N-methyl-d-aspartate receptor antagonist ketamine selectively attenuates spontaneous phasic activity of supraoptic vasopressin neurons in vivo

Nissen, R.; Hu, Bin; Renaud, Leo P.

doi:10.1016/0306-4522(94)90103-1

Cited by 59 publications

(57 citation statements)

References 22 publications

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“…The antidiuretic hormone vasopressin (VP) is synthesized as part of a prepropeptide precursor in the cell bodies of SON and PVN MCNs (Brownstein et al, 1980;de Bree, 2000). This precursor is processed during anterograde axonal transportation to terminals in the posterior pituitary gland, in which biologically active VP is stored until mobilized for secretion; a rise in plasma osmolality is detected by intrinsic MCN osmoreceptor mechanisms (Bourque et al, 2002;Zhang and Bourque, 2003) and by specialized osmoreceptive neurons in the circumventricular organs that project to the MCNs (Bourque et al, 1994;Bourque, 1998;McKinley et al, 1999;Anderson et al, 2000;McKinley et al, 2004) that provide direct excitatory inputs (van den Pol et al, 1990) to shape the firing activity of MCNs (Hu and Bourque, 1992;Nissen et al, 1994) for hormone secretion (Dyball et al, 1995;Onaka and Yagi, 2001). On release, VP travels through the blood stream to specific receptor targets located in the kidney in which it increases the permeability of the collecting ducts to water, reducing the renal excretion of water, thus promoting water conservation.…”

Section: Introductionmentioning

confidence: 99%

Transcription Factor Expression in the Hypothalamo-Neurohypophyseal System of the Dehydrated Rat: Upregulation of Gonadotrophin Inducible Transcription Factor 1 mRNA Is Mediated by cAMP-Dependent Protein Kinase A

Qiu¹,

Yao²,

Hindmarch³

et al. 2007

J. Neurosci.

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The supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamo-neurohypophyseal system (HNS) undergo a dramatic function-related plasticity during dehydration. We hypothesize that alterations in steady-state transcript levels might be partially responsible for this remodeling. In turn, regulation of transcript abundance might be mediated by transcription factors. We used microarrays to identify changes in the expression of mRNAs encoding transcription factors in response to water deprivation in the SON. We observed downregulation of 10 and upregulation of 28 transcription factor transcripts. For five of the upregulated mRNAs, namely gonadotropin inducible ovarian transcription factor 1 (Giot1), Giot2, cAMP-responsive element binding protein 3-like 1, CCAAT/enhancer binding protein ␤, and activating transcription factor 4, in situ hybridization was used to confirm the array results, demonstrating a significant increase in expression in SON and PVN magnocellular neurons (MCNs) after 3 d of water deprivation and, in some cases, upregulation in parvocellular PVN neurons. Using a viral vector expressing a potent inhibitor of cAMP-dependent protein kinase A (PKA), we show that the osmotically induced increase in the abundance of transcripts encoding Giot1 is mediated in vivo by the PKA pathway. We thus suggest that signaling pathways activated by dehydration in MCNs mediate transcription factor gene activation, which, in turn, regulate target genes that mediate HNS remodeling.

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Section: Introductionmentioning

confidence: 99%

Transcription Factor Expression in the Hypothalamo-Neurohypophyseal System of the Dehydrated Rat: Upregulation of Gonadotrophin Inducible Transcription Factor 1 mRNA Is Mediated by cAMP-Dependent Protein Kinase A

Qiu¹,

Yao²,

Hindmarch³

et al. 2007

J. Neurosci.

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“…Glutamatergic terminals are abundant on hypothalamic magnocellular neurons (20) and glutamate is responsible for the fast excitatory synaptic input to the magnocellular neurons (54,57). Glutamate appears to be essential for the onset and maintenance of bursting activity in both vasopressin and oxytocin neurons in vitro (18,21) and in vivo (31,35,36). Glutamate circuits also carry information from perinuclear zones surrounding the SON and PVN (5,6,10,21), as well as from circumventricular osmosensitive brain structures to the magnocellular neurons (12,38).…”

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confidence: 99%

Internuclear coupling of hypothalamic magnocellular nuclei by glutamate synaptic circuits

Boudaba¹,

Tasker²

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Magnocellular neurons of the supraoptic nucleus (SON) and paraventricular nucleus (PVN) display bursting activity that is synchronized under certain conditions. They receive excitatory synaptic inputs from intrahypothalamic glutamate circuits, some of which are activated by norepinephrine. Ascending noradrenergic afferents and intrahypothalamic glutamate circuits may be responsible for the generation of synchronous bursting among oxytocin neurons and/or asynchronous bursting among vasopressin neurons located in the bilateral supraoptic and paraventricular nuclei. Here, we tested whether magnocellular neurons of the PVN receive excitatory synaptic input from the contralateral PVN and the region of the retrochiasmatic SON (SONrx) via norepinephrine-sensitive internuclear glutamate circuits. Whole cell patch-clamp recordings were performed in PVN magnocellular neurons in coronal hypothalamic slices from male rats, and the ipsilateral SONrx region and contralateral PVN were stimulated using electrical and chemical stimulation. Electrical and glutamate microdrop stimulation of the ipsilateral SONrx region or contralateral PVN elicited excitatory postsynaptic potentials/currents (EPSP/Cs) in PVN magnocellular neurons mediated by glutamate release, revealing internuclear glutamatergic circuits. Microdrop application of norepinephrine also elicited EPSP/Cs, suggesting that these circuits could be activated by activation of noradrenergic receptors. Repetitive electrical stimulation and drop application of norepinephrine, in some cases, elicited bursts of action potentials. Our data reveal glutamatergic synaptic circuits that interconnect the magnocellular nuclei and that can be activated by norepinephrine. These internuclear glutamatergic circuits may provide the functional architecture to support burst generation and/or burst synchronization in hypothalamic magnocellular neurons under conditions of activation. supraoptic nucleus; paraventricular nucleus; oxytocin; vasopressin; excitatory postsynaptic currents; excitatory postsynaptic potentials MAGNOCELLULAR NEURONS of the hypothalamic supraoptic nucleus (SON) and paraventricular nucleus (PVN) release either of the two hormones, vasopressin and oxytocin, directly into the bloodstream from their axon terminals located in the neurohypophysis. Under a variety of physiological conditions (e.g., dehydration, hypovolemia, lactation), these neurons display bursting activities that produce a large increase in the circulating concentrations of oxytocin and vasopressin. There is considerable evidence to suggest that glutamate plays an important role in the generation of bursts in these neurons. Glutamatergic terminals are abundant on hypothalamic magnocellular neurons (20) and glutamate is responsible for the fast excitatory synaptic input to the magnocellular neurons (54, 57). Glutamate appears to be essential for the onset and maintenance of bursting activity in both vasopressin and oxytocin neurons in vitro (18, 21) and in vivo (31,35,36). Glutamate circuits also carry informa...

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“…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: 94%

“…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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N-methyl-d-aspartate receptor antagonist ketamine selectively attenuates spontaneous phasic activity of supraoptic vasopressin neurons in vivo

Cited by 59 publications

References 22 publications

Transcription Factor Expression in the Hypothalamo-Neurohypophyseal System of the Dehydrated Rat: Upregulation of Gonadotrophin Inducible Transcription Factor 1 mRNA Is Mediated by cAMP-Dependent Protein Kinase A

Transcription Factor Expression in the Hypothalamo-Neurohypophyseal System of the Dehydrated Rat: Upregulation of Gonadotrophin Inducible Transcription Factor 1 mRNA Is Mediated by cAMP-Dependent Protein Kinase A

Internuclear coupling of hypothalamic magnocellular nuclei by glutamate synaptic circuits

Glutamatergic Inputs Contribute to Phasic Activity in Vasopressin Neurons

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