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Enteric nervous system (ENS): The intrinsic nervous system in the gastrointestinal (GI) tract that governs that GI tract function. It is completely separate from the central nervous system (CNS) and can function independently of brain or spinal cord input.

Vagal motor neurons: Neurons in the vagus system that carry neural impulses from the brain to peripheral target organs. Their neuronal bodies reside in the dorsal motor nucleus of the vagus in the hindbrain. They are the main components of the parasympathetic nervous system and may directly innervate the intestinal epithelium, blood vessels or intestinal smooth muscle. They also synapse with the ENS to indirectly regulate intestinal function.

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Vagal sensory neurons: Neurons in the vagus system that carry peripheral sensory information to the brain. Their neuronal bodies reside in the nodose ganglia that are at the base of the skull and behind the carotid canal.

The gut microbiota regulates extrinsic enteric-associated neurons. (A) Vagal and spinal sensory and motor neurons innervate the mammalian digestive tract. Vagal and spinal sensory neuronal cell bodies reside in the ganglia adjacent to the brainstem or spine. A representative pseudounipolar vagal sensory neuron is shown above the nodose vagal ganglion. (B) Gut microbial signals may translocate across the intestinal epithelium and act on receptors on the nerve ends of extrinsic enteric-associated neurons (eEANs) to regulate eEAN function. Gut microbial stimulants also act on intestinal epithelial cells such as enteroendocrine cells (light and dark purple cells), which in turn may indirectly affect the development and function of eEANs. Created using BioRender.com. The nodose vagal ganglion drawing is based on Waise et al., 2018. DMV, dorsal motor nucleus of the vagus; DRG, dorsal root ganglion; MAMPs, microbe-associated molecular patterns; NTS, nucleus tractus solitarius.

Many other studies support the role of sensory eEANs in transducing enteric microbial information to the CNS. Cecal infection with the bacterial pathogen Campylobacter jejuni in mice leads to neuronal activation in the nucleus tractus solitarius, the first entrance of vagal afferents into the brain (Gaykema et al., 2004). Surgical disconnection of the vagal sensory nerve from the brain via vagotomy prevents the anxiety-reducing effect of beneficial Bifidobacterium longum in mice (Bercik et al., 2011). Similarly, the beneficial effects of Lactobacillus reuteri in a mouse autism model can be blocked following vagotomy (Sgritta et al., 2019). A recent study using zebrafish also suggests that specific enteric bacteria stimulate EECs to activate vagal sensory neurons through the production of tryptophan catabolites (Ye et al., 2021). Gut microbiota are also likely to modulate CNS function through spinal sensory nerve function. The branched-chain fatty acid isovalerate produced by gut bacteria directly activates EECs to stimulate the pelvic spinal sensory neurons (see Glossary, Box 2; Bellono et al., 2017). These studies highlight the crucial roles of eEANs in sensing and responding to diverse microbial stimuli.

Functional gastrointestinal disorders (FGIDs) are a group of prevalent GI diseases characterized by chronic or recurrent digestive symptoms, including abdominal pain or GI tract motility dysfunction (Drossman, 2006). Most FGID patients do not display identifiable structural or biochemical abnormalities in the GI tract (Drossman, 2006). Increasing evidence suggests that FGIDs may be attributed to abnormalities in the gut microbiome and dysfunctional gut-brain neuronal circuitry and communication (Collins, 2014; Mayer et al., 2014). FGIDs are common in both childhood and adults. Many studies suggest that early life events predispose individuals to childhood FGIDs and contribute to the development of FGIDs later in adulthood (Rasquin et al., 2006; Bonilla and Saps, 2013; Chitkara et al., 2008; Mendall and Kumar, 1998). These early life risk factors include enteric infection or antibiotic usage, both of which are associated with the disruption of normal gut microbiota (Bonilla and Saps, 2013; Mendall and Kumar, 1998). Perturbation of the gut microbiome during childhood development thus likely leads to the inappropriate formation and function of the ENS and eEANs, which would increase the risk of FGIDs.

To monitor cerebral autoregulation (CA) at the bedside, indices of cerebrovascular reactivity can serve as surrogate markers of CA. One of the most widely investigated cerebrovascular reactivity indices is the pressure reactivity index (PRx), defined as the moving linear Pearson correlation index between mean arterial pressure (MAP) and intracranial pressure (ICP), which correlates with outcome after aneurysmal subarachnoid hemorrhage (aSAH) and traumatic brain injury (TBI) [1]. Recently, the low-frequency sample or long-pressure reactivity index (L-PRx), which correlates well with PRx and is based on longer (1 min) average values of MAP and ICP, has been shown to be similarly associated with outcome after TBI and intracerebral hemorrhage [2,3,4]. Compared to PRx, however, L-PRx is likely less affected by high-frequency fluctuations and/or noise and can also display pressure reactivity changes that occur during slow MAP waves [5].

In the healthy brain, increases in MAP will induce cerebral vasoconstriction, with a subsequent decrease in ICP and cerebral blood volume. In cases of impaired cerebrovascular reactivity, increases in MAP will lead to an increase in ICP due to a passive response of the cerebral resistance vessels [1,2,3,4]. By this background, L-PRx permits a continuous estimation of cerebrovascular reactivity as a surrogate marker for CA, thereby reflecting the capacity of cerebral resistance vessels to modify their diameter in response to perfusion pressure changes [2,3,4]. After aSAH, CA is often compromised [19], and the normal hemodynamic response to SD can be inverted [20]. Different hemodynamic responses with different overlapping vascular components have been identified in the gyrencephalic brain [21,22,23]. Thus, progressively prolonged SD-induced spreading ischemia with intense vasoconstriction and transition from clustered SDs to a negative ultraslow potential were found when optoelectrodes were located directly over a newly developing delayed cerebral infarct detected by serial neuroimaging after SAH [24]. If it is associated with SD in clusters and ischemic hemodynamic responses, CA impairment could possibly be a predictor of these pathophysiological changes.

Additionally, the fact that L-PRx was more impaired in cases of higher ICP with potentially lower cerebral perfusion pressure appears to agree with our observation in patients with malignant hemispheric stroke, in which CA impairment followed a perfusion-dependent pattern, with more significant CA impairment at low cerebral perfusion levels [48]. Moreover, a pressure reactivity index such as L-PRx may also reflect a change in brain elasticity, which changes during SDs [49], and less adaptability to changes in MAP, produced by brain cytotoxic edema as a consequence of neuronal swelling [6] and dendritic beading that occurs during SDs [50]. However, this hypothesis needs to be tested in further studies. The pharmacological blocking of SDs could help answer those questions [21, 51, 52].

Here we found that L-PRx values during clustered SDs exceeded the cutoff value of 0.2, whereas L-PRx values of the combined single and clustered SDs did not. However, the presence of isolated SD still statistically differed from SD-free periods. In this sense, the elevation of the L-PRx value could still be meaningful, although it remained below the threshold value. Although some reports defined 0.3 as a cutoff value for autoregulatory failure, there is evidence from different authors during the last 25 years that support a cutoff value of 0.2 in indices such as PRx or L-PRx being associated with a significant disturbance of pressure reactivity and an increase in the mortality rate in different pathological conditions, such as TBI and intracerebral hemorrhage [3, 4, 12,13,14,15,16,17,18]. PRx values below 0.2 for a 2-h period have been associated with poor prognosis in patients with brain injury [13, 53]. Specific differences may arise in the measurement of ICP by using EVD and intraparenchymal devices. In this study, we presented data from two different cohorts that might differ slightly from their management protocols. Therefore, the true impact of SD on CA measured by either an EVD or an intraparenchymal probe for ICP monitoring should be taken cautiously. For example, the presence of an impaired CA during SD in clusters in HD patients, but not in BE patients, could reflect the effect of continuous measurements with an intraparenchymal probe instead of intermittent measurements through an EVD. In this regard, although EVD is the gold standard for ICP measurement [54], there is an ongoing debate regarding the choice of a monitoring device in patients with aSAH because it seems that EVD is associated with an increased risk of aneurysmal rebleeding, intracerebral hemorrhage, and infection, and guidelines to standardize indications for ICP measurement and therapeutic targets are scarce [55]. Intraparenchymal devices, on the contrary, are relatively easy to place and offer a lower rate of hemorrhage and infection, yet unlike EVD, they cannot be calibrated after placement [54, 55]. On the other hand, when using EVD, changes in intracranial elastance can occur as a result of therapeutic interventions during neurocritical care, such as CSF drainage [56], limiting the continuity of ICP data acquisition, which could impact CA measurements. Further evidence suggests that ICP monitoring by an open EVD may lead to a less reliable continuous assessment of CA [57].

The orexins (hypocretins) are a family of peptides found primarily in neurons in the lateral hypothalamus. Although the orexinergic system is generally thought to be the same across species, the orexins are involved in behaviors which show considerable interspecific variability. There are few direct cross-species comparisons of the distributions of cells and fibers containing these peptides. Here, we addressed the possibility that there might be important species differences by systematically examining and directly comparing the distribution of orexinergic neurons and fibers within the forebrains of species with very different patterns of sleep-wake behavior. be457b7860