Conformational changes of the smooth endoplasmic reticulum are facilitated by L-glutamate and its receptors in rat Purkinje cells.
The intraventricular administrations of L-glutamate or trans-1-amino-1,3-cyclopentanedicarboxylic acid (t-ACPD), which is an agonist for the metabotropic glutamate receptor, induced conformational changes of the smooth endoplasmic reticulum (SER) to form lamellar bodies, consisting of stacks of flattened cisterns in Purkinje cell dendrites of the rat cerebellum. The formation of lamellar bodies by t-ACPD or by anoxia was blocked by pretreatment of L(+)-2-amino-3-phosphonopropionic acid (L-AP3), which is an antagonist for the metabotropic glutamate receptor. Injections of N-methyl-D-aspartic acid (NMDA) and amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate, which are categorized as acting on ionotropic receptors of glutamate, did not cause the formation of lamellar bodies, although kainate condensed the dendritic cytoplasm and produced a swelling of surrounding astrocytes. The cisterns of lamellar bodies formed by t-ACPD were long and formed regular stacks. Many intercisternal bridges were arranged with a center-to-center distance of about 25 nm between apposed cisterns. The bridges appeared as short tubes about 15 nm in diameter and in length, a clear center of which linked the lumen of their cisterns. The present results revealed that an excess release of excitatory transmitter by brief anoxia activates metabotropic glutamate receptors, which transform the networks of SER that normally release Ca2+ widely to the neuronal cytoplasm into lamellar bodies. Large Ca2+ storage pools of lamellar bodies are formed by the association of opposing molecules that belong to different cisterns and may protect excess release of Ca2+ from their reservoirs.
Banno
T
T
Department of Anatomy, University of Tsukuba, Institute of Basic Medical Sciences, Ibaraki, Japan.
Kohno
K
K
D000409:Alanine / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D001049:Apnea / Q000139:chemically induced / Q000150:complications; D001919:Bradycardia / Q000139:chemically induced; D020013:Calcium Signaling / Q000187:drug effects; D003515:Cycloleucine / Q000031:analogs & derivatives / Q000494:pharmacology; D003712:Dendrites / Q000648:ultrastructure; D018871:Endoplasmic Reticulum, Smooth / Q000187:drug effects / Q000648:ultrastructure*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000008:administration & dosage / Q000494:pharmacology*; D002534:Hypoxia, Brain / Q000209:etiology / Q000473:pathology; D007150:Immunohistochemistry; D007276:Injections, Intraventricular; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D016202:N-Methylaspartate / Q000494:pharmacology; D009419:Nerve Tissue Proteins / Q000187:drug effects* / Q000502:physiology; D018696:Neuroprotective Agents / Q000494:pharmacology; D011689:Purkinje Cells / Q000648:ultrastructure*; D051381:Rats; D017208:Rats, Wistar; D018091:Receptors, AMPA / Q000819:agonists / Q000502:physiology; D018092:Kainic Acid Receptors / Q000819:agonists / Q000502:physiology; D018094:Receptors, Metabotropic Glutamate / Q000819:agonists* / Q000037:antagonists & inhibitors / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists / Q000502:physiology; D012119:Respiration / Q000187:drug effects; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / Q000494:pharmacology
D000409:Alanine; D003515:Cycloleucine; D018691:Excitatory Amino Acid Antagonists; D018698:Glutamic Acid; D007608:Kainic Acid; D016202:N-Methylaspartate; D009419:Nerve Tissue Proteins; D018696:Neuroprotective Agents; D018091:Receptors, AMPA; D018092:Kainic Acid Receptors; D018094:Receptors, Metabotropic Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; C000211:2-amino-3-phosphonopropionic acid; C036361:1-amino-1,3-dicarboxycyclopentane