Autoradiographic distribution of brainstem substance P binding sites in humans: Ontogenic study and relation to Sudden Infant Death Syndrome (SIDS)

Jordan, D. C.; Kermadi, I.; Rambaud, Caroline; Bouvier, Raymonde; Dijoud, F.; Martin, David P.; Kopp, Nicolas

doi:10.1007/bf01273322

Cited by 14 publications

(6 citation statements)

References 5 publications

(8 reference statements)

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“…In keeping with initial reports, Bergstrom et al [136] found no difference in Met-enkephalin concentration between SIDS and controls in medulla, pons, hypothalamus or cortex, but disclosed for the first time a significant increase in the concentrations of substance P in the medulla of SIDS infants [136]. In contrast, a more recent study on substance P in the brain stem of SIDS infants [138] indicated that there were no significant differences between SIDS and developmentally normal infants. In contrast, a more recent study on substance P in the brain stem of SIDS infants [138] indicated that there were no significant differences between SIDS and developmentally normal infants.…”

Section: Brain Stemsupporting

confidence: 58%

Neuropathology of sudden infant death (syndrome): literature review and evidence of a probable apoptotic degenerative cause

Sparks

Hunsaker

2002

Childs Nerv Syst

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Background: The agonizing enigma of sudden infant death syndrome (SIDS) endures. Contemporary research concentrates on the central nervous system (CNS) as the prime cause. Review and discussion: What follows is a review of the neuropathology of SIDS. A persuasive, but as yet unproved, hypothesis is that the lethal pathophysiologic derangement or mechanism in SIDS involves dysfunction of sleep-related cardiorespiratory homeostatic controls or failure to arouse or both. Neuropathological investigation of SIDS continues to be closely linked to the study of specific anatomic structures and regions of the CNS. The structures in these regions underpin and regulate normal cardiorespiratory function. It follows that dysfunction of one or more of these loci probably precipitates SIDS. Under this large umbrella review we include histological, immunohistochemical, and biochemical markers in the cerebrospinal fluid (CSF), ce-rebrum, cerebellum, brain stem, pituitary gland, and pineal gland. With variable effect, these regions are deemed to mediate the functionality of cardiorespiratory activity and the diurnal rhythms of sleep/arousal. The following factors, which (a) are associated with altered electrochemical or neural transmission and biochemical changes in the CNS and (b) predispose to systemic derangements that most probably precipitate SIDS, are subjects of ongoing investigation: evidence of delayed development; ischemic insult; degenerative changes; and synaptic alterations. Conclusion: On the basis of current data, we add to these theoretical constructs by postulating that apoptotic neurodegeneration constitutes the anatomic substrate accounting for the pathophysiologic mechanism and proximate cause of SIDS.

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Section: Brain Stemsupporting

confidence: 58%

Neuropathology of sudden infant death (syndrome): literature review and evidence of a probable apoptotic degenerative cause

Sparks

Hunsaker

2002

Childs Nerv Syst

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“…, ; Prandota ; Vege and Ole Rognum ; Kinney and Thach ) and upregulation of inflammatory mediators, such as IL‐1 β and substance P, is assumed to be responsible for SIDS (Jordan et al. ; Froen et al. ; Balan et al.…”

Section: Discussionmentioning

confidence: 99%

Maternal nicotinic exposure produces a depressed hypoxic ventilatory response and subsequent death in postnatal rats

Zhuang

Zhao

2014

Physiol Rep

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In this study, we asked whether a “full term” prenatal nicotinic exposure (fPNE, 6 mg·kg−1·day−1 nicotinic delivery) over the full gestation, compared to a traditional PNE (tPNE) over the last two‐thirds of the gestation, caused a higher mortality following a remarkable depressed hypoxic ventilatory response (dHVR) independent of brain and pulmonary edema and change in serum corticosterone. P12‐14 pups pretreated with tPNE, fPNE or their vehicle (tCtrl and fCtrl) were exposed to 5% O2 for up to 60 min followed by harvesting the brain and lungs or anesthetized to collect blood for detecting arterial blood pH/gases and serum cotinine and corticosterone levels. We found that fPNE had little effect on baseline VE and heart rate, but consistently induced a dHVR and prolonged apnea that were rarely observed after tPNE. The severity of the dHVR in PNE pups were closely correlated to an earlier appearance of lethal ventilatory arrest (the hypoxia‐induced mortality). PNE did not induce brain and pulmonary edema, but significantly increased serum corticosterone levels similarly in tPNE and fPNE pups. Moreover, the accumulated nicotinic dose given to the individual was significantly higher in fPNE than tPNE pups, though there was no difference in serum cotinine levels and arterial blood pH/gases between the two groups. Our results suggest that nicotinic exposure at the early stage of gestation achieved by fPNE, rather than tPNE, is critical in generating the dHVR and subsequent death occurring independently of brain/pulmonary edema and changes in arterial blood pH/gases and serum corticosterone.

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“…Based on previous physiological studies on SP‐mediated or ENK‐mediated respiratory activity, the present study, using morphological approaches to identify SP or ENK immunoreactivity and their relationship with neurotransmitters, as well as with NK1R‐ir neurons in the pre‐BötC, provides a foundation for understanding synaptic interaction underlying respiratory rhythmogenesis and modulation in the pre‐BötC network. Alteration of SP‐mediated or ENK‐mediated synaptic transmission may implicate respiratory disorders such as sudden infant death syndrome (Morin‐Surun et al ., 1992; Jordan et al ., 1997).…”

Section: Discussionmentioning

confidence: 99%

Substance P and enkephalinergic synapses onto neurokinin‐1 receptor‐immunoreactive neurons in the pre‐Bötzinger complex of rats

Liu

Wong‐Riley

Liu

et al. 2004

Eur J of Neuroscience

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Our previous studies have demonstrated that neurokinin-1 receptor (NK1R)-immunoreactive (ir) neurons in the pre-Bötzinger Complex (pre-BötC), the hypothesized kernel of respiratory rhythmogenesis, receive both glutamatergic excitatory and GABAergic or glycinergic inhibitory inputs. Neuromodulators, such as substance P (SP) and opioids, play important roles in normal respiratory activity and respiratory disorders. The identification of the relationship between neurotransmitters and NK1R-ir neurons at the cellular level is essential for understanding the synaptic interaction within the pre-BötC network. Using immunofluorescence and immunogold-silver staining, we wished to exploit SP and enkephalin (ENK) immunoreactivity and their relationships with glutamate, GABA, glycine, or NK1R in the pre-BötC in adult Sprague-Dawley rats. The pre-BötC contained a substantial amount of SP-ir and ENK-ir boutons. They were largely colocalized with glutamate and much less so with GABA. Glycine immunoreactivity was rarely found in either SP-ir or ENK-ir boutons. A number of SP-ir boutons were ENK-ir as well. Synapses were commonly found between SP-ir or ENK-ir terminals and NK1R-ir neurons in the pre-BötC. Most of them were asymmetric. Symmetric synapses made up 10% of all synapses examined between SP-ir boutons and NK1R-ir neurons, and 19% of ENK/NK1R synapses. Colocalization of SP and/or ENK with glutamate in boutons in the pre-BötC implies the combined synaptic release of excitatory amino acid and neuropeptides, which may exert combined post-synaptic effects onto NK1R-ir neurons and contribute to respiratory activity.

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Autoradiographic distribution of brainstem substance P binding sites in humans: Ontogenic study and relation to Sudden Infant Death Syndrome (SIDS)

Cited by 14 publications

References 5 publications

Neuropathology of sudden infant death (syndrome): literature review and evidence of a probable apoptotic degenerative cause

Neuropathology of sudden infant death (syndrome): literature review and evidence of a probable apoptotic degenerative cause

Maternal nicotinic exposure produces a depressed hypoxic ventilatory response and subsequent death in postnatal rats

Substance P and enkephalinergic synapses onto neurokinin‐1 receptor‐immunoreactive neurons in the pre‐Bötzinger complex of rats

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