Chronic lithium administration potentiates brain arachidonic acid signaling at rest and during cholinergic activation in awake rats
Studies were performed to determine if the reported ‘proconvulsant’ action of lithium in rats given cholinergic drugs is related to receptor‐initiated phospholipase A2 signaling via arachidonic acid. Regional brain incorporation coefficients k* of intravenously injected [1‐14C]arachidonic acid, whic...
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| Published in | Journal of neurochemistry Vol. 85; no. 6; pp. 1553 - 1562 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Science Ltd
01.06.2003
Blackwell |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-3042 1471-4159 |
| DOI | 10.1046/j.1471-4159.2003.01811.x |
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| Abstract | Studies were performed to determine if the reported ‘proconvulsant’ action of lithium in rats given cholinergic drugs is related to receptor‐initiated phospholipase A2 signaling via arachidonic acid. Regional brain incorporation coefficients k* of intravenously injected [1‐14C]arachidonic acid, which represent this signaling, were measured by quantitative autoradiography in unanesthetized rats at baseline and following administration of subconvulsant doses of the cholinergic muscarinic agonist, arecoline. In rats fed LiCl for 6 weeks to produce a therapeutically relevant brain lithium concentration, the mean baseline values of k* in brain auditory and visual areas were significantly greater than in rats fed control diet. Arecoline at doses of 2 and 5 mg/kg intraperitoneally increased k* in widespread brain areas in rats fed the control diet as well as the LiCl diet. However, the arecoline‐induced increments often were significantly greater in the LiCl‐fed than in the control diet‐fed rats. Lithium's elevation of baseline k* in auditory and visual regions may correspond to its ability in humans to increase auditory and visual evoked responses. Additionally, its augmentation of the k* responses to arecoline may underlie its reported ‘proconvulsant’ action with cholinergic drugs, as arachidonic acid and its eicosanoid metabolites can increase neuronal excitability and seizure propagation. |
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| AbstractList | Studies were performed to determine if the reported ‘proconvulsant’ action of lithium in rats given cholinergic drugs is related to receptor‐initiated phospholipase A2 signaling via arachidonic acid. Regional brain incorporation coefficients
k*
of intravenously injected [1‐
14
C]arachidonic acid, which represent this signaling, were measured by quantitative autoradiography in unanesthetized rats at baseline and following administration of subconvulsant doses of the cholinergic muscarinic agonist, arecoline. In rats fed LiCl for 6 weeks to produce a therapeutically relevant brain lithium concentration, the mean baseline values of
k*
in brain auditory and visual areas were significantly greater than in rats fed control diet. Arecoline at doses of 2 and 5 mg/kg intraperitoneally increased
k*
in widespread brain areas in rats fed the control diet as well as the LiCl diet. However, the arecoline‐induced increments often were significantly greater in the LiCl‐fed than in the control diet‐fed rats. Lithium's elevation of baseline
k*
in auditory and visual regions may correspond to its ability in humans to increase auditory and visual evoked responses. Additionally, its augmentation of the
k*
responses to arecoline may underlie its reported ‘proconvulsant’ action with cholinergic drugs, as arachidonic acid and its eicosanoid metabolites can increase neuronal excitability and seizure propagation. Studies were performed to determine if the reported `proconvulsant' action of lithium in rats given cholinergic drugs is related to receptor-initiated phospholipase A2 signaling via arachidonic acid. Regional brain incorporation coefficients k* of intravenously injected [1- super(14) C]arachidonic acid, which represent this signaling, were measured by quantitative autoradiography in unanesthetized rats at baseline and following administration of subconvulsant doses of the cholinergic muscarinic agonist, arecoline. In rats fed LiCl for 6 weeks to produce a therapeutically relevant brain lithium concentration, the mean baseline values of k* in brain auditory and visual areas were significantly greater than in rats fed control diet. Arecoline at doses of 2 and 5 mg/kg intraperitoneally increased k* in widespread brain areas in rats fed the control diet as well as the LiCl diet. However, the arecoline-induced increments often were significantly greater in the LiCl-fed than in the control diet-fed rats. Lithium's elevation of baseline k* in auditory and visual regions may correspond to its ability in humans to increase auditory and visual evoked responses. Additionally, its augmentation of the k* responses to arecoline may underlie its reported `proconvulsant' action with cholinergic drugs, as arachidonic acid and its eicosanoid metabolites can increase neuronal excitability and seizure propagation. Studies were performed to determine if the reported 'proconvulsant' action of lithium in rats given cholinergic drugs is related to receptor-initiated phospholipase A2 signaling via arachidonic acid. Regional brain incorporation coefficients k* of intravenously injected [1-14C]arachidonic acid, which represent this signaling, were measured by quantitative autoradiography in unanesthetized rats at baseline and following administration of subconvulsant doses of the cholinergic muscarinic agonist, arecoline. In rats fed LiCl for 6 weeks to produce a therapeutically relevant brain lithium concentration, the mean baseline values of k* in brain auditory and visual areas were significantly greater than in rats fed control diet. Arecoline at doses of 2 and 5 mg/kg intraperitoneally increased k* in widespread brain areas in rats fed the control diet as well as the LiCl diet. However, the arecoline-induced increments often were significantly greater in the LiCl-fed than in the control diet-fed rats. Lithium's elevation of baseline k* in auditory and visual regions may correspond to its ability in humans to increase auditory and visual evoked responses. Additionally, its augmentation of the k* responses to arecoline may underlie its reported 'proconvulsant' action with cholinergic drugs, as arachidonic acid and its eicosanoid metabolites can increase neuronal excitability and seizure propagation. Studies were performed to determine if the reported 'proconvulsant' action of lithium in rats given cholinergic drugs is related to receptor-initiated phospholipase A2 signaling via arachidonic acid. Regional brain incorporation coefficients k* of intravenously injected [1-14C]arachidonic acid, which represent this signaling, were measured by quantitative autoradiography in unanesthetized rats at baseline and following administration of subconvulsant doses of the cholinergic muscarinic agonist, arecoline. In rats fed LiCl for 6 weeks to produce a therapeutically relevant brain lithium concentration, the mean baseline values of k* in brain auditory and visual areas were significantly greater than in rats fed control diet. Arecoline at doses of 2 and 5 mg/kg intraperitoneally increased k* in widespread brain areas in rats fed the control diet as well as the LiCl diet. However, the arecoline-induced increments often were significantly greater in the LiCl-fed than in the control diet-fed rats. Lithium's elevation of baseline k* in auditory and visual regions may correspond to its ability in humans to increase auditory and visual evoked responses. Additionally, its augmentation of the k* responses to arecoline may underlie its reported 'proconvulsant' action with cholinergic drugs, as arachidonic acid and its eicosanoid metabolites can increase neuronal excitability and seizure propagation.Studies were performed to determine if the reported 'proconvulsant' action of lithium in rats given cholinergic drugs is related to receptor-initiated phospholipase A2 signaling via arachidonic acid. Regional brain incorporation coefficients k* of intravenously injected [1-14C]arachidonic acid, which represent this signaling, were measured by quantitative autoradiography in unanesthetized rats at baseline and following administration of subconvulsant doses of the cholinergic muscarinic agonist, arecoline. In rats fed LiCl for 6 weeks to produce a therapeutically relevant brain lithium concentration, the mean baseline values of k* in brain auditory and visual areas were significantly greater than in rats fed control diet. Arecoline at doses of 2 and 5 mg/kg intraperitoneally increased k* in widespread brain areas in rats fed the control diet as well as the LiCl diet. However, the arecoline-induced increments often were significantly greater in the LiCl-fed than in the control diet-fed rats. Lithium's elevation of baseline k* in auditory and visual regions may correspond to its ability in humans to increase auditory and visual evoked responses. Additionally, its augmentation of the k* responses to arecoline may underlie its reported 'proconvulsant' action with cholinergic drugs, as arachidonic acid and its eicosanoid metabolites can increase neuronal excitability and seizure propagation. |
| Author | Bell, Jane M. Basselin, Mireille Chang, Lisa Seemann, Ruth Rapoport, Stanley I. |
| Author_xml | – sequence: 1 givenname: Mireille surname: Basselin fullname: Basselin, Mireille – sequence: 2 givenname: Lisa surname: Chang fullname: Chang, Lisa – sequence: 3 givenname: Ruth surname: Seemann fullname: Seemann, Ruth – sequence: 4 givenname: Jane M. surname: Bell fullname: Bell, Jane M. – sequence: 5 givenname: Stanley I. surname: Rapoport fullname: Rapoport, Stanley I. |
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| Keywords | Rat Enzyme phospholipase A2 Rodentia Central nervous system Excitability Lithium Esterases Arachidonic acid brain Phospholipase A Carboxylic ester hydrolases Signal transduction muscarinic Cholinergic receptor Vertebrata Mammalia Neuron Eicosanoid Hydrolases Muscarinic receptor Brain (vertebrata) stimulation |
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| Snippet | Studies were performed to determine if the reported ‘proconvulsant’ action of lithium in rats given cholinergic drugs is related to receptor‐initiated... Studies were performed to determine if the reported 'proconvulsant' action of lithium in rats given cholinergic drugs is related to receptor-initiated... Studies were performed to determine if the reported `proconvulsant' action of lithium in rats given cholinergic drugs is related to receptor-initiated... |
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| SubjectTerms | Animals arachidonic acid Arachidonic Acid - administration & dosage Arachidonic Acid - pharmacokinetics Arachidonic Acid - physiology Arecoline - administration & dosage Autoradiography Biochemistry and metabolism Biological and medical sciences Body Weight - drug effects brain Brain - drug effects Brain - metabolism Carbon Radioisotopes Central nervous system Cholinergic Agonists - administration & dosage Drug Administration Routes Drug Administration Schedule Fundamental and applied biological sciences. Psychology lithium Lithium Chloride - administration & dosage Male muscarinic phospholipase A2 Rats Rats, Inbred F344 Rest - physiology Seizures - chemically induced Seizures - prevention & control Signal Transduction - drug effects Signal Transduction - physiology stimulation Time Vertebrates: nervous system and sense organs Wakefulness - physiology |
| Title | Chronic lithium administration potentiates brain arachidonic acid signaling at rest and during cholinergic activation in awake rats |
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