Activation of N-methyl-D-aspartate receptors regulates basal electrical activity of oxytocin and vasopressin neurons in lactating rats

Moos, Françoise; Rossi, Karoline Alves; Richard, Ph.

doi:10.1016/s0306-4522(96)00536-2

Cited by 40 publications

(46 citation statements)

References 31 publications

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“…In our experiments, values for parameters like IF, BD, and SD in organotypic cultures (IF, 9.1 Hz; BD, 22 s; SD, 18 s) were similar to those in vivo (IF, 9.2 Hz; BD, 29 s; SD, 17 s), and in agreement with those reported in vivo (Poulain and Wakerley, 1982;Nissen et al, 1995;Moos et al, 1997;Gouzènes et al, 1998). In contrast, VP neurons in acute slices displayed longer bursts (75 s) and silent periods (49 s).…”

Section: Discussionsupporting

confidence: 90%

“…Our data therefore argue against an essential role for DAPs in the generation of phasic pattern in VP neurons. An alternative possibility, already proposed in previous reports (Andrew and Dudek, 1984;Nissen et al, 1994Nissen et al, , 1995Moos et al, 1997;, is that such phasic activity is controlled by synaptic activity from glutamatergic inputs.…”

Section: Role Of Daps In Phasic Activitymentioning

confidence: 92%

“…In vivo experiments unambiguously showed that glutamate receptor blockers reversibly interrupted phasic activity in VP neurons (Nissen et al, 1994(Nissen et al, , 1995Moos et al, 1997), whereas glutamatergic receptor agonists triggered (Nissen et al, 1995) or accelerated phasic activity. Glutamate was shown to be the sole source of EPSPs in coronal slices in vitro (van den Pol et al, 1990;Wuarin and Dudek, 1993;Yang et al, 1994;Richard and Bourque, 1995;Jourdain et al, 1998).…”

Section: Role Of Glutamatergic Inputs In Phasic Activitymentioning

confidence: 93%

“…However, in this preparation, synaptic activity is mostly impaired and usually reduced to miniature synaptic currents/ potentials (Wuarin and Dudek, 1993;Brussaard et al, 1996Brussaard et al, , 1997Kabashima et al, 1997;Kombian et al, 2000), probably because axon terminals are severed from their glutamatergic cell bodies. In vivo, application of glutamate receptor antagonists like ketamine (Nissen et al, 1994), D(Ϫ)-2-amino-5-phosphonopentanoic acid (D-AP-5) (Nissen et al, 1995;Moos et al, 1997), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (Nissen et al, 1995), or kynurenic acid blocks phasic activity in VP neurons, suggesting that glutamatergic inputs play a key role in governing phasic activity. It is still not clear why this is not the case in vitro.…”

Section: Introductionmentioning

confidence: 99%

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Glutamatergic Inputs Contribute to Phasic Activity in Vasopressin Neurons

Israël

Poulain²,

Oliet³

2010

J. Neurosci.

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Many neurons in the CNS display rhythmic patterns of activity to optimize excitation-secretion coupling. However, the mechanisms of rhythmogenesis are only partially understood. Magnocellular vasopressin (VP) neurons in the hypothalamus display a phasic activity that consists of alternative bursts of action potentials and silent periods. Previous observations from acute slices of adult hypothalamus suggested that VP cell rhythmicity depends on intrinsic membrane properties. However, such activity in vivo is nonregenerative. Here, we studied the mechanisms of VP neuron rhythmicity in organotypic slice cultures that, unlike acute slices, preserve functional synaptic connections. Comparative analysis of phasic firing of VP neurons in vivo, in acute slices, and in the cultures revealed that, in the latter, the activity was closely related to that observed in vivo. It was synaptically driven, essentially from glutamatergic inputs, and did not rely on intrinsic membrane properties. The glutamatergic synaptic activity was sensitive to osmotic challenges and -opioid receptor activation, physiological stimuli known to affect phasic activity. Together, our data thus strongly suggest that phasic activity in magnocellular VP neurons is controlled by glutamatergic synaptic inputs rather than by intrinsic properties.

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Section: Discussionsupporting

confidence: 90%

Section: Role Of Daps In Phasic Activitymentioning

confidence: 92%

Section: Role Of Glutamatergic Inputs In Phasic Activitymentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Glutamatergic Inputs Contribute to Phasic Activity in Vasopressin Neurons

Israël

Poulain²,

Oliet³

2010

J. Neurosci.

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“…The neurohormones oxytocin (OT) and vasopressin (VP) are synthesized in the magnocellular neurosecretory cells (MNCs) of the supraoptic nucleus (SON) and paraventricular nucleus of the hypothalamus and released into the bloodstream in the posterior pituitary. Since secretion of these hormones depends on the activity of MNCs and this is tightly coupled to the efficacy of excitatory synapses (Nissen et al, 1995;Moos et al, 1997;Jourdain et al, 1998;Shibuya et al, 2000;Hrabovszky and Liposits, 2008), modulation of glutamatergic neurotransmission is an important mechanism for adjusting neuroendocrine output.…”

Section: Introductionmentioning

confidence: 99%

Opposing Actions of Endothelin-1 on Glutamatergic Transmission onto Vasopressin and Oxytocin Neurons in the Supraoptic Nucleus

Zampronio¹,

Kuzmiski²,

Florence³

et al. 2010

J. Neurosci.

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Endothelin (ET-1) given centrally has many reported actions on hormonal and autonomic outputs from the CNS. However, it is unclear whether these effects are due to local ischemia via its vasoconstrictor properties or to a direct neuromodulatory action. ET-1 stimulates the release of oxytocin (OT) and vasopressin (VP) from supraoptic magnocellular (MNCs) neurons in vivo; therefore, we asked whether ET-1 modulates the excitatory inputs onto MNCs that are critical in sculpting the activity of these neurons. To investigate whether ET-1 modulates excitatory synaptic transmission, we obtained whole-cell recordings and analyzed quantal glutamate release onto MNCs in the supraoptic nucleus (SON). Neurons identified as VP-containing neurosecretory cells displayed a decrease in quantal frequency in response to ET-1 (10 -100 pM). This decrease was mediated by ET A receptor activation and production of a retrograde messenger that targets presynaptic cannabinoid-1 receptors. In contrast, neurons identified as OT-containing MNCs displayed a transient increase in quantal glutamate release in response to ET-1 application via ET B receptor activation. Application of TTX to block action potentialdependent glutamate release inhibited the excitatory action of ET-1 in OT neurons. There were no changes in quantal amplitude in either MNC type, suggesting that the effects of ET-1 were via presynaptic mechanisms. A gliotransmitter does not appear to be involved as ET-1 failed to elevate astrocytic calcium in the SON. Our results demonstrate that ET-1 differentially modulates glutamate release onto VPversus OT-containing MNCs, thus implicating it in the selective regulation of neuroendocrine output from the SON.

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Expression of ionotropic glutamate receptor subunit mRNAs in the hypothalamic paraventricular nucleus of the rat

et al. 2000

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The hypopthalamic paraventricular nucleus (PVN) coordinates multiple aspects of homeostatic regulation, including pituitary-adrenocortical function, cardiovascular tone, metabolic balance, fluid/electrolyte status, parturition and lactation. In all cases, a substantial component of this function is controlled by glutamate neurotransmission. In this study, the authors performed a high-resolution in situ hybridization analysis of ionotropic glutamate receptor subunit expression in the PVN and its immediate surround. N-methyl-D-aspartate (NMDA) receptor 1 (NMDAR1), NMDAR2A, and NMDAR2B mRNAs were expressed highly throughout the PVN and its perinuclear region as well as in the subparaventricular zone. NMDAR2C/2D expression was limited to subsets of neurons in magnocellular and hypophysiotrophic regions. In contrast with NMDA subunit localization, AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate)-preferring and kainate (KA)-preferring receptor subunit mRNAs were expressed heterogeneously in the PVN and surround. Glutamate receptor 1 (GluR1) mRNA labeling was most intense in preautonomic subregions, whereas GluR2, GluR4, GluR5, and KA2 were expressed in hypophysiotrophic cell groups. It is noteworthy that GluR5 mRNA expression was particularly robust in the dorsolateral region of the medial parvocellular PVN, suggesting localization in corticotropin-releasing hormone neurons. All four AMPA subunits and GluR6 and GluR7 mRNAs were expressed highly in the perinuclear PVN region and the subparaventricular zone. These data suggest the capacity for multifaceted regulation of PVN function by glutamate, with magnocellular neurons preferentially expressing NMDA subunits, preautonomic neurons preferentially expressing AMPA subunits, and hypophysiotrophic neurons preferentially expressing KA subunits. Localization of all species in the perinuclear PVN suggests that glutamate input to the immediate region of the PVN may modulate its function, perhaps by communication with local gamma-aminobutyric acid neurons.

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Activation of N-methyl-D-aspartate receptors regulates basal electrical activity of oxytocin and vasopressin neurons in lactating rats

Cited by 40 publications

References 31 publications

Glutamatergic Inputs Contribute to Phasic Activity in Vasopressin Neurons

Glutamatergic Inputs Contribute to Phasic Activity in Vasopressin Neurons

Opposing Actions of Endothelin-1 on Glutamatergic Transmission onto Vasopressin and Oxytocin Neurons in the Supraoptic Nucleus

Expression of ionotropic glutamate receptor subunit mRNAs in the hypothalamic paraventricular nucleus of the rat

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