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1Latest Papers from Table of Contents or Articles in PressP. Abbot ; J. Abe ; J. Alcock ; S. Alizon ; J. A. Alpedrinha ; M. Andersson ; J. B. Andre ; M. van Baalen ; F. Balloux ; S. Balshine ; N. Barton ; L. W. Beukeboom ; J. M. Biernaskie ; T. Bilde ; G. Borgia ; M. Breed ; S. Brown ; R. Bshary ; A. Buckling ; N. T. Burley ; M. N. Burton-Chellew ; M. A. Cant ; M. Chapuisat ; E. L. Charnov ; T. Clutton-Brock ; A. Cockburn ; B. J. Cole ; N. Colegrave ; L. Cosmides ; I. D. Couzin ; J. A. Coyne ; S. Creel ; B. Crespi ; R. L. Curry ; S. R. Dall ; T. Day ; J. L. Dickinson ; L. A. Dugatkin ; C. El Mouden ; S. T. Emlen ; J. Evans ; R. Ferriere ; J. Field ; S. Foitzik ; K. Foster ; W. A. Foster ; C. W. Fox ; J. Gadau ; S. Gandon ; A. Gardner ; M. G. Gardner ; T. Getty ; M. A. Goodisman ; A. Grafen ; R. Grosberg ; C. M. Grozinger ; P. H. Gouyon ; D. Gwynne ; P. H. Harvey ; B. J. Hatchwell ; J. Heinze ; H. Helantera ; K. R. Helms ; K. Hill ; N. Jiricny ; R. A. Johnstone ; A. Kacelnik ; E. T. Kiers ; H. Kokko ; J. Komdeur ; J. Korb ; D. Kronauer ; R. Kummerli ; L. Lehmann ; T. A. Linksvayer ; S. Lion ; B. Lyon ; J. A. Marshall ; R. McElreath ; Y. Michalakis ; R. E. Michod ; D. Mock ; T. Monnin ; R. Montgomerie ; A. J. Moore ; U. G. Mueller ; R. Noe ; S. Okasha ; P. Pamilo ; G. A. Parker ; J. S. Pedersen ; I. Pen ; D. Pfennig ; D. C. Queller ; D. J. Rankin ; S. E. Reece ; H. K. Reeve ; M. Reuter ; G. Roberts ; S. K. Robson ; D. Roze ; F. Rousset ; O. Rueppell ; J. L. Sachs ; L. Santorelli ; P. Schmid-Hempel ; M. P. Schwarz ; T. Scott-Phillips ; J. Shellmann-Sherman ; P. W. Sherman ; D. M. Shuker ; J. Smith ; J. C. Spagna ; B. Strassmann ; A. V. Suarez ; L. Sundstrom ; M. Taborsky ; P. Taylor ; G. Thompson ; J. Tooby ; N. D. Tsutsui ; K. Tsuji ; S. Turillazzi ; F. Ubeda ; E. L. Vargo ; B. Voelkl ; T. Wenseleers ; S. A. West ; M. J. West-Eberhard ; D. F. Westneat ; D. C. Wiernasz ; G. Wild ; R. Wrangham ; A. J. Young ; D. W. Zeh ; J. A. Zeh ; A. Zink
Nature Publishing Group (NPG)
Published 2011Staff ViewPublication Date: 2011-03-25Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: *Altruism ; Animals ; *Biological Evolution ; Cooperative Behavior ; Female ; Game Theory ; *Genetic Fitness ; Genetics, Population ; Heredity ; Humans ; Male ; *Models, Biological ; Phenotype ; Reproducibility of Results ; *Selection, Genetic ; Sex RatioPublished by: -
2Articles: DFG German National LicensesStaff View
ISSN: 1460-9568Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: It has been suggested that, after ischaemia, activation of proteases such as calpains could be involved in cytoskeletal degradation leading to neuronal cell death. In vivo, calpain inhibitors at high doses have been shown to reduce ischaemic damage and traumatic brain injury, however, the relationship between calpain activation and cell death remains unclear. We have investigated the role of calpain activation in a model of ischaemia based on organotypic hippocampal slice cultures using the appearance of spectrin breakdown products (BDPs) as a measure of calpain I activation. Calpain I activity was detected on Western blot immediately after a 1-h exposure to ischaemia. Up to 4 h post ischaemia, BDPs were found mainly in the CA1 region and appeared before uptake of the vital dye propidium iodide (PI). 24 h after the insult, BDPs were detected extensively in CA1 and CA3 pyramidal cells, all of which was PI-positive. However, there were many more PI-positive cells that did not have BDPs, indicating that the appearance of BDPs does not necessarily accompany ischaemic cell death. Inhibition of BDP formation by the broad-spectrum protease inhibitor leupeptin was not accompanied by any neuroprotective effects. The more specific and more cell-permeant calpain inhibitor MDL 28170 had a clear neuroprotective effect when added after the ischaemic insult. In contrast, when MDL 28170 was present throughout the entire pre- and post-incubation phases, PI labelling actually increased, indicating a toxic effect. These results suggest that calpain activation is not always associated with cell death and that, while inhibition of calpains can be neuroprotective under some conditions, it may not always lead to beneficial outcomes in ischaemia.Type of Medium: Electronic ResourceURL: -
3Articles: DFG German National LicensesStaff View
ISSN: 1432-0533Keywords: Epilepsy ; Hippocampus ; Rat ; Somatostatin ; Tetanus toxinSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract A loss of inhibitory interneurons has been reported in the hippocampus following seizure activity in various animal models of epilepsy and in human epileptic tissue. The question of whether particular populations of inhibitory neurons are similarly affected by the chronic block of inhibition tha tresults after tetanus toxin injections directly into the brain has not previously been addressed. In the present study a unilateral intrahippocampal injection of tetanus toxin into the ventral hippocampus was used to produce a chronic epileptic syndrome characterised by brief seizures that recurred intermittently for 6–8 weeks. The results reveal, for the first time, the morphological changes in somatostatin interneurons following tetanus toxin-induced seizures in the rat. A bilateral short-term increase in immunoreactivity of somatostatin neurons is present 1 week after injection. This is accompanied by an increased intensity of somatostatin-immunoreactive axon terminals in the outer molecular layer of the dentate gyrus, which is more marked on the contralateral side. A chronic and significant loss of somatostatin-immunoreactive neurons was noted in the hilus of the dentate gyrus 2 months later. The significance of the chronic loss of the hilar somatostatin neurons in the control of excitatory activity in the dentate gyrus and whether the acute morphological changes are due to a direct action of the toxin on release mechanisms or as a result of seizure activity are discussed.Type of Medium: Electronic ResourceURL: -
4Articles: DFG German National LicensesStaff View
ISSN: 1432-0533Keywords: Key words Epilepsy ; Hippocampus ; Rat ; Somatostatin ; Tetanus toxinSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract A loss of inhibitory interneurons has been reported in the hippocampus following seizure activity in various animal models of epilepsy and in human epileptic tissue. The question of whether particular populations of inhibitory neurons are similarly affected by the chronic block of inhibition that results after tetanus toxin injections directly into the brain has not previously been addressed. In the present study a unilateral intrahippocampal injection of tetanus toxin into the ventral hippocampus was used to produce a chronic epileptic syndrome characterised by brief seizures that recurred intermittently for 6–8 weeks. The results reveal, for the first time, the morphological changes in somatostatin interneurons following tetanus toxin-induced seizures in the rat. A bilateral short-term increase in immunoreactivity of somatostatin neurons is present 1 week after injection. This is accompanied by an increased intensity of somatostatin-immunoreactive axon terminals in the outer molecular layer of the dentate gyrus, which is more marked on the contralateral side. A chronic and significant loss of somatostatin-immunoreactive neurons was noted in the hilus of the dentate gyrus 2 months later. The significance of the chronic loss of the hilar somatostatin neurons in the control of excitatory activity in the dentate gyrus and whether the acute morphological changes are due to a direct action of the toxin on release mechanisms or as a result of seizure activity are discussed.Type of Medium: Electronic ResourceURL: -
5Articles: DFG German National LicensesStaff View
ISSN: 1432-119XSource: Springer Online Journal Archives 1860-2000Topics: BiologyMedicineNotes: Abstract The use of sodium sulphide-perfused material for the immunocytochemical demonstration of microglia and astrocytes is described. An intracerebroventricular injection of kainic acid (KA) was used to induce neuronal degeneration and subsequent axonal sprouting in the hippocampus. Animals under deep anaesthesia were killed by perfusion with either 4% paraformaldehyde alone or with 1% sodium sulphide followed by 4% paraformaldehyde solution. Microglial cells were identified with OX-42, a monoclonal antibody towards CR3 complement receptors, and astrocytes with a polyclonal antibody to glial fibrillary acidic protein (GFAP). The present study reveals a marked enhancement in the immunoreactivity of activated microglial cells in sodium sulphide perfused tissues compared to those observed in tissues fixed in paraformaldehyde alone. GFAP immunoreactivity of the astrocytes was not compromised by the use of sodium sulphide. The results clearly show the suitability of sodium sulphide perfused tissues for immunocytochemical procedures and should provide a useful tool for investigation of the role of neuroglial cells in axonal sprouting.Type of Medium: Electronic ResourceURL: