Effects of emodin on synaptic transmission in rat hippocampal CA1 pyramidal neurons in vitro

Autor: Hiroshi Hasuo, Jian-Wen Gu, Takashi Akasu, Mitsue Takeya
Rok vydání: 2005
Předmět:
Male
Adenosine
Emodin
Adenosine Deaminase
Excitotoxicity
In Vitro Techniques
Pharmacology
Neurotransmission
Biology
Bicuculline
Inhibitory postsynaptic potential
medicine.disease_cause
Hippocampus
Synaptic Transmission
Neuroprotection
Cellular and Molecular Neuroscience
chemistry.chemical_compound
Theophylline
Quinoxalines
Excitatory Amino Acid Agonists
medicine
Animals
Drug Interactions
Enzyme Inhibitors
Rats
Wistar

Dose-Response Relationship
Drug

Pyramidal Cells
musculoskeletal
neural
and ocular physiology

Glutamate receptor
Excitatory Postsynaptic Potentials
Neural Inhibition
Valine
Rats
Electrophysiology
medicine.anatomical_structure
Purinergic P1 Receptor Antagonists
nervous system
chemistry
Biochemistry
Schaffer collateral
Excitatory postsynaptic potential
Excitatory Amino Acid Antagonists
Zdroj: Neuropharmacology. 49:103-111
ISSN: 0028-3908
DOI: 10.1016/j.neuropharm.2005.02.003
Popis: Rhubarb extracts provide neuroprotection after brain injury, but the mechanism of this protective effect is not known. The present study tests the hypothesis that rhubarb extracts interfere with the release of glutamate by brain neurons and, therefore, reduce glutamate excitotoxicity. To this end, the effects of emodin, an anthraquinone derivative extracted from Rheum tanguticum Maxim. Ex. Balf, on the synaptic transmission of CA1 pyramidal neurons in rat hippocampus were studied in vitro. The excitatory postsynaptic potential (EPSP) was depressed by bath-application of emodin (0.3-30 microM). Paired-pulse facilitation (PPF) of the EPSP was significantly increased by emodin. The monosynaptic inhibitory postsynaptic potential (IPSP) recorded in the presence of glutamate receptor antagonists (DNQX and AP5) was not altered by emodin. Emodin decreased the frequency, but not the amplitude, of the miniature EPSP (mEPSP). The inhibition of the EPSP induced by emodin was blocked by either 8-CPT, an adenosine A1 receptor antagonist, or by adenosine deaminase. These results suggest that emodin inhibits the EPSP by decreasing the release of glutamate from Schaffer collateral/commissural terminals via the activation of adenosine A1 receptors in rat hippocampal CA1 area and that the neuroprotective effects of rhubarb extracts may result from decreased glutamate excitotoxicity.
Databáze: OpenAIRE