{"id":"9a9ebebb-f8c0-5b17-aae2-9567a74c5a12","stable_key":"9a47f338-d127-5e4d-abf6-e99056833a69:d-aspartate-terminal-glutamate","predicate":"potentiates_tested","statement":"D-aspartate at 10 micromolar enhanced potassium-evoked glutamate release in cortical synaptosomes superfused with TBOA; NMDA, AMPA/kainate and mGlu5 antagonists attenuated or prevented the effect.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"8361393b-99f3-5e3a-80ab-4678c496eaa7","mechanism_event_label":"Receptor-sensitive feedback changed release under an uptake-blocked assay condition.","subject":{"id":"b3404670-6db1-517f-b9a0-27ecfaac558b","slug":"d-aspartate","display_name":"D-Aspartate","entity_type_key":"small_molecule"},"object":{"id":"fb9f458d-456f-5c07-8f65-b4c6334c1e1d","slug":"mouse-cortical-terminal-glutamate-release","display_name":"Glutamate release from mouse cortical synaptosomes","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"8361393b-99f3-5e3a-80ab-4678c496eaa7","stable_key":"9a47f338-d127-5e4d-abf6-e99056833a69:d-aspartate-terminal-glutamate-event","event_type":"observed_relationship","label":"Receptor-sensitive feedback changed release under an uptake-blocked assay condition.","description":"D-aspartate at 10 micromolar enhanced potassium-evoked glutamate release in cortical synaptosomes superfused with TBOA; 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15 mM potassium stimulus, 10 micromolar TBOA.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"This is evoked release under transporter blockade, not basal release in an intact human brain.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit.","comparator":null,"unit":null,"notes":"","entity":{"slug":"d-aspartate","display_name":"D-Aspartate","entity_type_key":"small_molecule"}},{"dimension":"plain_language","value_text":"Receptor-sensitive feedback changed release under an uptake-blocked assay condition.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"e9aa1aba-3c4a-5529-87c0-feea8dcaf044","evidence_kind":"source_excerpt","locator":"Lines 232-238","start_line":232,"end_line":238,"excerpt":"## d-aspartate-terminal-glutamate\nReceptor-sensitive feedback changed release under an uptake-blocked assay condition.\nD-aspartate at 10 micromolar enhanced potassium-evoked glutamate release in cortical synaptosomes superfused with TBOA; NMDA, AMPA/kainate and mGlu5 antagonists attenuated or prevented the effect.\nModel: Mouse cortical terminals; 15 mM potassium stimulus, 10 micromolar TBOA.\nLimitations: This is evoked release under transporter blockade, not basal release in an intact human brain.\nEvidence access: Primary full text\nOlanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288","model_system":"Mouse cortical terminals; 15 mM potassium stimulus, 10 micromolar TBOA.","directness":"reported_statement","verification_status":"source_derived_draft","notes":"Original curation paraphrase; evidence access and experimental limitations specified.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"3751103e-e256-5615-b24f-39cc76ccfb47","stable_key":"import-9a47f338-d127-5e4d-abf6-e99056833a69","title":"D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19)","document_type":"imported_text","citation_label":"AI-assisted research curation; primary references, access levels and experimental limitations individually identified. 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