Malnutrition and REM-sleep Deprivation Modulate in Rats the Impairment of Spreading Depression by a Single Sub-convulsing Dose of Pilocarpine

Vasconcelos, Carlos Augusto Carvalho de; Oliveira, João Augusto Farias de; Costa, Luis André de Oliveira; Guedes, Rubem Carlos Araújo

doi:10.1080/10284150412331281031

Cited by 22 publications

(7 citation statements)

References 36 publications

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“…17,18 As we have previously demonstrated in laboratory animals, drugs used with therapeutic purposes in neurological diseases present distinct effectiveness as a function of the nutritional status of the organism. 23,35,36 In line with the above evidence, we found that early malnutrition enhanced the antagonistic effects of lithium on CSD. These findings collectively indicate that the responsiveness of the CSD to distinct compounds may not be the same for all types of pharmacological substances.…”

Section: Lithium/nutrition Interaction On Csdsupporting

confidence: 88%

Lithium/nutrition interaction in the brain: A single lithium administration impairs spreading depression in malnourished, but not in well-nourished rats

Aguiar

Guedes

2011

Nutritional Neuroscience

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Lithium salts exert electrophysiological and behavioral effects in animals and humans and have been used clinically in the treatment of bipolar disorders. Little is known about the lithium/nutrition interaction in the developing brain. This work aimed to determine, in adult rats, whether treatment with a single dose of lithium chloride (LiCl) would influence the propagation of the brain excitability-related phenomenon known as cortical spreading depression (CSD). Male well-nourished (W; fed a lab chow diet with 22% protein; n=22) and previously protein-malnourished rats (M; fed a low-quality 8% protein diet; proteins mostly from vegetable source; n=20) were treated at 75-80 days of age with a single intraperitoneal injection of either 50 mg/kg LiCl (n=9 W and 10 M rats) or saline (n=13 W and 10 M rats). When the pups were 90-110 days, CSD was elicited at the frontal cortex and recorded during 4 hours at two cortical parietal points. In malnourished, but not in well-nourished rats, lithium treatment lowered CSD velocities (P < 0.05), in comparison with saline-injected animals. In a third group (n=23), in which the low-protein diet was quantitatively corrected to 22%, the lithium effect disappeared (n=12), compared to saline (n=11). Our results demonstrate a facilitating effect of malnutrition on the CSD-impairing action of a single lithium administration, suggesting a lithium/nutrition interaction.

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Section: Lithium/nutrition Interaction On Csdsupporting

confidence: 88%

Lithium/nutrition interaction in the brain: A single lithium administration impairs spreading depression in malnourished, but not in well-nourished rats

Aguiar

Guedes

2011

Nutritional Neuroscience

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“…The possible relationship between CSD and brain excitability has been investigated in our laboratory using the acute pilocarpine administration paradigm; both convulsing (Guedes and Cavalheiro, 1997) and sub-convulsing dosing with a single injection of pilocarpine (Vasconcelos et al, 2004; Guedes and Vasconcelos, 2008) decelerated CSD. In the present study, we treated young animals (PND35) over 21 days with a sub-convulsing dose of pilocarpine and confirmed its CSD decelerating action.…”

Section: Discussionmentioning

confidence: 99%

Sub-Convulsing Dose Administration of Pilocarpine Reduces Glycemia, Increases Anxiety-Like Behavior and Decelerates Cortical Spreading Depression in Rats Suckled on Various Litter Sizes

Francisco

Guedes

2018

Front. Neurosci.

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Epilepsy and malnutrition constitute two worldwide health problems affecting behavior and brain function. The cholinergic agonist pilocarpine (300–380 mg/kg; single administration) reproduces the human type of temporal lobe epilepsy in rats. Pilocarpine-induced epilepsy in rodents has been associated with glycemia, learning and memory and anxiety disturbances. Cortical spreading depression (CSD) is a neural response that has been linked to brain excitability disorders and its diseases, and has been shown to be antagonized by acute pilocarpine. This study aimed to further investigate the effect of chronic pilocarpine at a sub-convulsing dose on weight gain, blood glucose levels, anxiety-like behavior and CSD. In addition, we tested whether unfavorable lactation-induced malnutrition could modulate the pilocarpine effects. Wistar rats were suckled under normal size and large size litters (litters with 9 and 15 pups; groups L9 and L15, respectively). From postnatal days (PND) 35–55, these young animals received a daily intraperitoneal injection of pilocarpine (45 mg/kg/day), or vehicle (saline), or no treatment (naïve). On PND58, the animals were behaviorally tested in an open field apparatus. This was immediately followed by 6 h fasting and blood glucose measurement. At PND60–65, CSD was recorded, and its parameters (velocity of propagation, amplitude, and duration) were calculated. Compared to the control groups, pilocarpine-treated animals presented with reduced weight gain and lower glycemia, increased anxiety-like behavior and decelerated CSD propagation. CSD velocity was higher (p < 0.001) in the L15 groups in comparison to the corresponding groups in the L9 condition. The results demonstrate an influence of chronic (21-day) administration of a sub-convulsing, very low dose (45 mg/kg) of pilocarpine on CSD propagation, anxiety-like behavior, glycemia and body weight. Furthermore, data reinforce the hypothesis of a relationship between CSD and brain excitability. The lactation condition seems to differentially modulate these effects.

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“…Slow wave sleep is also associated with reductions in brain temperature and metabolic demand for oxygen and glucose, as well as replenishment of ATP and glycogen stores (Aalling et al, 2018;Caporale et al, 2021). REM sleep deprivation decreases the threshold for cortical spreading depressions which are found frequently after acquired brain injuries and thought to contribute to secondary brain injury (De Vasconcelos et al, 2004;Levesque et al, 2021). Interestingly, a recent study of analgesia and sedation after a variety of brain injuries found that benzodiazepine treatment increased the incidence of cortical spreading depressions (Hertle et al, 2012).…”

Section: Sleeping With One Eye Open Sleep Architecture Is Disrupted During Critical Illnessmentioning

confidence: 99%

Cognitive Dysfunction After Analgesia and Sedation: Out of the Operating Room and Into the Pediatric Intensive Care Unit

Turner

Sullivan

Drury

et al. 2021

Front. Behav. Neurosci.

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In the midst of concerns for potential neurodevelopmental effects after surgical anesthesia, there is a growing awareness that children who require sedation during critical illness are susceptible to neurologic dysfunctions collectively termed pediatric post-intensive care syndrome, or PICS-p. In contrast to healthy children undergoing elective surgery, critically ill children are subject to inordinate neurologic stress or injury and need to be considered separately. Despite recognition of PICS-p, inconsistency in techniques and timing of post-discharge assessments continues to be a significant barrier to understanding the specific role of sedation in later cognitive dysfunction. Nonetheless, available pediatric studies that account for analgesia and sedation consistently identify sedative and opioid analgesic exposures as risk factors for both in-hospital delirium and post-discharge neurologic sequelae. Clinical observations are supported by animal models showing neuroinflammation, increased neuronal death, dysmyelination, and altered synaptic plasticity and neurotransmission. Additionally, intensive care sedation also contributes to sleep disruption, an important and overlooked variable during acute illness and post-discharge recovery. Because analgesia and sedation are potentially modifiable, understanding the underlying mechanisms could transform sedation strategies to improve outcomes. To move the needle on this, prospective clinical studies would benefit from cohesion with regard to datasets and core outcome assessments, including sleep quality. Analyses should also account for the wide range of diagnoses, heterogeneity of this population, and the dynamic nature of neurodevelopment in age cohorts. Much of the related preclinical evidence has been studied in comparatively brief anesthetic exposures in healthy animals during infancy and is not generalizable to critically ill children. Thus, complementary animal models that more accurately “reverse translate” critical illness paradigms and the effect of analgesia and sedation on neuropathology and functional outcomes are needed. This review explores the interactive role of sedatives and the neurologic vulnerability of critically ill children as it pertains to survivorship and functional outcomes, which is the next frontier in pediatric intensive care.

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Malnutrition and REM-sleep Deprivation Modulate in Rats the Impairment of Spreading Depression by a Single Sub-convulsing Dose of Pilocarpine

Cited by 22 publications

References 36 publications

Lithium/nutrition interaction in the brain: A single lithium administration impairs spreading depression in malnourished, but not in well-nourished rats

Lithium/nutrition interaction in the brain: A single lithium administration impairs spreading depression in malnourished, but not in well-nourished rats

Sub-Convulsing Dose Administration of Pilocarpine Reduces Glycemia, Increases Anxiety-Like Behavior and Decelerates Cortical Spreading Depression in Rats Suckled on Various Litter Sizes

Cognitive Dysfunction After Analgesia and Sedation: Out of the Operating Room and Into the Pediatric Intensive Care Unit

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