Evidence that Activation of the Hypothalamo-Pituitary-Adrenal Axis by Electrical Stimulation of the Noradrenergic A1 Group Is Not Mediated by Noradrenaline

Gartside, Sarah E.; Suaud-Chagny, Marie-Françoise; Tappaz, Marcel

doi:10.1159/000126982

Cited by 14 publications

(7 citation statements)

References 45 publications

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“…Other cells in the A2 region also display Fos-like immunoreactivity following i.c.v. LPS injection, and the neurochemical identity of these other neurons needs to be ascertained as various neurotransmitter systems coexist here alongside the noradrenergic neurons [56]. Our results confirm previous findings by Li et a.…”

Section: Discussionsupporting

confidence: 90%

“…Such gross lesioning studies may also damage other fiber tracts originating in the NTS and hence the specific effects of removal of noradrenaline cannot be fully determined. Indeed, the noradrenergic neurons themselves possess additional transmitters [56]and it is possible that these rather than noradrenaline itself are the mediators of A2 effects on the HPA axis. Noradrenaline depletion reduces the Fos response of the PVN to IL-1β [13]as do knife cuts to the ascending projections from the brainstem to the PVN, but these knife cuts do not alter the numbers of Fos-positive cells seen in the region of the NTS, whereas foot shock following such lesions leads to a decrease in the Fos within the NTS but not the PVN [19].…”

Section: Discussionmentioning

confidence: 99%

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Central LPS-Induced <i>c-fos</i> Expression in the PVN and the A1/A2 Brainstem Noradrenergic Cell Groups Is Altered by Adrenalectomy

et al. 1999

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The A1 and A2 brainstem noradrenergic cell groups project to the hypothalamic paraventricular nucleus (PVN), which is involved in integrating the stress response. Bi-directional communication between the brain and immune system is well established, with both neuroendocrine and immune responses being activated by lipopolysaccharide (LPS). The mechanisms underlying such activation and differences between alternative routes of administration remain unclear. We examined activation of the PVN and A1/A2 cell groups, by assessing c-fos mRNA, or counting Fos-positive neurons in either the PVN or in brainstem A1/A2 cell groups 3 h after intracerebroventricular (i.c.v.) LPS, in control and adrenalectomized (ADX) rats. We also measured corticotropin-releasing hormone (CRH) mRNA in the PVN, and plasma corticosterone (CORT) levels. A group of ADX/CORT-replaced animals received i.c.v. LPS, and CRH mRNA and Fos peptide in the PVN were analysed. ADX increased CRH mRNA in the PVN, as did LPS, but no enhancement of this response was seen in LPS/ADX animals. C-fos mRNA also increased in both the PVN and the A2 cell group following LPS, but this response was potentiated by ADX. Fos peptide-containing cells increased in the PVN and A2 following LPS, and this change was amplified by ADX. Only 11.25% of Fos was found in DBH-positive (putative noradrenergic) neurons, suggesting activation of neurons containing other transmitters. ADX/LPS/CORT animals showed numbers of Fos neurons in the brainstem, and CRH mRNA levels in the PVN which were comparable to intact/LPS animals. Central LPS activates the hypothalamo-pituitary-adrenal axis, a process mediated partly by brainstem noradrenergic neurons, suggesting the involvement of afferent/efferent pathways within the brain. Peripheral administration of LPS involves activation of vagal inputs leading to the nucleus tractus solitarius. We suggest that centrally administered LPS activates the A2 cell group by a mechanism independent of the vagus. In the absence of CORT, despite the lack of a CRH mRNA response, an exaggerated c-fos and peptide response to LPS is observed, which is reversed following CORT pretreatment.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Central LPS-Induced <i>c-fos</i> Expression in the PVN and the A1/A2 Brainstem Noradrenergic Cell Groups Is Altered by Adrenalectomy

et al. 1999

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“…In the periphery, ATP is known to function as a cotransmitter with NE in a number of tissues innervated by the sympathetic system (Burnstock, 1990;von Kugelgen and Starke, 1991). Central noradrenergic neurons might be expected to use similar cotransmission, especially as more evidence accumulates for the involvement of nonadrenergic neurotransmission (Gartside et al, 1995).In the present investigation, perifused explants of the rat hypothalamoneurohypophyseal system (HNS) were used to study the role of ATP and NE in the regulation of VP and oxytocin release. Specifically, the effects of ␣ 1 -adrenergic and purinergic receptor activation and the interactions of these agents were evaluated.…”

mentioning

confidence: 99%

Purinergic and Adrenergic Agonists Synergize in Stimulating Vasopressin and Oxytocin Release

Kapoor

Sladek

2000

J. Neurosci.

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The A1 catecholamine neurons of the caudal ventrolateral medulla transmit hemodynamic information to the vasopressin (VP) neurons in the hypothalamus. These neurons corelease ATP with norepinephrine. Perifused explants of the hypothalamoneurohypophyseal system were used to investigate the role of these substances on VP release. ATP (100 M) increased VP release 1.5-fold ( p ϭ 0.027). The response was rapid but unsustained. It was blocked by the P 2 receptor antagonist pyridoxal-phosphate-6-azophenyl-2Ј,4Ј-disulphonic acid (PPADS). The ␣ 1 -adrenergic agonist phenylephrine (PE; 100 M) also increased VP release by 1.5-fold ( p ϭ 0.014). Again, the response was rapid and unsustained. However, simultaneous perifusion of explants with ATP (100 M) and PE (100 M) resulted in a threefold to fourfold increase in VP release, which was sustained for as long as 4 hr. There was a similar synergistic effect of ATP and PE on oxytocin release. Interestingly, the synergistic response was delayed ϳ40 min relative to the response to either agent alone. Several experiments were performed to elucidate the cellular mechanisms of this synergism. The effect was blocked by PPADS, a protein kinase C inhibitor (bisindolylmaleimide I HCl), and actinomycin, an inhibitor of gene transcription. These data suggest that P 2X receptor activation, PKC-mediated phosphorylation, and gene transcription are required for the synergistic response. The marked synergism of these coreleased agents is probably important to achieve sustained increases in plasma VP in response to prolonged hypotension. These observations may also have broad applications to CNS function, because ATP may be coreleased at noradrenergic synapses throughout the CNS. Key words: norepinephrine; ATP; vasopressin; supraoptic nucleus; catecholamine; neurohypophysis; purinergic transmission; blood pressure regulationVasopressin (VP)-synthesizing neurons of the supraoptic and paraventricular nuclei (SON and PVN) receive direct, excitatory input from the A1 noradrenergic neurons of the caudal ventrolateral medulla (Alonso and Assenmacher, 1984;Day et al., , 1992Shioda et al., 1992;Ginsberg et al., 1994;Smith et al., 1995). In addition to norepinephrine (NE), various substances are colocalized or coreleased from the A1 neurons, including neuropeptide Y, substance P, and ATP (Everitt et al., 1984;Sawchenko et al., 1985;Blessing et al., 1986;Beroukas et al., 1989;Lundberg et al., 1989;Bittencourt et al., 1991;Sperlagh et al., 1998). Although abundant evidence supports the importance of the A1 pathway for stimulation of VP release in response to moderate decreases in blood pressure (Raby and Renaud, 1989;Smith et al., 1995), studies directed at demonstrating that NE is the primary transmitter mediating this response were not successful (Day et al., 1990). Adrenoceptor antagonists did not block A1 activation of VP cells, prompting the suggestion that these neurons use a substance other than NE as their principal transmitter (Day et al., 1990). In addition, injections of the broad-spectrum exci...

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“…We have also demonstrated that the administration of both ionotropic receptor antagonists attenuated the neuroendocrine responses following VNAB and DRN stimulation in a dose-dependent manner. It was previously reported that electrical stimulation of either the VNAB or the DRN caused the release of NE and 5-HT, respectively, in the hypothalamus [24, 25, 26]. Importantly, in the present study the animals were anesthetized with pentobarbital which may enhance GABAergic inhibition and modify the neuroendocrine responses.…”

Section: Discussionmentioning

confidence: 79%

Involvement of Endogeneous Glutamate in the Stimulatory Effect of Norepinephrine and Serotonin on the Hypothalamo-Pituitary-Adrenocortical Axis

Feldman

Weidenfeld²

2004

Neuroendocrinology

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The effects of ionotropic glutamate receptor antagonists on the pituitary adrenal responses following injections of norepinephrine (NE) and serotonin (5-HT) receptor agonists into the hypothalamic paraventricular nucleus (PVN) or electrical stimulation of central NE and 5-HT pathways were studied in anesthetized male rats. PVN injections of an α₁-adrenergic receptor agonist or a serotonergic 5-HT_1A receptor agonist markedly increased both adrenocorticotropin (ACTH) and corticosterone (CS) serum levels. These responses were significantly inhibited by separate pre-injection of the selective non-NMDA and NMDA glutamate receptor subtype antagonists into the PVN in a dose-dependent manner. Electrical stimulation of either the ventral noradrenergic bundle or the dorsal raphe nucleus markedly increased serum ACTH and CS. These responses were also significantly attenuated by pre-injection of the above glutamate ionotropic receptor antagonists in a dose-dependent manner. These results suggest that glutamatergic interneurons in the PVN, acting via non-NMDA and NMDA receptors, may act as an excitatory mechanism in the NE and 5-HT control of hypothalamic ACTH secretagogues.

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Evidence that Activation of the Hypothalamo-Pituitary-Adrenal Axis by Electrical Stimulation of the Noradrenergic A1 Group Is Not Mediated by Noradrenaline

Cited by 14 publications

References 45 publications

Central LPS-Induced <i>c-fos</i> Expression in the PVN and the A1/A2 Brainstem Noradrenergic Cell Groups Is Altered by Adrenalectomy

Central LPS-Induced <i>c-fos</i> Expression in the PVN and the A1/A2 Brainstem Noradrenergic Cell Groups Is Altered by Adrenalectomy

Purinergic and Adrenergic Agonists Synergize in Stimulating Vasopressin and Oxytocin Release

Involvement of Endogeneous Glutamate in the Stimulatory Effect of Norepinephrine and Serotonin on the Hypothalamo-Pituitary-Adrenocortical Axis

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