Glutamate transport in rat cerebellar granule cells is impaired by inorganic epileptogenic agents

Mafra, Roberta Amaral; Araújo, Demétrius Antônio Machado de; Beirão, Paulo Sérgio Lacerda; Cruz, Jáder Santos

doi:10.1016/s0304-3940(01)02069-9

Cited by 8 publications

(5 citation statements)

References 19 publications

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“…), ceftriaxone may, in particular, reduce inhibition of GluTs by some polyvalent metal ions (Co, Ni, Mn) (Mafra et al . ; Mutkus et al . ).…”

Section: Drugs and Compounds That Both Modulate Glutamate Uptake And mentioning

confidence: 99%

“…It cannot be ruled out that such structural/conformational modifications influence availability of GLT1 at the cell surface or render GLT1 monomers more susceptible to dimerization. Furthermore, because of the pronounced metal-chelating properties of b-lactams (Ji et al 2005), ceftriaxone may, in particular, reduce inhibition of GluTs by some polyvalent metal ions (Co, Ni, Mn) (Mafra et al 2001;Mutkus et al 2005).…”

Section: Analgesic Effects Of Up-regulation Of Glut By Viral Gene Tramentioning

confidence: 99%

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High‐affinity glutamate transporters in chronic pain: an emerging therapeutic target

Gegelashvili

Bjerrum

2014

Journal of Neurochemistry

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Neurons responsible for sensing noxious stimuli and conducting pain signals from periphery to the spinal cord are predominantly glutamatergic. Members of the SLC1A family of highaffinity glutamate transporters (GluTs) are differentially expressed in sensory neurons and surrounding glial cells. These plasma membrane proteins along with glutamate/ cystine exchanger, light chain of cystine/glutamate exchanger, are responsible for fine tuning of extracellular glutamate concentrations and, thus, for modulation of excitatory signalling in the spinal cord. Emerging data point at key roles of GluTs in molecular mechanisms of chronic pain and analgesia, incl. development of opioid tolerance. Pharmacological inhibition or antisense down-regulation of spinal GluTs can induce/aggravate pain behaviours, whereas increasing of expression of GluTs by viral gene transfer or positive pharmacological modulators can mitigate chronic pain. Furthermore, some drugs, originally introduced for targeting different pathological conditions, but in parallel exhibiting analgesic properties (e.g. anti-convulsants valproate and riluzole, b-lactam-and tetracycline antibiotics, tricyclic anti-depressants), can enhance glutamate transport in the spinal cord. Thus, molecular modulation of GluTs may turn into prospective therapeutic approach for the management of chronic pain. However, precise pharmacological targeting of this transport system requires in-depth elucidation of molecular factors and signalling pathways underlying expression and activity of individual GluT subtypes, including their splice variants.

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“…), ceftriaxone may, in particular, reduce inhibition of GluTs by some polyvalent metal ions (Co, Ni, Mn) (Mafra et al . ; Mutkus et al . ).…”

Section: Drugs and Compounds That Both Modulate Glutamate Uptake And mentioning

confidence: 99%

Section: Analgesic Effects Of Up-regulation Of Glut By Viral Gene Tramentioning

confidence: 99%

High‐affinity glutamate transporters in chronic pain: an emerging therapeutic target

Gegelashvili

Bjerrum

2014

Journal of Neurochemistry

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“…Animal experiments aiming at determining the mechanisms of cerebellar seizures describe damage to the Purkinje cells (Gonzalez-Maciel et al, 2001), and some metabolic alterations in the cerebellum following seizures, such as a decrease in cerebellar GABA content (Carmody and Brennan, 2010). It was also noted that cerebellar granule cell glutamate transporters are inhibited during seizure-like conditions in vitro, which may also have implications in vivo (Mafra et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemistry of cerebellar seizures: Mossy fiber afferents play an important role in seizure spread and initiation in the rat

et al. 2015

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“…Studies with nickel and other metals, such as manganese, indicate that in their volatile form, these metals can be taken up in the primary olfactory neurons and be transported transneuronally to olfactory bulbs and even further into other areas of the brain (9). Animal studies suggest that inhibition of the glutamate transporter may be one mechanism explaining the seizures induced by nickel exposure (10).…”

Section: Discussionmentioning

confidence: 99%

First Epileptic Seizure Induced by Occupational Nickel Poisoning

Denays¹,

Kumba

Lison

et al. 2005

Epilepsia

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Summary: Toxic causes of seizures are numerous: alcohol and other substances of abuse, drugs, and industrial and household products. However, in the absence of a clearly suggestive history and/or associated symptoms and signs, identification of the toxic origin of new-onset seizures may be extremely difficult. We report here the case of a patient admitted in our hospital after a single generalized tonic-clonic seizure. The remarkable coincidence that a colleague of his, with whom he was working to clean the same workshop, had been admitted 1 week earlier for respiratory distress, coma, and de novo nonconvulsive focal status epilepticus, led us to consider a possible toxicologic etiology. Urine analysis revealed a high nickel concentration, suggestive of acute nickel poisoning. Key Words: Seizures-PoisoningNickel.Toxic causes of seizures are numerous: alcohol and other substances of abuse, drugs, and industrial and household products. However, in the absence of a clearly suggestive history and/or associated symptoms and signs, identification of the toxic origin of new-onset seizures may be extremely difficult. We report here the case of a patient admitted in our hospital after a single generalized tonic-clonic seizure. The remarkable coincidence that a colleague of his, with whom he was working to clean the same workshop, had been admitted 1 week earlier for respiratory distress, coma, and de novo nonconvulsive focal status epilepticus, led us to suspect a possible common toxic origin. CASE REPORTThe patient was a 43-year-old man admitted to our hospital after an inaugural generalized tonic-clonic seizure. His medical and surgical history was unremarkable. The patient did not take or had not recently stopped any medication. He did not abuse alcohol or any other substance and did not recently modify his sleep or food habits. No familial history of epilepsy was known. He had worked for a couple of weeks in a car body-repair workshop where he was cleaning the ceilings of the building. On admission, physical and neurologic examinations were normal, Accepted January 27, 2005. Address correspondence and reprint requests to Dr. D. De Bels at Intensive care Unit, Salle 92, Brugmann University Hospital, Free University of Brussels, 4 Van Gehuchten Plein, B 1020 Brussels, Belgium. E-mail: david.debels@chu-brugmann.be except for a mild drowsiness attributed to a postictal state. No meningeal signs were seen. Prolactin and lactate levels were high on admission, 36.8 ng/ml (2.5-11) and 122.8 mg/dl (9-16), respectively. HbCO was normal (<5%). Glycemia and other routine blood analyses were within normal values. EEG performed a few hours later showed diffuse slow waves. Brain CT and MRI scans were normal. A diagnosis of first idiopathic generalized seizure was presumed, until we were informed that a colleague of the patient, with whom he was working to clean the same workshop, had been admitted 1 week earlier in the same hospital for respiratory distress, coma, and de novo nonconvulsant focal status epilepticus [global aphasia a...

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Glutamate transport in rat cerebellar granule cells is impaired by inorganic epileptogenic agents

Cited by 8 publications

References 19 publications

High‐affinity glutamate transporters in chronic pain: an emerging therapeutic target

High‐affinity glutamate transporters in chronic pain: an emerging therapeutic target

Immunohistochemistry of cerebellar seizures: Mossy fiber afferents play an important role in seizure spread and initiation in the rat

First Epileptic Seizure Induced by Occupational Nickel Poisoning

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