Acetylcholine determination of cerebrospinal fluid in aneurysmal subarachnoid hemorrhage

Kawamata, Takakazu; Takeshita, Mikihiko; Ujiié, Hiroshi; Sato, Kazuei; Izawa, Masahiro; Kagawa, Mizuo; Takakura, Kintomo

doi:10.1016/0090-3019(94)90034-5

Cited by 6 publications

(3 citation statements)

References 29 publications

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“…For that reason, BFB neurons might be easily affected by any pathological event in the subarachnoid space that has the potential to exert cellular injury in the juxtaposed brain parenchyma. Cholinergic lesions after SAH might cause the lowering of acetylcholine (ACh) concentration in the cerebrospinal fluid in humans (25). Thus, several findings link the cognitive decline in patients after SAH to a lesion of the cholinergic BFB: either dissector-based cell counts (52) or other counting protocols has not revealed considerable differences (19).…”

Section: Induction Of Experimental Sahmentioning

confidence: 99%

Degeneration of Cholinergic Rat Basal Forebrain Neurons After Experimental Subarachnoid Hemorrhage

et al. 2008

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Section: Induction Of Experimental Sahmentioning

confidence: 99%

Degeneration of Cholinergic Rat Basal Forebrain Neurons After Experimental Subarachnoid Hemorrhage

et al. 2008

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“…In conditions involving a clinical situation and chronic stress, these non-ACTH factors modulate HPA axis function at the pituitary or adrenal level and induce the hypersecretion of cortisol without increasing the ACTH level: that is, ACTH secretion is dissociated from the cortisol level (Pignatelli et al 1998;Bornstein et al 2008). Some studies have reported that non-ACTH factors (cytokines and neurotransmitters) in the cerebrospinal fluid are elevated and that the sympathetic nervous system is activated during the first few days or weeks after aSAH (Kawamata et al 1994;Naredi et al 2000Naredi et al , 2006Fassbender et al 2001). A dissociation of ACTH from the cortisol levels within the first 1 -2 weeks after an aSAH has already been reported in previous studies (Bendel et al 2008;Poll et al 2010).…”

Section: Discussionmentioning

confidence: 96%

Abnormal diurnal pattern of cortisol secretion in patients after aneurysmal subarachnoid hemorrhage

Shin

Joo

Chung

et al. 2010

Stress

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Substantial evidence suggests that impairment of the hypothalamus?pituitary system can occur following an aneurysmal subarachnoid hemorrhage (aSAH). Given that the diurnal cortisol rhythm is primarily controlled by the hypothalamus?pituitary system, this study examined whether changes in diurnal cortisol rhythm occurred after aSAH. Cortisol concentrations were measured in the saliva samples collected from patients after aSAH and other types of cerebral hemorrhage (non-aSAH) in the post-awakening period and at night (21:00?h), and the cortisol awakening response (CAR) and diurnal cortisol decline were determined. The area under the cortisol curve from immediately after to 45?min after awakening (CARauc) in the aSAH patient group was comparable to that in the non-aSAH or healthy control groups. However, an obvious cortisol peak was not found after the awakening period, and the morning/nighttime cortisol ratio in the aSAH patient group was significantly lower than that in other examined groups due to higher nighttime cortisol concentrations. In aSAH patients, the CARauc and nighttime cortisol concentrations were negatively correlated with the Fisher CT grade. These results indicate that the diurnal cortisol rhythm is not regulated normally after aSAH, and cortisol secretory activity decreases as the volume of subarachnoid bleeding increases. Our findings will be helpful to understand altered hypothalamus?pituitary?adrenal axis function after aSAH.

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“…For example, in animal models of aSAH, increased parasympathetic tone, either directly through stimulation of the sphenopalatine ganglion or by activation of perivascular α 7 -AChR, improves outcome [10,11]. Furthermore, acetylcholine levels in cerebrospinal fluid after aSAH are significantly lower in the acute phase of illness, suggesting that reduced Ach receptor activity may play a role in SAH injury [12]. α 7 -AChR agonists have been reported to offer benefit after a number of hemorrhagic insults to the brain including intracerebral hemorrhage [13], traumatic brain injury [14], and SAH [15].…”

Section: Introductionmentioning

confidence: 99%

α7-Acetylcholine Receptor Signaling Reduces Neuroinflammation After Subarachnoid Hemorrhage in Mice

et al. 2021

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Aneurysmal subarachnoid hemorrhage (aSAH) causes a robust inflammatory response which leads worse brain injury and poor outcomes. We investigated if stimulation of nicotinic acetylcholine α 7 receptors (α 7 -AChR) (receptors shown to have anti-inflammatory effects) would reduce inflammation and improve outcomes. To investigate the level of peripheral inflammation after aSAH, inflammatory markers were measured in plasma samples collected in a cohort of aSAH patients. To study the effect of α 7 -AChR stimulation, SAH was induced in adult mice which were then treated with a α 7 -AChR agonist, galantamine, or vehicle. A battery of motor and cognitive tests were performed 24 h after subarachnoid hemorrhage. Mice were euthanized and tissue collected for analysis of markers of inflammation or activation of α 7 -AChR-mediated transduction cascades. A separate cohort of mice was allowed to survive for 28 days to assess long-term neurological deficits and histological outcome. Microglia cell culture subjected to hemoglobin toxicity was used to assess the effects of α 7 -AChR agonism. Analysis of eighty-two patient plasma samples confirmed enhanced systemic inflammation after aSAH. α 7 -AChR agonism reduced neuroinflammation at 24 h after SAH in male and female mice, which was associated with improved outcomes. This coincided with JAK2/STAT3 and IRAK-M activity modulations and a robust improvement in neurological/cognitive status that was effectively reversed by interfering with various components of these signaling pathways. Pharmacologic inhibition partially reversed the α 7 -AChR agonist's benefits, supporting α 7 -AChR as a target of the agonist's therapeutic effect. The cell culture experiment showed that α 7 -AChR agonism is directly beneficial to microglia. Our results demonstrate that activation of α 7 -AChR represents an attractive target for treatment of SAH. Our findings suggest that α 7 -AChR agonists, and specifically galantamine, might provide therapeutic benefit to aSAH patients.

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Acetylcholine determination of cerebrospinal fluid in aneurysmal subarachnoid hemorrhage

Cited by 6 publications

References 29 publications

Degeneration of Cholinergic Rat Basal Forebrain Neurons After Experimental Subarachnoid Hemorrhage

Degeneration of Cholinergic Rat Basal Forebrain Neurons After Experimental Subarachnoid Hemorrhage

Abnormal diurnal pattern of cortisol secretion in patients after aneurysmal subarachnoid hemorrhage

α7-Acetylcholine Receptor Signaling Reduces Neuroinflammation After Subarachnoid Hemorrhage in Mice

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