Changing patterns of Fos expression in brainstem catecholaminergic neurons during the rat oestrous cycle

Conde, Gillian; Bicknell, R.J.; Herbison, Allan E.

doi:10.1016/0006-8993(94)01385-u

Cited by 47 publications

(26 citation statements)

References 35 publications

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“…During most of the reproductive cycle estrogen receptor-␣ signaling inhibits GnRH, but in the late follicular stage it switches to positive feedback and causes a surge in GnRH and luteinizing hormone (LH) release. C1 cells may participate in the GnRH/LH surge but the evidence for this is limited (41,95,167). Alternatively, C1 neurons may inhibit GnRH, in particular, in response to physical stressors to conserve energy.…”

Section: C1 and Female Reproductive Functionmentioning

confidence: 99%

C1 neurons: the body's EMTs

Guyenet

Stornetta

Bochorishvili

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

245

262

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The C1 neurons reside in the rostral and intermediate portions of the ventrolateral medulla (RVLM, IVLM). They use glutamate as a fast transmitter and synthesize catecholamines plus various neuropeptides. These neurons regulate the hypothalamic pituitary axis via direct projections to the paraventricular nucleus and regulate the autonomic nervous system via projections to sympathetic and parasympathetic preganglionic neurons. The presympathetic C1 cells, located in the RVLM, are probably organized in a roughly viscerotopic manner and most of them regulate the circulation. C1 cells are variously activated by hypoglycemia, infection or inflammation, hypoxia, nociception, and hypotension and contribute to most glucoprivic responses. C1 cells also stimulate breathing and activate brain stem noradrenergic neurons including the locus coeruleus. Based on the various effects attributed to the C1 cells, their axonal projections and what is currently known of their synaptic inputs, subsets of C1 cells appear to be differentially recruited by pain, hypoxia, infection/inflammation, hemorrhage, and hypoglycemia to produce a repertoire of stereotyped autonomic, metabolic, and neuroendocrine responses that help the organism survive physical injury and its associated cohort of acute infection, hypoxia, hypotension, and blood loss. C1 cells may also contribute to glucose and cardiovascular homeostasis in the absence of such physical stresses, and C1 cell hyperactivity may contribute to the increase in sympathetic nerve activity associated with diseases such as hypertension. C1 neurons; blood pressure; brain stem BEST KNOWN for their contribution to the control of arterial pressure (AP), the C1 neurons have also been implicated in many other physiological processes ranging from neuroendocrine responses to infection and inflammation, glucose homeostasis, reproduction, breathing, thermoregulation, hypothalamo-pituitary axis (HPA)-mediated stress responses, and food consumption. The purpose of this review is to summarize the most salient information concerning the C1 cells, to point out some of the remaining gaps in our current knowledge, and to suggest a few unifying physiological principles that could account for these seemingly disparate observations. Based on the various effects attributed to the C1 cells and what is currently known of their synaptic inputs, we propose that these neurons are, figuratively speaking, the body's "emergency medical technicians." By this we imply that these neurons produce stereotyped autonomic, metabolic, and neuroendocrine responses designed to help the organism survive major acute physical stresses such as accidental, pathological, or dive-related hypoxia or physical injury and its associated cohort of acute infection, blood loss, and hypotension. These emergency responses include, in the short term and depending on the stress, vasoconstriction, cardioinhibition, or acceleration, breathing stimulation, antidiuresis, changes in metabolism, and gastrointestinal (GI) functions designed to conserve pe...

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Section: C1 and Female Reproductive Functionmentioning

confidence: 99%

C1 neurons: the body's EMTs

Guyenet

Stornetta

Bochorishvili

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

245

262

View full text Add to dashboard Cite

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“…IHC was performed as described previously (Conde et al 1995) but on unfixed frozen 12 µm cryostat sections. Sections through the PVN were fixed in 4% paraformaldehyde for 10 min prior to immunostaining.…”

Section: Immunohistochemistry (Ihc)mentioning

confidence: 99%

Serotonin depletion does not alter lipopolysaccharide-induced activation of the rat paraventricular nucleus

Renshaw²,

Lightman³

et al. 1998

Journal of Endocrinology

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We have investigated the effects of serotonin depletion on immune-mediated activation of the hypothalamopituitary-adrenal (HPA) axis. Corticotrophin-releasing factor (CRF) mRNA, c-fos mRNA and Fos peptide responses in the paraventricular nucleus (PVN) together with circulating levels of corticosterone were assessed in response to i.p. injections of three doses of lipopolysaccharide (LPS) both in control animals and animals pretreated with p-chlorophenylalanine (PCPA).Conscious animals received either an i.p. injection of 0·5 ml saline or 200 mg/kg PCPA in 0·5 ml saline on 2 consecutive days. This treatment resulted in a 93% depletion of serotonin on the fourth day. On day 4, animals received i.p. injections of LPS (2·5 mg/0·5 ml saline, 250 µg/0·5 ml or 50 µg/0·5 ml; E. coli 055:B5), or saline injections as controls.Pretreatment with PCPA had no effect on the basal levels of corticosterone, or on the elevated levels induced by the three doses of LPS. Fos peptide and c-fos mRNA were undetectable in control animals, and Fos-like immunoreactivity increased in a dosedependent manner following i.p. LPS in both control and PCPA-pretreated animals. C-fos mRNA expression induced by LPS was unaffected by serotonin depletion. Following the lowest dose of LPS, CRF mRNA did not change above control levels, however, the medium and high doses of LPS produced a significant (P<0·05) increase in CRF mRNA levels in both depleted and intact animals.To confirm the temporal effects of serotonin depletion on activation of the HPA axis we collected plasma at 30 min, 1, 2, 3, 4, 5 and 6 h after LPS in both intact and serotonin-depleted animals. No significant differences in plasma corticosterone levels were found at any of the time points between intact and depleted animals.It appears that, at least under these experimental conditions, serotonergic inputs do not seem to play a major role in mediating the effects of LPS on changes in mRNA levels in the PVN or on the subsequent activation of the HPA axis.

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“…Estrogen has been demonstrated to increase the electrical excitability of NE neurons projecting to the preoptic area (332) and also to stimulate Fos (333) and tyrosine hydroxylase (334) gene expression in A2 neurons. Furthermore, the number of A2 neurons expressing Fos increases on proestrus before the onset of the LH surge (333,335). Hence, estrogen may facilitate a diurnal pattern of NE secretion within the preoptic area by stimulating the A2 subpopulation to elevate NE release in the morning/early afternoon of proestrus (307,335).…”

Section: Neurotensinmentioning

confidence: 99%

“…Furthermore, the number of A2 neurons expressing Fos increases on proestrus before the onset of the LH surge (333,335). Hence, estrogen may facilitate a diurnal pattern of NE secretion within the preoptic area by stimulating the A2 subpopulation to elevate NE release in the morning/early afternoon of proestrus (307,335). In addition, there is good evidence for a presynaptic inhibition of NE release by ␤END in the preoptic area of the rat, and an estrogen-induced decrease in this tonic input may further contribute to the elevation of preoptic NE concentrations at the time of the LH surge (336 -339).…”

Section: Neurotensinmentioning

confidence: 99%