{"id":{"repo_id":"lund","oai_identifier":"oai:lup.lub.lu.se:3a617885-2a27-475b-88df-c6e19514eb48"},"canonical_url":"https://search.dev.ndltd.org/etd/lund/oai:lup.lub.lu.se:3a617885-2a27-475b-88df-c6e19514eb48","repository":{"repo_id":"lund","name":"University of Lund","base_url":"https://lup.lub.lu.se/oai"},"display":{"title":"Cell coupling and exocytosis measured in intact mouse pancreatic islets Control of {delta}-cell secretion","abstract":"Patch-clamp and capacitance measurements were applied to α-, β- and δ-cells in intact mouse pancreatic islets. The maximum rate of β-cell exocytosis during a depolarization to 0 mV was 14 granules/s, <5% of that observed in isolated β-cells. β-cell exocytosis exhibited bell-shaped voltage dependence and peaked at +20 mV. At physiological membrane potentials (≤-20 mV), the maximum rate of release was ~4 granules/s. Exocytosis in β-cell depends on Ca2+-influx via L-type Ca2+-channels, whereas N-type Ca2+-channels are important in α-cells. δ-cell exocytosis exhibits a post-stimulation component not observed in the other islet cell types. Ca2+-imaging in conjunction with capacitance measurements revealed that this feature results from Ca2+-induced Ca2+-release (CICR) via ryanodine receptor 3 (RyR3). Both somatostatin release measurements and patch-clamp experiments indicate that R-type Ca2+-channels are tightly coupled to CICR. The latency between Ca2+-influx through R-type Ca2+-channels and CICR was <6 ms. However, unlike what is observed in skeletal muscle, where association has been reported to be equally tight, Ca2+-influx is required in the δ-cells and no CICR can be evoked by depolarization alone. Glucose regulates CICR via promoting intracellular Ca2+ sequestration and cAMP/PKA-mediated modulation of RyR3. Electrophysiological analysis of cell coupling in intact islets reveals that every β-cell is electrically coupled to seven other β-cells. Coupling is sufficient to account for the synchronization and propagation of the cytosolic Ca2+-oscillations but small changes in β-cell electrical activity can be predicted to have strong effects on the synchronization which may contribute to the loss of pulsatile insulin secretion in type-2 diabetes.","abstract_html":"Patch-clamp and capacitance measurements were applied to α-, β- and δ-cells in intact mouse pancreatic islets. The maximum rate of β-cell exocytosis during a depolarization to 0 mV was 14 granules/s, &lt;5% of that observed in isolated β-cells. β-cell exocytosis exhibited bell-shaped voltage dependence and peaked at +20 mV. At physiological membrane potentials (≤-20 mV), the maximum rate of release was ~4 granules/s. Exocytosis in β-cell depends on Ca2+-influx via L-type Ca2+-channels, whereas N-type Ca2+-channels are important in α-cells. δ-cell exocytosis exhibits a post-stimulation component not observed in the other islet cell types. Ca2+-imaging in conjunction with capacitance measurements revealed that this feature results from Ca2+-induced Ca2+-release (CICR) via ryanodine receptor 3 (RyR3). Both somatostatin release measurements and patch-clamp experiments indicate that R-type Ca2+-channels are tightly coupled to CICR. The latency between Ca2+-influx through R-type Ca2+-channels and CICR was &lt;6 ms. However, unlike what is observed in skeletal muscle, where association has been reported to be equally tight, Ca2+-influx is required in the δ-cells and no CICR can be evoked by depolarization alone. Glucose regulates CICR via promoting intracellular Ca2+ sequestration and cAMP/PKA-mediated modulation of RyR3. Electrophysiological analysis of cell coupling in intact islets reveals that every β-cell is electrically coupled to seven other β-cells. Coupling is sufficient to account for the synchronization and propagation of the cytosolic Ca2+-oscillations but small changes in β-cell electrical activity can be predicted to have strong effects on the synchronization which may contribute to the loss of pulsatile insulin secretion in type-2 diabetes.","abstract_has_math":false,"creators":["Zhang, Quan"],"institution":"Department of Clinical Sciences, Lund University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2008,"date_issued":"2008","date_published":"2008","updated_at":"2026-07-24T02:59:49Z","subjects":["Endocrinology and Diabetes"],"languages":["eng"],"rights":["info:eu-repo/semantics/openAccess"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["urn:isbn:978-91-85897-78-0"],"render_values":[{"text":"urn:isbn:978-91-85897-78-0","href":null,"code":true}]}]},"links":{"outbound_url":"https://lup.lub.lu.se/record/1024510","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Zhang, Quan"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2008"]},{"key":"dc:publisher","label":"Institution","values":["Department of Clinical Sciences, Lund University"]},{"key":"dc:type","label":"Dc Type","values":["thesis/doccomp","info:eu-repo/semantics/doctoralThesis","text"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Endocrinology and Diabetes"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["info:eu-repo/semantics/openAccess"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://lup.lub.lu.se/record/1024510","urn:isbn:978-91-85897-78-0","https://portal.research.lu.se/files/3886264/1054333.pdf"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Patch-clamp and capacitance measurements were applied to α-, β- and δ-cells in intact mouse pancreatic islets. The maximum rate of β-cell exocytosis during a depolarization to 0 mV was 14 granules/s, <5% of that observed in isolated β-cells. β-cell exocytosis exhibited bell-shaped voltage dependence and peaked at +20 mV. At physiological membrane potentials (≤-20 mV), the maximum rate of release was ~4 granules/s. Exocytosis in β-cell depends on Ca2+-influx via L-type Ca2+-channels, whereas N-type Ca2+-channels are important in α-cells. δ-cell exocytosis exhibits a post-stimulation component not observed in the other islet cell types. Ca2+-imaging in conjunction with capacitance measurements revealed that this feature results from Ca2+-induced Ca2+-release (CICR) via ryanodine receptor 3 (RyR3). Both somatostatin release measurements and patch-clamp experiments indicate that R-type Ca2+-channels are tightly coupled to CICR. The latency between Ca2+-influx through R-type Ca2+-channels and CICR was <6 ms. However, unlike what is observed in skeletal muscle, where association has been reported to be equally tight, Ca2+-influx is required in the δ-cells and no CICR can be evoked by depolarization alone. Glucose regulates CICR via promoting intracellular Ca2+ sequestration and cAMP/PKA-mediated modulation of RyR3. Electrophysiological analysis of cell coupling in intact islets reveals that every β-cell is electrically coupled to seven other β-cells. Coupling is sufficient to account for the synchronization and propagation of the cytosolic Ca2+-oscillations but small changes in β-cell electrical activity can be predicted to have strong effects on the synchronization which may contribute to the loss of pulsatile insulin secretion in type-2 diabetes."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:source","label":"Dc Source","values":["Lund University Faculty of Medicine Doctoral Dissertation Series; 2008:25 (2008)","ISSN: 1652-8220"]},{"key":"dc:title","label":"Title","values":["Cell coupling and exocytosis measured in intact mouse pancreatic islets Control of {delta}-cell secretion"]}]}],"canonical_facts":{"dc:creator":["Zhang, Quan"],"dc:date":["2008"],"dc:description":["Patch-clamp and capacitance measurements were applied to α-, β- and δ-cells in intact mouse pancreatic islets. The maximum rate of β-cell exocytosis during a depolarization to 0 mV was 14 granules/s, <5% of that observed in isolated β-cells. β-cell exocytosis exhibited bell-shaped voltage dependence and peaked at +20 mV. At physiological membrane potentials (≤-20 mV), the maximum rate of release was ~4 granules/s. Exocytosis in β-cell depends on Ca2+-influx via L-type Ca2+-channels, whereas N-type Ca2+-channels are important in α-cells. δ-cell exocytosis exhibits a post-stimulation component not observed in the other islet cell types. Ca2+-imaging in conjunction with capacitance measurements revealed that this feature results from Ca2+-induced Ca2+-release (CICR) via ryanodine receptor 3 (RyR3). Both somatostatin release measurements and patch-clamp experiments indicate that R-type Ca2+-channels are tightly coupled to CICR. The latency between Ca2+-influx through R-type Ca2+-channels and CICR was <6 ms. However, unlike what is observed in skeletal muscle, where association has been reported to be equally tight, Ca2+-influx is required in the δ-cells and no CICR can be evoked by depolarization alone. Glucose regulates CICR via promoting intracellular Ca2+ sequestration and cAMP/PKA-mediated modulation of RyR3. Electrophysiological analysis of cell coupling in intact islets reveals that every β-cell is electrically coupled to seven other β-cells. Coupling is sufficient to account for the synchronization and propagation of the cytosolic Ca2+-oscillations but small changes in β-cell electrical activity can be predicted to have strong effects on the synchronization which may contribute to the loss of pulsatile insulin secretion in type-2 diabetes."],"dc:format":["application/pdf"],"dc:identifier":["https://lup.lub.lu.se/record/1024510","urn:isbn:978-91-85897-78-0","https://portal.research.lu.se/files/3886264/1054333.pdf"],"dc:language":["eng"],"dc:publisher":["Department of Clinical Sciences, Lund University"],"dc:rights":["info:eu-repo/semantics/openAccess"],"dc:source":["Lund University Faculty of Medicine Doctoral Dissertation Series; 2008:25 (2008)","ISSN: 1652-8220"],"dc:subject":["Endocrinology and Diabetes"],"dc:title":["Cell coupling and exocytosis measured in intact mouse pancreatic islets Control of {delta}-cell secretion"],"dc:type":["thesis/doccomp","info:eu-repo/semantics/doctoralThesis","text"]},"updated_at":"2026-07-24T02:59:49Z"}