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Angaben zur Quelle [Bearbeiten]

Autor     Oscar Herreras, Carlota Large, José M. Ibarz, George G. Somien, Rafael Martin del Rio
Titel    Role of Neuronal Synchronizing Mechanisms in the Propagation of Spreading Depression in the in wivo Hippocampus
Zeitschrift    The Journal of Neuroscience
Ausgabe    14
Datum    November 1994
Nummer    11
Seiten    7087-7098
URL    http://www.jneurosci.org/content/14/11/7087.long

Literaturverz.   

no
Fußnoten    no
Fragmente    1


Fragmente der Quelle:
[1.] Tmm/Dublette/Fragment 011 04 - Diskussion
Zuletzt bearbeitet: 2014-04-28 21:03:41 Hindemith
Dublette, Fragment, Herreras et al 1994, KeineWertung, SMWFragment, Schutzlevel, Tmm, ZuSichten

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Untersuchte Arbeit:
Seite: 11, Zeilen: 4-23
Quelle: Herreras et al 1994
Seite(n): 7087, Zeilen: r.col: 8ff
Widely accepted hypotheses hold that the primary event responsible for both the initiation and the propagation of SD is the release of some substance from neuronal elements to the extracellular compartment, which initially excites and then depresses adjacent neurons. The slowness of diffusion of the mediator would account for the low velocity of SD propagation. Among the substances proposed to mediate SD propagation are potassium (Grafstein, 1963; Bures et al., 1974) and excitatory amino acids (Fabricius et al., 1993). There are, however, observations that are difficult to reconcile with either of these two propositions.

SD had been interpreted as a composite process or a sequence of several linked events. To solve its genesis, a most important question concerns identification of the very first step in the chain reaction. In the extant literature, however, generally more attention has been given to the major depolarization and the attending extracellular potential shift than to the antecedent events. Among antecedents heralding the onset of SD that have been reported, are a slight increase of extracellular potassium, a small positive shift preceding the fast negative shift of the extracellular potential and several types of fast field activity including a short burst of action potentials or intense synaptic noise (Leao, 1944; Higashida et al., 1974). Even a silence of spontaneous or evoked activity has occasionally been described prior to other signs (Higashida et al., 1974). Not all of these early signs are obligatory prodromals of the large, accelerating, regenerative depolarization that is typical of the process.

Widely accepted hypotheses hold that the primary event responsible for both the initiation and the propagation of SD is the release of some substance from neuronal elements to the extracellular compartment, which initially excites and then depresses adjacent neurons. The slowness of diffusion of the mediator would account for the low velocity of SD propagation. Among the substances proposed to mediate SD propagation are potassium (Grafstein, 1956; Brinley et al., 1960; BureS and Kiivanek, 1960) and excitatory amino acids (Van Harreveld, 1959; SiesjG and Bengtsson, 1989; Fabricius et al., 1993). There are, however, observations that are difficult to reconcile with either of these two propositions (Lehmenkiihler, 1990; Herreras and Somjen, 1993a,b; see also Discussion).

SD had been interpreted as a composite process or a sequence of several linked events. To solve its genesis, a most important question concerns identification of the very first step in the chain reaction. In the extant literature, however, generally more attention has been given to the major depolarization and the attending extracellular potential shift (ΔV0) than to the antecedent events. Among antecedents heralding the onset of SD that have been reported, are a slight increase of extracellular potassium ([K+]0), a small positive shift preceding the fast negative shift of the extracellular potential (ΔV0) (Marshall, 1959) and several types of fast field activity including a short burst of action potentials or intense synaptic noise (Leao, 1944; Grafstein 1956; Rosenblueth and Garcia-Ramos, 1966; Ichijo and Ochs, 1970; Higashida et al., 1974; Somjen and Aitken, 1984; Haglund and Schwartzkroin, 1990; Herreras and Somjen, 1993a). Even a silence of spontaneous or evoked activity has occasionally been described prior to other signs (Grafstein, 1956; Morlock et al., 1964; Muiioz, 1970; Higashida et al., 1974). Not all of these early signs are obligatory prodromals of the large, accelerating, regenerative depolarization that is typical of the process

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