity

Liu¹

2013

Handbook of the Cerebellum and Cerebellar Disorders

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Stellate and basket cells in the molecular layer of the cerebellum are inhibitory interneurons which control the activity of Purkinje cells. Recent studies using genetic approaches have revealed the important function of these interneurons during behavioral tasks, motor coordination, and motor learning. Synaptic transmission onto cerebellar interneurons and interneuron inhibition onto Purkinje cells can be dynamically regulated by synaptic activity. The capacity of molecular layer interneurons to undergo activity-dependent changes in synaptic transmission and membrane excitability provides a cellular mechanism that underlies cerebellar learning and memory.

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The Activation of Excitatory Glutamate Receptors Evokes a Long-Lasting Increase in the Release of GABA from Cerebellar Stellate Cells

Cited by 55 publications

References 39 publications

Presynaptic LTP and LTD of Excitatory and Inhibitory Synapses

Presynaptic LTP and LTD of Excitatory and Inhibitory Synapses

Glutamate-dependent ectodomain shedding of neuregulin-1 type II precursors in rat forebrain neurons

Stellate Cells: Synaptic Processing and Plasticity

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