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A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats

Post-stroke depression (PSD) is the most recurrent of all psychiatric complications resulting from an ischemic stroke. A greater majority (about 60%) of ...

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A Complex Diving-For-Food Task to Investigate Social Organization and Interactions in Rats

For many species, where status is a vital motivator that can affect health, social hierarchies influence behavior. Social hierarchies that include ...

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A Metric Test for Assessing Spatial Working Memory in Adult Rats Following Traumatic Brain Injury

Impairments to sensory, short-term, and long-term memory are common side effects after traumatic brain injury (TBI). Due to the ethical limitations of ...

Ben-Gurion University of the Negev

Soroka Medical Center, Ben-Gurion University of the Negev

Isoflurane-anesthetized rats submitted to a closed head injury (CHI) display a significant decrease of their blood glutamate levels. Having demonstrated that a decrease of blood L-glutamate (glutamate) causes an increase of the driving force for a spontaneous brain-to-blood glutamate efflux, and consequently affords brain neuroprotection, we investigated here the possible mechanisms which can affect blood glutamate levels. Reasoning that the spontaneous decrease of blood glutamate levels post CHI could be part of a stress response, we observed that the stress involved in tail artery catheterization under isoflurane anesthesia does not affect blood glutamate levels. Investigating in naïve rats the stress effectors, we found that corticotropin-releasing factor (CRF) significantly decreased blood glutamate levels. Pretreatment with antalarmine (a selective type-1 CRF receptor antagonist) occludes the CRF-mediated decrease in blood glutamate levels. In contrast, the adrenocorticotrophic hormone (ACTH) did not affect blood glutamate levels. Investigating the effectors of the sympathetic/adrenomedullary system, we observed that in naïve rats, adrenaline but not noradrenaline decreased blood glutamate levels. Confirming the role of adrenaline, propranolol pretreatment (a non-selective beta-antagonist) prevented the spontaneous decrease of blood glutamate observed post CHI. On the strength of these results, we further observed that isoproterenol (a beta(1/2)-selective adrenoreceptor agonist) produced a marked sustained decrease in blood glutamate levels. These results suggest that stress induces a decrease of blood glutamate levels partly via the activation of peripheral CRF receptors and the activation of the beta-adrenoreceptors. We propose that this newly identified component of the stress response could be a peripherally mediated defense mechanism of the injured brain against the deleterious effects of excess glutamate.

Regulation of blood L-glutamate levels by stress as a possible brain defense mechanism.

Isoflurane-anesthetized rats subjected to traumatic brain injury (TBI) show a transient reduction in blood L-glutamate levels. Having previously observed that isoproterenol produces a sustained decrease in blood glutamate levels in naive rats, we investigated the possible effects of nonselective and selective β1 and β2 adrenergic agonists and antagonists both on blood glutamate levels and on the neurological outcomes of rats subjected to TBI.

β2 adrenergic-mediated reduction of blood glutamate levels and improved neurological outcome after traumatic brain injury in rats.

Decreasing blood glutamate concentrations after traumatic brain injury accelerates brain-to-blood glutamate efflux, leading to improved neurologic outcomes. The authors hypothesize that treatment with blood glutamate scavengers should reduce neuronal cell loss, whereas administration of glutamate should worsen outcomes. The authors performed histologic studies of neuronal survival in the rat hippocampus after traumatic brain injury and treatment with blood glutamate scavengers.

Effect of glutamate and blood glutamate scavengers oxaloacetate and pyruvate on neurological outcome and pathohistology of the hippocampus after traumatic brain injury in rats.

The Aintree intubating catheter (Cook® Medical Inc., Bloomington, IN, USA) has been shown to successfully facilitate difficult intubations when other methods have failed. The Aintree intubating catheter (Cook® Medical Inc., Bloomington, IN, USA) has a fixed length of 56 cm, and it has been suggested in the literature that it may be too short for safe use in patients who are tall.

Novel use of an exchange catheter to facilitate intubation with an Aintree catheter in a tall patient with a predicted difficult airway: a case report.

Several motor-function scales have been developed to assess neurological function in animal models of stroke, subarachnoid hemorrhage and closed head injury. We hypothesize that the location of arterial and venous catheters, even in the absence of brain injury, may impact rats' motor performance. Our study examined the effect of catheter location, rate of infection and the time required for catheter placement. We further describe an original technique of tail artery cannulation without exposure of the artery. Sixty-one rats were anesthetized and randomly assigned to one of seven groups, including no catheter, tail artery or artery + vein catheters, or femoral artery or artery + vein catheters. A neurological severity score (NSS) was determined at 1 h, 24 h and 48 h after surgical preparation or catheter placement. NSS at 1 h after placement of unilateral and bilateral femoral catheters was higher than the NSS observed at 1 h after placement of tail arterial and venous catheters (P < 0.01). The NSS also was higher at 24 h in the bilateral femoral catheter groups as compared with the tail catheter groups (P < 0.05). There were no differences in the NSS observed between the groups that had tail catheters and the sham group at 1 h, 24 h or 48 h. Infection rate at the site of catheter placement and the time required for catheter placement was also higher in the femoral catheter groups (P < 0.001). Thus, we propose that the line location may bias a study's results and lead to deceptive interpretations of neurological assessment following rat head injury. Compared to femoral vessels, tail blood vessels are preferable locations for lines placement.

Anatomical location of arterial and venous lines significantly affects motor performance in rats.

Excessive concentrations of L-glutamate (glutamate) have been found to posses neurotoxic properties. This study investigates how stress induced by strong physical exercise effects blood glutamate, 2-ketoglutarate, Alanine aminotransferase (ALT) and Aspartate Aminotransferase (AST) levels. The relationship between muscle damage caused by strong physical exercise and blood glutamate levels was also examined. Twenty-two healthy volunteers engaged in intense veloergometry ("spinning") for a duration of 60 minutes. Two 10 minute peaks of extremely intense exercise were performed at 10 minutes and 50 minutes after the start of exercise. After 60 minutes of exercise, volunteers were monitored for an additional 180 minutes in resting conditions. Blood samples for determination of glutamate and 2-ketoglutarate levels were collected prior to exercise and then every 30 min for entire experiment. Blood samples were also taken at those time points to measure glutamate, 2-ketoglutarate, AST, ALT, creatine phosphokinase (CPK), myoglobin, lactate and venous blood gas levels. Blood glutamate levels were significantly elevated throughout the exercise session (P less than 0.001) and then returned to baseline levels at the cessation of exercise. 2-ketoglutarate, a product of glutamate metabolism, reached significantly elevated levels at 30 minutes (P less than 0.01) from the start of exercise and remained elevated up to 240 minutes post exercise initiation (P less than 0.001). AST and ALT levels were elevated at 60 minutes when compared to baseline. AST levels remained elevated at 240 minutes, unlike ALT levels which returned to baseline values at 240 minutes. Strong physical exercise leads to a significant elevation in blood glutamate, most likely as a result of skeletal muscle damage. 2-ketoglutarate was also found to be elevated for long periods of time, reflecting an ongoing process of glutamate breakdown. Elevated concentrations of AST and ALT in plasma reflect the importance of these enzymes in the maintenance of stable blood glutamate concentrations.

Effects of strong physical exercise on blood glutamate and its metabolite 2-ketoglutarate levels in healthy volunteers.

Patients who undergo surgical procedures that impair the integrity of the chest wall frequently experience extremely severe postoperative pain. Opiates and weaker analgesics, such as nonsteroidal anti-inflammatory drugs (NSAIDs), are not sufficiently effective in achieving control of severe pain and might cause respiratory and gastrointestinal complications. In the past decade, there has been an increased interest in the use of regional nerve blocks for post-thoracoscopy and post-thoracotomy analgesia.

ArticleTotal : 3	Year
Publication title Cited by 11	2019
Publication title	2021
Publication title Cited by 4	2021

Article	Year
Regulation of blood L-glutamate levels by stress as a possible brain defense mechanism. Experimental neurology\| PubMed ID: 20493841	2010
β2 adrenergic-mediated reduction of blood glutamate levels and improved neurological outcome after traumatic brain injury in rats. Journal of neurosurgical anesthesiology\| PubMed ID: 21979171	2012
Effect of glutamate and blood glutamate scavengers oxaloacetate and pyruvate on neurological outcome and pathohistology of the hippocampus after traumatic brain injury in rats. Anesthesiology\| PubMed ID: 22129535	2012
Novel use of an exchange catheter to facilitate intubation with an Aintree catheter in a tall patient with a predicted difficult airway: a case report. Journal of medical case reports\| PubMed ID: 22502764	2012
Anatomical location of arterial and venous lines significantly affects motor performance in rats. Animal science journal = Nihon chikusan Gakkaiho\| PubMed ID: 22943533	2012
Effects of strong physical exercise on blood glutamate and its metabolite 2-ketoglutarate levels in healthy volunteers. Acta neurobiologiae experimentalis\| PubMed ID: 23377269	2012
Ultrasound-guided serratus anterior plane block for analgesia after thoracic surgery. Journal of pain research\| PubMed ID: 30881105	2019

Michael Dubilet

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