School of Nursing Class of 1983

Top Row: Barbara A. Fleckenstein, Anne M. Phelan, Julie-Ann Gersin, Laura E. Kemper, Mary Ann McCulloch, Meryl I. Faber, Karen E. Morton, Jennifer S. Miller, Catherine A. Chichester, Dana R. Piper, Harold K. Lohwasser, Michelle A. Lyons, Julia C. Kelly, Deborah L. Rossman, Amy L. Keskey, John F. Nama, Linda Borucki, Michelle M. Bradley, Caroline M. Fischer, Lisa A. Kuhnlein

Row 2: Karen M. Pardo, Laura L. Price, Mollie A. McDonald, Jan M. Grable, Janna S. Nichols, Laura A. Quain, Patricia M. Battel, Claudia J. Koch, Maureen G. D'hondt, Trudy J. Tervo, Linda A. Walz, Cheryl K. Ebling, Patricia A. Merte, Lauri R. Klock, Maria A. Lomibao, Mary E. Eisenhauer, Ellen B. Malvern, Josephine A. Polesnak

Row 3: Yvonne D. Krisel, Rosemary T. Coyne, Janey A. Porterfield, Deborah A. Mulawa, Janet E. Lovelace, Susan P. O'brien, Margaret T. Perrone, Brenda K. Luckhardt, Terry A. Layher, Sharon A. Potonac, Susan K. Watson, Janet A. Servatowski

Row 4: Vivian A. Reeves, Tracey A. Weeks, Marilyn K. Morgan, Terrilynn Phillips, Susan S. Kirk, Robert J. Ziola, Fred Roberts, Karen S. Myron, Pamela M. Przybylski, Mary Jo F. Lafata, Janet A. Scapini, Mary J. Swails

Row 5: Julie E. Reitz, Julie A. Symons, Ave M. Reagor, Catherine A. Regan, Marsha A. Glass, Susan M. Derubeis, Judy L. Goode, Jennifer P. Wylie, Janet L. Nowak, Karen M. Ulfig, Cynthia E. West, Carol A. Czarnecki, Gloria J. Verdi, Lisa D. Singleton

Row 6: Cynthia Wiggins, Monica L. Babyak, Gail M. Ray, Karen S. Desloover, Ladonna L. Christian-Combs, Deborah J. Dunnaback, Deborah A. Cecchini, Nancy A. Neville, Julia H. Grove, Wendy A. Weinfurtner, Susan M. Twigg, Jolynne Vanotteren, Lori A. Clark, Susan T. Savidge

Row 7: Marianne Ojeda, Ann M. Tucker, Lisa A. Valiquette, Sharon J. Bergmann, Elizabeth A. Rice, Marjorie R. Hovis, Laura I. Berry, Janice B. Lindberg, Rhetaugh G. Dumas, Susan B. Steckel, Helen L. Erickson, Kathleen M. Oshea, Tricia A. Richardson, Cheryl L. Sanders, Ann L. Shcoene, Anita M. Bargardi, Constance S. Siler, Anne L. Scott

Row 8: Gassenie Thomas, Victoria L. cadagin, Sheryl A. Strace, Joyce I. Sourbeck, Mary S. Donald, Cindy Tollis, Miriam L. Allis, Julie J. Watson, Patricia A. Shefferly, Nina M. Squire, Carol J. Debrodt, Jennifer A. Dreps, Cynthia B. Stone, Martha A. House, Elizabeth A. Hull, Laurie J. Bommarito, Erin A. Swain, Lisa D. Davis

Row 9: Lisa W. Barak, Charlotte L. Allport, Karen J. Baker, Julie M. Sweet, Pamela R. Armfield, Kathleen A. Hornick, Marcianna M. Davis, Joann L. Holdridge, Barbara A. Black, Scott L. Baker, Lawrene S. Gardipee, Julie A. Hemsteger, Mary Ann Barz, Carla L. Arnett, Danielle L. Bonam, Janice S. Brady, Karen L. Eischer, Amy A. Hing, Marcia L. Hassig, Heidi G. Henn

Bibliography on low temperature characteristics of steel:

Mode of access: Internet.

Teutsch-Evangelisches Judenthum: das ist, Gründlicher Beweisz ausz den Heil. Propheten Gottes : dasz wir Evangelische in Teutschland grösten Theils dem jüdischen Volck im Alten Testament ietzo gleich: ... nebenst angehängtem treuen Raht und Vorschlag Gottes ... ietzige Friedens Tractaten fruchtbarlich anzustellen und das heutige fast jüdische Christenthum in Teutschland ausz dem Schlaaff der Heucheley und Sicherheit zuerwecken: zum ernsten Busz-Spiegel ... /

Title and imprint partially from Faber du Faur.

Zur Kenntnis der Benziloxime /

Thesis (doctoral)--Ruprecht-Carls-Universitat zu Heidelberg, 1893.

Uber reihenentwickelungen analytischer funktionen.

Thesis (doctoral)--

Klinisches uber den

Mode of access: Internet.

Elements of chemistry: for the use of colleges, academies, and schools /

Mode of access: Internet.

Ca2+-activated K+(BK) channel inactivation contributes to spike broadening during repetitive firing in the rat lateral amygdala

In many neurons, trains of action potentials show frequency-dependent broadening. This broadening results from the voltage-dependent inactivation of K+ currents that contribute to action potential repolarisation. In different neuronal cell types these K+ currents have been shown to be either slowly inactivating delayed rectifier type currents or rapidly inactivating A-type voltage-gated K+ currents. Recent findings show that inactivation of a Ca2+-dependent K+ current, mediated by large conductance BK-type channels, also contributes to spike broadening. Here, using whole-cell recordings in acute slices, we examine spike broadening in lateral amygdala projection neurons. Spike broadening is frequency dependent and is reversed by brief hyperpolarisations. This broadening is reduced by blockade of voltage-gated Ca2+ channels and BK channels. In contrast, broadening is not blocked by high concentrations of 4-aminopyridine (4-AP) or alpha-dendrotoxin. We conclude that while inactivation of BK-type Ca2+-activated K+ channels contributes to spike broadening in lateral amygdala neurons, inactivation of another as yet unidentified outward current also plays a role.

Opioids Inhibit Lateral Amygdala Pyramidal Neurons by Enhancing A Dendritic Potassium Current

Pyramidal neurons in the lateral amygdala discharge trains of action potentials that show marked spike frequency adaptation, which is primarily mediated by activation of a slow calcium-activated potassium current. We show here that these neurons also express an alpha-dendrotoxin- and tityustoxin-Kalpha-sensitive voltage-dependent potassium current that plays a key role in the control of spike discharge frequency. This current is selectively targeted to the primary apical dendrite of these neurons. Activation of mu-opioid receptors by application of morphine or D-Ala(2)-N-Me-Phe(4)-Glycol(5)-enkephalin (DAMGO) potentiates spike frequency adaptation by enhancing the alpha-dendrotoxin-sensitive potassium current. The effects of mu-opioid agonists on spike frequency adaptation were blocked by inhibiting G-proteins with N-ethylmaleimide (NEM) and by blocking phospholipase A(2). Application of arachidonic acid mimicked the actions of DAMGO or morphine. These results show that mu-opioid receptor activation enhances spike frequency adaptation in lateral amygdala neurons by modulating a voltage-dependent potassium channel containing Kv1.2 subunits, through activation of the phospholipase A(2)-arachidonic acid-lipoxygenases cascade.

Independent roles of calcium and voltage-dependent potassium currents in controlling spike frequency adaptation in lateral amygdala pyramidal neurons

The calcium-dependent afterhyperpolarization (AHP) that follows trains of action potentials is responsible for controlling action potential firing patterns in many neuronal cell types. We have previously shown that the slow AHP contributes to spike frequency adaptation in pyramidal neurons in the rat lateral amygdala. In addition, a dendritic voltage-gated potassium current mediated by Kv1.2-containing channels also suppresses action potential firing in these neurons. In this paper we show that this voltage-gated potassium current and the slow AHP act together to control spike frequency adaptation in lateral amygdala pyramidal neurons. The two currents have similar effects on action potential number when firing is evoked either by depolarizing current injections or by synaptic stimulation. However, they differ in their control of firing frequency, with the voltage-gated potassium current but not the slow AHP determining the initial frequency of action potential firing. This dual mechanism of controlling firing patterns is unique to lateral amygdala neurons and is likely to contribute to the very low levels of firing seen in lateral amygdala neurons in vivo.

SK channels regulate excitatory synaptic transmission and plasticity in the lateral amygdala

At glutamatergic synapses, calcium influx through NMDA receptors (NMDARs) is required for long-term potentiation (LTP); this is a proposed cellular mechanism underlying memory and learning. Here we show that in lateral amygdala pyramidal neurons, SK channels are also activated by calcium influx through synaptically activated NMDARs, resulting in depression of the synaptic potential. Thus, blockade of SK channels by apamin potentiates fast glutamatergic synaptic potentials. This potentiation is blocked by the NMDAR antagonist AP5 (D(-)-2-amino-5-phosphono-valeric acid) or by buffering cytosolic calcium with BAPTA. Blockade of SK channels greatly enhances LTP of cortical inputs to lateral amygdala pyramidal neurons. These results show that NMDARs and SK channels are colocalized at glutamatergic synapses in the lateral amygdala. Calcium influx through NMDARs activates SK channels and shunts the resultant excitatory postsynaptic potential. These results demonstrate a new role for SK channels as postsynaptic regulators of synaptic efficacy.

Synaptic activation of transient receptor potential channels by metabotropic glutamate receptors in the lateral amygdala

Classical mammalian transient receptor potential channels form non-selective cation channels that open in response to activation of phospholipase C-coupled metabotropic receptors, and are thought to play a key role in calcium homeostasis in non-excitable cells. Within the nervous system transient receptor potential channels are widely distributed but their physiological roles are not well understood. Here we show that in the rat lateral amygdala transient receptor potential channels mediate an excitatory synaptic response to glutamate. Activation of group l etabotropic glutamate receptors on pyramidal neurons in the lateral amygdala with either exogenous or synaptically released glutamate evokes an inward current at negative potentials with a current voltage relationship showing a region of negative slope and steep outward rectification. This current is blocked by inhibiting G protein function with GTP-beta-S, by inhibiting phospholipase C or by infusing transient receptor potential antibodies into lateral amygdala pyramidal neurons. Using RT-PCR and Western blotting we show that transient receptor potential 1, transient receptor potential 4 and transient receptor potential 5 are present in the lateral amygdala. Single cell PCR confirms the presence of transient receptor potential 1 and transient receptor potential 5 in pyramidal neurons and we show by co-immunoprecipitation that transient receptor potential 1 and transient receptor potential 5 co-assemble as a heteromultimers in the amygdala. These results show that in lateral amygdala pyramidal neurons synaptically released glutamate activates transient receptor potential channels, which we propose are likely to be heteromultimeric channels containing transient receptor potential 1 and transient receptor potential 5/transient receptor potential 4. (c) 2005 Published by Elsevier Ltd on behalf of IBRO.