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24 publication(s) depuis Septembre 2004:

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02/2006 | Neuron Glia Biol   IF 5.5
Neuron-glia interactions in the hypothalamus.
Panatier A, Oliet SH

The supraoptic (SON) and paraventricular (PVN) magnocellular nuclei of the hypothalamus undergo reversible anatomical remodeling under conditions of intense secretion of neurohypophysial hormones, such as lactation and chronic dehydration. This morphological plasticity is characterized by a pronounced reduction in astrocytic coverage of neurons, which results in an increased number and extent of directly juxtaposed somatic and dendritic surfaces. As a consequence, astrocyte-mediated clearance of glutamate from the extracellular space is altered, which causes an increased concentration and range of action of the excitatory amino acid in the extracellular space. This leads to a reduction of synaptic efficacy at excitatory and inhibitory inputs through the activation of presynaptic metabotropic glutamate receptors. By contrast, the action of glio transmitters released from astrocytes and acting on adjacent magnocellular neurons is limited during such anatomical remodeling. This includes glia derived ATP mediating potentiation of glutamatergic transmission, a process compromised by the neuronal-glial reorganization.Together, these studies on hypothalamic magnocellular nuclei provide new insights on the contribution of glial cells on neuronal activity.

2006 | Novartis Found Symp   IF 1.4
Functional neuronal-glial anatomical remodelling in the hypothalamus.
Oliet SH, Panatier A, Piet R

The supraoptic nucleus (SON) of the hypothalamus undergoes a striking anatomical remodelling under conditions of intense stimulations like chronic dehydration, parturition and lactation. This morphological plasticity modifies the astrocytic coverage of magnocellular neurons and their synaptic afferent inputs. These changes occur within a few hours and are completely reversible upon the cessation of the stimulation. By comparing synaptic transmission and diffusion properties before and during this neuroglial remodelling, we have been able to show that the astrocytic environment of neurons contributes to the regulation of synaptic and extrasynaptic transmission. It appears that the presence of fine astrocytic processes enveloping synapses and neuronal elements ensures two important functions. First, they control the level of activation of presynaptic metabotropic glutamate autoreceptors located on glutamatergic terminals, thereby regulating synaptic strength at excitatory synapses. Second, they constitute a physical barrier to diffusion, limiting spatially and temporally spill-over of neurotransmitters and, as a consequence, extrasynaptic transmission, a process essential for intercellular communication. Using the neuroglial anatomical remodelling of the SON as an experimental model has brought new insights into the role of glial cells in the regulation of synaptic transmission and signal processing in the brain.

05/2005 | Eur J Neurosci   IF 2.8
Voltage-gated Ca2+ channel subtypes mediating GABAergic transmission in the rat supraoptic nucleus.
Bhaukaurally K, Panatier A, Poulain DA, Oliet SH

The supraoptic nucleus receives an abundant gamma-aminobutyric acid (GABA)ergic input which is inhibited by activation of various presynaptic metabotropic receptors. We here analysed the subtypes of voltage-gated Ca2+ channels intervening in the control of transmitter release at these synapses. To address this issue, we tested various specific inhibitors of Ca2+ channels on evoked inhibitory postsynaptic currents (IPSCs). Blocking N- and P-type voltage-gated Ca2+ channels with 1 micromomega-conotoxin-GVIA and 20 nmomega-agatoxin-IVA, respectively, dramatically reduced IPSC amplitude. Q- and L-type Ca2+ channels also contributed to GABAergic transmission, although to a lesser extent, as revealed by applications of 200 nmomega-agatoxin-IVA and of the dihydropyridines nifedipine (10 microm) and nimodipine (10 microm). Evoked IPSCs were insensitive to SNX-482 (300 nm), a blocker of some R-type Ca2+ channels. Analysis of selective blockade by the various antagonists suggested that multiple types of Ca2+ channels synergistically interact to trigger exocytosis at some individual GABA release sites. We next investigated whether inhibition of GABA release in response to the activation of metabotropic glutamate, GABA and adenosine receptors involved the modulation of these presynaptic Ca2+ channels. This was not the case, as the inhibitory actions of selective agonists of these receptors were unaffected by the presence of the different Ca2+ channel antagonists. This finding suggests that these metabotropic receptors modulate GABAergic transmission through a different mechanism, downstream of Ca2+ entry in the terminals, or upstream through the activation of K+ channels.

We analyzed the subtypes of group III metabotropic glutamate receptors (mGluRs) modulating inhibitory and excitatory transmission in the rat supraoptic nucleus. Bath application of the agonist l-AP4 at 200 microM, a concentration that activates all group III mGluR subtypes, inhibited the frequency but not the amplitude of miniature inhibitory and excitatory postsynaptic currents, indicating a presynaptic site of action. l-AP4 at low concentrations (10 microM), as well as ACPT-1 (50 microM), a specific mGluR III agonist, inhibited transmission at GABAergic and glutamatergic synapses to the same extent as 200 microM l-AP4. Because the potency of l-AP4 and ACPT-1 is much higher on mGluR4 and mGluR8 than on mGluR7, these results are consistent with the presence of high-affinity group III mGluRs regulating transmitter release in this nucleus. In agreement with these findings, DCPG (30 microM), a selective mGluR8 agonist, induced a significant depression of inhibitory and excitatory synaptic currents. Group III mGluRs such as mGluR8, because of their high affinity for glutamate, are particularly well suited to detect small changes in the concentration of this excitatory amino acid in the extracellular space. Their presence, therefore, may favor the negative feedback control exerted by glutamate on its own release as well as the intersynaptic crosstalk mediated by glutamate spillover on adjacent synapses.