132,449 research outputs found
Presynaptic potentials and facilitation of transmitter release in the squid giant synapse.
Presynaptic potentials were studied during facilitation of transmitter
release in the squid giant synapse. Changes in action potentials were found to
cause some, but not all, of the facilitation during twin-pulse stimulation. During
trains of action potentials, there were no progressive changes in presynaptic action
potentials which could account for the growth of facilitation. Facilitation could still
be detected in terminals which had undergone conditioning depolarization or
hyperpolarization. Facilitation could be produced by small action potentials in low
[Ca++]o and by small depolarizations in the presence of tetrodotoxin. Although the
production of facilitation varied somewhat with presynaptic depolarization, nevertheless,
approximately equal amounts of facilitation could be produced by depolarizations
which caused the release of very different amounts of transmitter.This work was supported by National Science Foundation research grant (GB-36949, a National
Institutes of Health career award to Dr. Bittner, and National Research Council (Canada) and Grass
Fellowships to Dr. Charlton.Neuroscienc
Kant oder Hegel? (hrsg. v. D. Henrich)
Bittner R. Kant oder Hegel? (hrsg. v. D. Henrich). Zeitschrift für philosophische Forschung. 1985;39(2):317-321
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Evolution of abilities to regenerate neurons in central nervous systems
This work was supported by a Kappa Kappa Gamma Graduate Fellowship Award to C. E. H. and NIH grant NS-11861 and RCDA NS-00070 to G. D. B.Neuroscienc
Robert Bittner Attestation Document
Tan document with title, Nationalsozialistische Deutsche Arbeiterpartei. Includes printed and typewritten information.
Information Provided by Michael D. Bulmash:
German National Socialist Workers Party (NSDAP) document attesting to a Robert Bittner being a party member as well as a member of the SA or Sturmabteilung. It further attests that there are no doubts that Bittner will continue to support the movement of Adolf Hitler. This document was signed by Kreisamtsleiter Fliegner.https://digital.kenyon.edu/bulmash/2210/thumbnail.jp
Aline, Königin von Golconda
N. Bittner f. ; de Pian inv.Beschriftungen mit Bleistift: „D X“, „Aline. Königinn von Colconda. / Ballet.“Herstellungsangaben: "N. Bittner f. N. 24.", "de Pian. inv.
Robert Bittner Pledge Document
Tan document with title, Nierderschrift über die Bereidigung des. Includes typewritten and printed information with two signatures.
Information Provided by Michael D. Bulmash: A document from 1942 wherein Robert Bittner takes an oath that in the name of God he will be dutiful to the Führer and the nation.https://digital.kenyon.edu/bulmash/2211/thumbnail.jp
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Mechanisms for the maintenance and eventual degradation of neurofilament proteins in the distal segments of severed goldfish Mauthner axons
Cellular mechanisms that might affect the degradation of neurofilament proteins (NFPs) were examined in the distal segments
of severed goldfish Mauthner axons (M-axons), which do
not degenerate for more than 2 months after severance. Calpain
levels, as determined by reactivity to a polyclonal antibody,
remained constant for 80 d postseverance in distal segments
of M-axons and then declined from 80 to 85 d
postseverance. Calpain activity in rat brain, as determined by a
spectrophotometric assay, was much higher than calpain activity
in control and severed goldfish brain, spinal cord, muscle,
or M-axons. Calpain activity was extremely low in M-axons
compared with that in all other tissues and remained low for up
to 80 d postseverance in distal segments of M-axons. Phosphorylated
NFPs, as determined by Stains-All treatment of SDS
gels, were maintained for up to 72 d postseverance and then decreased noticeably at 75 d postseverance when NFP breakdown
products appeared on silver-stained gels. By 85 d postseverance,
phosphorylated NFPs no longer were detected, and
NFP breakdown products were the most prominent bands on
silver-stained gels. These results suggest that the distal segments
of M-axons survive for months after severance, because
NFPs are maintained in a phosphorylated state that stabilizes
and protects NFPs from degradation by low levels of calpain
activity in the M-axon; the distal segments of severed M-axons
degenerate eventually when NFPs no longer are maintained in
a phosphorylated state and become susceptible to degradation,
possibly by low levels of calpain activity in the M-axon.This work was supported by an Advanced Technology Project Grant to G.D.B.Neuroscienc
QUANTITATIVE ASPECTS OF TRANSMITTER RELEASE
The opener-stretcher motor neuron in crayfish makes 50 endings upon each of 1200 muscle
fibers . We have calculated the quantal content of junctional potentials produced by individual
terminals and by the whole cell at various physiological frequencies . The results
show that when the motor neuron is active at 20 impulses/second, it releases 50 quanta/
impulse per muscle fiber, or a total of 4 .5 X 109 quanta/hr. These figures are similar to
those for vertebrate muscles per fiber, but larger for the entire neuron because the opener
motor unit is so large. On the basis that the quanta correspond to synaptic vesicles each
containing 103-104 molecules of transmitter, the release rate must be around 10 -11 mole/hr.
This value is within an order of magnitude of the release figures obtained for mammalian
neurons by collecting transmitter in perfusates, but it is far lower than the value reported
for a crustacean inhibitory neuron. If the membrane materials surrounding each vesicle
were lost in the release process, the replacement synthesis would involve 24 mm , of membrane/
hr. We conclude that the metabolic load in terms of transmitter synthesis is probably
sustainable, but that the release mechanism must operate in such a way that vesicle membrane
materials are neither lost nor incorporated into the terminal membrane .Supported in part by grants (NB-02944, NB-
08609-01) from the U . S . Public Health Service to
Dr. Kennedy and Dr . BittnerNeuroscienc
Kodierungstechniken im Wandel: Das Zusammenspiel von Analytik und Synthese im Gegenwartsdeutschen
Interazioni molecolari tra l’omeostasi del ferro e del molibdeno in mitocondri di Cucumis sativus L
Il molibdeno (Mo) è un micronutriente essenziale in quasi tutti gli organismi comprese le piante [1]. Il Mo, sotto forma di molibdato, è complessato con un pterina per formare il cofattore-molibdeno (Moco), che è biologicamente funzionale e che viene inserito nei cosiddetti molibdo-enzimi. Il molibdeno è quindi coinvolto in processi metabolici essenziali o importanti come assimilazione dell'azoto, sintesi dell’acido abscissico (ABA) e catabolismo delle purine. Un’alterazione del metabolismo del Mo ha effetti drammatici sulla crescita e sulla resa della pianta.
Recentemente, è stato evidenziato come il metabolismo del Mo interagisca fortemente con quello del ferro (Fe) [2]. Scopo di questo lavoro è quello di indagare la mutua regolazione dei meccanismi fondamentali alla base dell’assorbimento e della compartimentazione subcellulare di Mo e Fe in piante di cetriolo (Cucumis sativus) cresciute in diverse condizioni nutrizionali di Mo e di Fe.
Piante di cetriolo sono state allevate nelle seguenti condizioni: controllo (+Fe+Mo), carenza di Fe (-Fe+Mo), carenza di Mo (+Fe-Mo) o entrambe le carenze (-Fe-Mo).
Analisi ionomiche condotte tramite ICP-MS dei tessuti vegetali e di mitocondri purificati dalle radici hanno permesso di osservare come le carenze di Fe e di Mo determinino forti variazioni nel contenuto dei vari micro e macro elementi sia a livello dell'intera pianta che a livello subcellulare. Inoltre è stata osservata una variazione della distribuzione mitocondriale del Fe e del Mo in piante +Fe-Mo e –Fe+Mo. Attraverso un’analisi proteomica sono state valutate le alterazioni indotte dalle carenze di tali nutrienti a livello mitocondriale. Sono state identificate oltre cento proteine i cui livelli di espressione sono significativamente alterati in almeno uno dei trattementi nutrizionali utilizzati. I dati preliminari ottenuti suggeriscono una significativa intarazione tra il metabolismo del Fe e del Mo a livello mitocondriale.
[1]Bittner and Mendel (2010) Springer-Verlag, Plant Cell Monogr 17:119-143.
[2]Bittner (2014) Front. Plant Sci. 5:28
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