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  • Presynaptic terminals  (1)
  • Vasoactive intestinal polypeptide  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 62 (1986), S. 663-668 
    ISSN: 1432-1106
    Keywords: CA1 ; Hippocampus ; Long-term potentiation ; Ca-uptake ; Subcellular fractionation ; Presynaptic terminals
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A combined electrophysiological and neurochemical study was performed on the CA1 area of hippocampal slices in an attempt to identify changes in presynaptic nerve terminal function in long-term potentiation (LTP). After controlled induction of LTP in CA1, the activated region was subjected to subcellular fractionation followed by 45Ca2+ uptake determinations. Synaptosomes prepared from slices in which LTP has been induced showed a faster risetime and a higher level of saturation for K+-induced Ca-uptake than those derived from unstimulated and stimulated control slices. These findings point to a participation of presynaptic terminals in long-term potentiation.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1106
    Keywords: Myenteric plexus ; Guinea pig ; Acetylcholine ; Vasoactive intestinal polypeptide ; Differential release ; Cotransmission
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of electrical field stimulation on the release of acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) from superfused strips of myenteric plexus-longitudinal muscle (MPLM) of guinea-pig ileum and on the transmitter content of the tissue was investigated at different frequencies and in the presence and absence of choline hemicholinium-3 and colchicine. Low frequency electrical field stimulation released ACh by more than 4 times the basal release; the simultaneously detected VIP secretion was increased only slightly above the resting level. During high frequency stimulation (50 Hz) the release of VIP was greatly increased (to 5 times the resting release) whereas the release of ACh increased to only 150% of the basal output. When choline was present, the ACh content of the tissue itself was not altered by electrical stimulation indicating a rate of synthesis sufficient to maintain release. It was reduced in a frequency-dependent manner in the absence of exogenous choline or in the presence of 10 μM hemicholinium-3 (an inhibitor of choline uptake) by up to 54% of the original content. A similar but even larger reduction took place in the amount of ACh released. Neither the secretion of VIP nor the tissue VIP content was altered by these treatments. Long-lasting (〉60 min) high-frequency (50 Hz) stimulation resulted in the depletion of the VIP pool (by 25%) while the ACh content remained unaltered. The stimulus-induced depletion of the VIP pool was increased when colchicine reduced the amount of VIP released and the VIP content of the stimulated tissue up to 50%; it caused a small hemicholinium-like effect on the release of ACh and on the ACh content of the tissue when the tissue was stimulated for an extended length of time (120 to 180 min) at low frequency (5 Hz) but otherwise had little effect. Depolarization by elevated potassium concentration or by veratridine increased the ACh release by 150–280% and the VIP release by 125–200% of the resting release and was thus equivalent to electrical stimulation at 8–10 Hz. At the end of prolonged chemical depolarization (60 min) the ACh content was reduced to 60–80% and the VIP content to 80–90% of the non-stimulated values respectively. These results are interpreted in terms of the different intracellular dynamics of ACh and VIP and their respective storage vesicles.
    Type of Medium: Electronic Resource
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