Relationship of substance P and gliosis in medulla oblongata in neonatal sudden infant death syndrome

Obonai, Toshimasa; Takashima, Sachio; Becker, Laurence E.; Asanuma, Masami; Mizuta, Ryuzo; H, Horie; Tanaka, Junichi

doi:10.1016/s0887-8994(96)00217-2

Cited by 42 publications

(20 citation statements)

References 14 publications

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“…In NS, the mismatch between the reported increase by Obonai et al (1996) in SIDS of immunohistochemical SP (associated with astrogliosis) and our lack of evidence for changes in the density of SP binding sites did not sustain a primary role in SIDS for this brainstem integrative structure.…”

Section: Discussioncontrasting

confidence: 79%

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

Jordan

Kermadi

Rambaud

et al. 1997

J. Neural Transmission

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The precise distribution of substance P (SP) binding sites in the human brainstem was investigated in normal cases (3 fetuses and 24 new-borns) and in 9 cases of Sudden Infant Death Syndrome (SIDS) by in vitro quantitative autoradiography. We discussed the widely but uneven distribution of SP binding sites as regards to the role of SP in brainstem cardio-respiratory ontogenic control and its possible involvement in SIDS.

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Section: Discussioncontrasting

confidence: 79%

“…If the hypothesis of an alteration of this brainstem control regulation in Sudden Infant Death Syndrome (SIDS) is generally accepted today, little information has been recently published concerning SP involvement in SIDS brainstem (Obonai et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

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

Jordan

Kermadi

Rambaud

et al. 1997

J. Neural Transmission

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“…Few earlier studies with small sample size have been performed in relation to SP expression in brainstems of SIDS (60–63). Our group (11) defined localization, morphology, and functional aspects of TrN in different developmental stages of human brain development for the first time in cases of sudden perinatal death victims.…”

Section: Evidence Of Involvement Of Spinal Trigeminal Nucleus In Respmentioning

confidence: 99%

Substance P/Neurokinin 1 and Trigeminal System: A Possible Link to the Pathogenesis in Sudden Perinatal Deaths

Mehboob

2017

Front. Neurol.

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Sudden demise of a healthy fetus or a neonate is a very tragic episode in the life of parents. These deaths have been a mystery since ages but still remain unexplained. This review proposes the involvement of trigeminal nerve, neurotransmitter substance P (SP), and its receptor neurokinin 1 (NK-1R) in regulation of cardiorespiratory control in fetuses and newborns. Anomalies and immaturity of neuroregulatory systems such as trigeminal system in medulla oblongata of brainstem may provide a possible mechanism of sudden perinatal deaths. Vulnerable infants are born with respiratory center immaturity which in combination with any stressor such as cold, hypoxia, and smoking may lead to cessation of breathing and ventilatory response. SP/NK-1R may be involved in regulating the ventilatory control in neonates while it is decreased in fetal and adult life in humans, and any alterations from these may lead to irreversible sleep apnea and fatal breathing, ultimately sudden death. This review summarizes the studies performed to highlight the expression of SP or NK-1R in sudden perinatal deaths and proposes the involvement of trigeminal ganglion along with its nerve and SP/NK-1R expression alteration as one of the possible pathophysiological underlying mechanism. However, further studies are required to explore the role of SP, NK-1R, and trigeminal system in the pathogenesis of sudden infant deaths, sudden intrauterine deaths, stillbirths, and sudden deaths later in human life.

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“…The neurotransmitters included acetylcholine, catecholamines, Substance P, glutamate (via NMDA and non-NMDA receptors), and serotonin (Kinney et al, 1995;H. C. Kinney, McHugh, Miller, Belliveau, & Assmann, 2002;Kinney et al, 2003;Machaalani & Waters, 2003;Obonai et al, 1996;Panigrahy et al, 1997Panigrahy et al, , 2000Paterson et al, 2006;Takashima & Becker, 1991). Structural abnormalities were also reported in cardiorespiratory-related regions, including hypoplasia of the arcuate nucleus (the putative homologue of respiratory chemosensitive fields at the ventral medullary surface in experimental animals) (Biondo, Lavezzi, Tosi, Turconi, & Matturri, 2003;Filiano, Choi, & Kinney, 1990;Filiano & Kinney, 1992;Matturri, Biondo, Mercurio, & Rossi, 2000); apoptosis (Machaalani, Rodriguez, & Waters, 2007;Machaalani & Waters, 2008), and dendritic spine abnormalities (Quattrochi, 1985Takashima, 1985Takashima, 1990.…”

Section: Initial Neuropathologic Studies In Sids Brainstemsmentioning

confidence: 99%

Brainstem mechanisms underlying the sudden infant death syndrome: Evidence from human pathologic studies

Kinney

2009

Developmental Psychobiology

108

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The brainstem hypothesis is one of the leading hypotheses concerning the sudden infant death syndrome (SIDS). It states that SIDS, or an important subset of SIDS, is due to abnormal brainstem mechanisms in the control of respiration, chemosensitivity, autonomic regulation, and/or arousal which impairs the infant's response to life-threatening, but often occurring, stressors during sleep (e.g., hypoxia, hypercarbia, asphyxia, hyperthermia) and leads to sudden death in a vulnerable developmental period. In this review, we summarize neuropathologic evidence from SIDS cases that support this hypothesis, beginning with the seminal report of subtle brainstem gliosis three decades ago. We focus upon recent neurochemical studies in our laboratory concerning the neurotransmitter serotonin (5-HT) and its key role in mediating protective responses to homeostatic stressors via medullary circuits. The possible fetal origin of brainstem defects in SIDS is reviewed, including evidence for adverse effects of prenatal exposure to maternal cigarette smoking and alcohol upon the postnatal development of human brainstem 5-HT pathways.

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Relationship of substance P and gliosis in medulla oblongata in neonatal sudden infant death syndrome

Cited by 42 publications

References 14 publications

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

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

Substance P/Neurokinin 1 and Trigeminal System: A Possible Link to the Pathogenesis in Sudden Perinatal Deaths

Brainstem mechanisms underlying the sudden infant death syndrome: Evidence from human pathologic studies

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