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Release from synaptosomes

Also in cultured neuroendocrine pinealocytes K+-induced release of Asp was both Ca +-dependent and sensitive to botulinum toxin (Yatsushiro et al., 1997). To rule out involvement of exchange mechanisms in the K -induced release of Asp the authors used dihydrokainate, which is a non-transported inhibitor (see above) of the excitatory amino acid carrier (GLTl) found in the pinealocytes (Yamada et al., 1997). This treatment did not affect the K+-induced release, but inhibited Na -dependent sequestration of Asp into the pinealocytes. In addition they showed that the pinealocytes, which contain both the L-form the D-form of Asp, released only L-Asp upon membrane depolarization. This makes it further [Pg.49]


Grady, S., Marks, M.J., Wonnacott, S., Collins, A.C. Characterization of nicotinic receptor-mediated [3H]dopamine release from synaptosomes prepared from mouse striatum. J. Neurochem. 59 848,1992. [Pg.35]

Kulak JM, McIntosh JM, Yoshikami D, Olivera BM (2001) Nicotine-evoked transmitter release from synaptosomes functional association of specific presynaptic acetylcholine receptors and voltage-gated calcium channels. J Neurochem 77 1581-9 Kuner R, Grunewald KH, Eisenhardt G et al (1999) Role of heteromer formation in GABAb receptor function. Science 283 74-7... [Pg.404]

Grady SR, Murphy KL, Cao J, Marks MJ, McIntosh JM, Collins AC (2002) Characterization of nicotinic agonist-induced [(3)H]dopamine release from synaptosomes prepared from four mouse brain regions. J Pharmacol Exp Ther 301 651-60 Graham B, Redman S (1994) A simulation of action potentials in synaptic boutons during presynaptic inhibition. J Neurophysiol 71 538 49... [Pg.518]

McMahon HT, Foran P, Dolly JO et al. (1992) Tetanus toxin and botulinum toxins type A and B inhibit gitamate, gamma-aminobutyric acid, aspartate, and met-enkephalin release from synaptosomes. Clues to the focus of action. J. Biol. Chem. 267 21338-43. [Pg.213]

Since ChAc is relatively easily released from synaptosome membranes, it is necessary to keep in mind that only a minor portion of the enzyme can be bound to membranes. If there are microenvironmental changes in pH within the terminal (e.g., due to the hydrolysis of ACh) a larger proportion of the enzyme could be membrane bound. [Pg.37]

METABOLISM OF PHOSPHATIDIC ACID AND PHOSPHATIDYLINOSITOL IN RELATION TO TRANSMITTER RELEASE FROM SYNAPTOSOMES... [Pg.419]


See other pages where Release from synaptosomes is mentioned: [Pg.197]    [Pg.304]    [Pg.98]    [Pg.107]    [Pg.107]    [Pg.183]    [Pg.40]    [Pg.201]    [Pg.382]    [Pg.301]    [Pg.448]    [Pg.207]    [Pg.60]    [Pg.191]    [Pg.49]    [Pg.49]    [Pg.247]    [Pg.295]    [Pg.112]    [Pg.51]    [Pg.328]    [Pg.98]   


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Aspartate release from synaptosomes

Dopamine release from synaptosomes

Glutamate release from synaptosomes

NE Release from Cardiac Synaptosomes

Noradrenaline release from synaptosomes

Synaptosomal

Synaptosome

Synaptosome/synaptosomal

Synaptosomes

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