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Neurotransmitter released from neurons is known to signal to neighbouring neurons and glia. Here we demonstrate an additional signalling pathway in which glutamate is released from astrocytes and causes an NMDA (N-methyl-D-aspartate) receptor-mediated increase in neuronal calcium. Internal calcium was elevated and glutamate release stimulated by application(More)
Earlier studies in live pancreatic acinar cells identified new cellular structures at the cell plasma membrane called 'pits' and 'depressions', where membrane-bound secretory vesicles dock and fuse to release vesicular contents. In the current study, using atomic force microscopy we identify similar structures at the plasma membrane of GH-secreting cells of(More)
The mechanism responsible for the ability of bradykinin to cause calcium-dependent release of glutamate from astrocytes in vitro was investigated. The glutamate transport inhibitor, dihydrokainate, did not block bradykinin-induced glutamate release, and bradykinin did not cause cell swelling. These data exclude the involvement of glutamate transporters or(More)
An MCM-41 type mesoporous silica nanosphere-based (MSN) controlled-release delivery system has been synthesized and characterized using surface-derivatized cadmium sulfide (CdS) nanocrystals as chemically removable caps to encapsulate several pharmaceutical drug molecules and neurotransmitters inside the organically functionalized MSN mesoporous framework.(More)
Bradykinin induces receptor-mediated calcium-dependent release of glutamate from cultured astrocytes through a mechanism that is neither due to cell-swelling mechanism nor due to the reversal of the glutamate transporter. Astrocytes may thus release glutamate using a mechanism resembling the neuronal vesicular release of neurotransmitters. Synaptobrevin is(More)
Bradykinin caused a receptor-mediated increase in release of the excitatory amino acids (EAAs) glutamate and aspartate from Schwann cell cultures obtained from dorsal root ganglia (DRG) together with an increase in the cytoplasmic level of free calcium. Perturbations which inhibited brady-kinin-induced calcium mobilization prevented the release of EAAs from(More)
The role of subtypes of excitatory amino acid receptor in synaptic transmission in the spinal dorsal horn has been studied in an in vitro slice preparation with well-preserved afferent inputs to the dorsal horn. Intracellular recordings were made from 30 dorsal horn neurons in laminae I-III of 18-28 day old rats. Superfusion of the slice with a Mg2+ zero(More)
We synthesized a MCM-41-type mesoporous silica nanosphere (MSN)-based gene transfection system, where second generation (G2) polyamidoamines (PAMAMs) were covalently attached to the surface of MSN. The G2-PAMAM-capped MSN material (G2-MSN) was used to complex with a plasmid DNA (pEGFP-C1) that encodes for an enhanced green fluorescence protein. The gene(More)
ATP caused a dose-dependent, receptor-mediated increase in the release of glutamate and aspartate from cultured astrocytes. Using calcium imaging in combination HPLC we found that the increase in intracellular calcium coincided with an increase in glutamate and aspartate release. Competitive antagonists of P(2) receptors blocked the response to ATP. The(More)
Bradykinin is a nonapeptide that plays a central role in the production of pain and inflammation. A horizontal spinal cord slice preparation with attached dorsal root and dorsal root ganglion was used to study the effect of bradykinin on afferent fibers. Intracellular recordings were made from dorsal root ganglion and dorsal horn neurons. Bath application(More)