Low level lead (Pb2+) exposure may produce lasting deficits in learning and memory by altering calcium (Ca2+) dependent processes. Isolated presynaptic nerve terminals from rat hippocampus were loaded with the intracellular (Ca2+) indicator Fura-2. The changes in cytoplasmic free calcium ([Ca2+]i) were measured by stopped-flow fluorescence spectroscopy following depolarization with elevated potassium on a millisecond time scale (Lentzner et al., 1992). Depolarization promoted a rapid increase in Ca2+i which occured in two kinetically distinguishable phases: a fast component, representing the activity of rapidly inactivating Ca2+ channels (τ ~ 60 msec), and a slow component, which is comprised of slowly inactivating Ca2+ channels (τ ~ 1sec) and Na+/Ca2+ exchange operating in the \"reverse\" mode. Low concentrations of Pb2+ (0.1-0.5 μΜ ) blocked competitively both the rapidly and slowly inactivating channels. At higher concentrations (≥1μΜ) , Pb2+ permeated the rapidly inactivating channels. Pb2+ permeation was accompanied by a subsequent rise in intracellular Ca2+ even in the absence of extracellular Ca2+. The rise in Ca2+ was reduced by thapsigargin, suggesting Pb2+ activates the release of Ca2+ from intracellular stores, possibly an IP3 sensitive store. The Ca2+ release was greatest in younger animals and gradually declined during postnatal development.
","abstract_html":"<p>Low level lead (Pb<sup>2+</sup>) exposure may produce lasting deficits in learning and memory by altering calcium (Ca<sup>2+</sup>) dependent processes. Isolated presynaptic nerve terminals from rat hippocampus were loaded with the intracellular (Ca<sup>2+</sup>) indicator Fura-2. The changes in cytoplasmic free calcium ([Ca<sup>2+</sup>]<sub>i</sub>) were measured by stopped-flow fluorescence spectroscopy following depolarization with elevated potassium on a millisecond time scale (Lentzner et al., 1992). Depolarization promoted a rapid increase in Ca<sup>2+</sup><sub>i</sub> which occured in two kinetically distinguishable phases: a fast component, representing the activity of rapidly inactivating Ca<sup>2+</sup> channels (τ ~ 60 msec), and a slow component, which is comprised of slowly inactivating Ca<sup>2+</sup> channels (τ ~ 1sec) and Na<sup>+</sup>/Ca<sup>2+</sup> exchange operating in the "reverse" mode. Low concentrations of Pb<sup>2+</sup> (0.1-0.5 μΜ ) blocked competitively both the rapidly and slowly inactivating channels. At higher concentrations (≥1μΜ) , Pb<sup>2+</sup> permeated the rapidly inactivating channels. Pb<sup>2+</sup> permeation was accompanied by a subsequent rise in intracellular Ca<sup>2+</sup> even in the absence of extracellular Ca<sup>2+</sup>. The rise in Ca<sup>2+</sup> was reduced by thapsigargin, suggesting Pb<sup>2+</sup> activates the release of Ca<sup>2+</sup> from intracellular stores, possibly an IP<sub>3</sub> sensitive store. The Ca<sup>2+</sup> release was greatest in younger animals and gradually declined during postnatal development.</p>","abstract_has_math":false,"creators":["Rhodes, Troy E."],"institution":null,"degree_name":"Doctor of Philosophy (PhD)","degree_level":"Dissertation","degree_discipline":null,"degree_department":null,"school":null,"contributors":["Dieter K. Bartschat","Peter F. Blackmore","barbara Y. Hargrave","Gerald J. Pepe","Paul H. Ratz"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":1996,"date_issued":"1996-07-01T07:00:00Z","date_published":"1996-07-01T07:00:00Z","updated_at":"2026-07-24T03:34:46Z","subjects":["Lead activation","Calcium channel","Rats","Nerve","Neurology","Toxicology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["9780591048674"],"render_values":[{"text":"9780591048674","href":null,"code":true}]}]},"links":{"outbound_url":"https://digitalcommons.odu.edu/biomedicalsciences_etds/72","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Dieter K. Bartschat","Peter F. Blackmore","barbara Y. Hargrave","Gerald J. Pepe","Paul H. Ratz"]},{"key":"dc:creator","label":"Author","values":["Rhodes, Troy E."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2019-05-14T07:00:00Z"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Doctor of Philosophy (PhD)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Lead activation","Calcium channel","Rats","Nerve","Neurology","Toxicology"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["9780591048674","https://digitalcommons.odu.edu/biomedicalsciences_etds/72"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Low level lead (Pb2+) exposure may produce lasting deficits in learning and memory by altering calcium (Ca2+) dependent processes. Isolated presynaptic nerve terminals from rat hippocampus were loaded with the intracellular (Ca2+) indicator Fura-2. The changes in cytoplasmic free calcium ([Ca2+]i) were measured by stopped-flow fluorescence spectroscopy following depolarization with elevated potassium on a millisecond time scale (Lentzner et al., 1992). Depolarization promoted a rapid increase in Ca2+i which occured in two kinetically distinguishable phases: a fast component, representing the activity of rapidly inactivating Ca2+ channels (τ ~ 60 msec), and a slow component, which is comprised of slowly inactivating Ca2+ channels (τ ~ 1sec) and Na+/Ca2+ exchange operating in the \"reverse\" mode. Low concentrations of Pb2+ (0.1-0.5 μΜ ) blocked competitively both the rapidly and slowly inactivating channels. At higher concentrations (≥1μΜ) , Pb2+ permeated the rapidly inactivating channels. Pb2+ permeation was accompanied by a subsequent rise in intracellular Ca2+ even in the absence of extracellular Ca2+. The rise in Ca2+ was reduced by thapsigargin, suggesting Pb2+ activates the release of Ca2+ from intracellular stores, possibly an IP3 sensitive store. The Ca2+ release was greatest in younger animals and gradually declined during postnatal development.
"]},{"key":"dc:title","label":"Title","values":["Lead Activation of a Developmentally Regulated Calcium Channel in Rat Hippocampal Nerve Terminals"]}]}],"canonical_facts":{"dc:contributor":["Dieter K. Bartschat","Peter F. Blackmore","barbara Y. Hargrave","Gerald J. Pepe","Paul H. Ratz"],"dc:creator":["Rhodes, Troy E."],"dc:date.available":["2019-05-14T07:00:00Z"],"dc:description.abstract":["Low level lead (Pb2+) exposure may produce lasting deficits in learning and memory by altering calcium (Ca2+) dependent processes. Isolated presynaptic nerve terminals from rat hippocampus were loaded with the intracellular (Ca2+) indicator Fura-2. The changes in cytoplasmic free calcium ([Ca2+]i) were measured by stopped-flow fluorescence spectroscopy following depolarization with elevated potassium on a millisecond time scale (Lentzner et al., 1992). Depolarization promoted a rapid increase in Ca2+i which occured in two kinetically distinguishable phases: a fast component, representing the activity of rapidly inactivating Ca2+ channels (τ ~ 60 msec), and a slow component, which is comprised of slowly inactivating Ca2+ channels (τ ~ 1sec) and Na+/Ca2+ exchange operating in the \"reverse\" mode. Low concentrations of Pb2+ (0.1-0.5 μΜ ) blocked competitively both the rapidly and slowly inactivating channels. At higher concentrations (≥1μΜ) , Pb2+ permeated the rapidly inactivating channels. Pb2+ permeation was accompanied by a subsequent rise in intracellular Ca2+ even in the absence of extracellular Ca2+. The rise in Ca2+ was reduced by thapsigargin, suggesting Pb2+ activates the release of Ca2+ from intracellular stores, possibly an IP3 sensitive store. The Ca2+ release was greatest in younger animals and gradually declined during postnatal development.
"],"dc:identifier":["9780591048674","https://digitalcommons.odu.edu/biomedicalsciences_etds/72"],"dc:subject":["Lead activation","Calcium channel","Rats","Nerve","Neurology","Toxicology"],"dc:title":["Lead Activation of a Developmentally Regulated Calcium Channel in Rat Hippocampal Nerve Terminals"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Doctor of Philosophy (PhD)"]},"updated_at":"2026-07-24T03:34:46Z"}