scholarly journals Immunocytochemical evidence for SNARE protein-dependent transmitter release from guinea pig horizontal cells

2010 ◽  
Vol 31 (8) ◽  
pp. 1388-1401 ◽  
Author(s):  
Helen Lee ◽  
Nicholas C. Brecha
2010 ◽  
Vol 518 (10) ◽  
pp. 1647-1669 ◽  
Author(s):  
Chenying Guo ◽  
Arlene A. Hirano ◽  
Salvatore L. Stella ◽  
Michaela Bitzer ◽  
Nicholas C. Brecha

1989 ◽  
Vol 67 (6) ◽  
pp. 669-674 ◽  
Author(s):  
Koki Shigenobu ◽  
Tatsuya Mori ◽  
Katsuo Kamata ◽  
Yutaka Kasuya

Microelectrode and mechanical studies were performed with isolated guinea pig myocardium (right ventricular free walls and papillary muscles) to examine the effects of platelet-activating factor (PAF) and lysophosphatidylcholine (LPC). Low concentrations of PAF (10−8 to 10−6 M, a range equivalent to the blood concentrations that produce marked hypotension in vivo) had no effects on action potential configuration and contractile force. High concentrations (10−5 to 10−4 M) of PAF and LPC per se elicited slow response action potentials with concomitant contraction (restored contraction) in the myocardium depolarized with elevated K+ (25 mM); they also augmented slow responses and restored contractions produced by a low concentration of isoproterenol (10−8 M). Although these results suggested there was an increase in slow Ca current, the slow responses and restored contractions thus produced were greatly suppressed or abolished by the addition of a β-adrenoceptor blocking agent, sotalol (10−5 M), and by pretreatment with reserpine (5 mg/kg i.p., 24 h prior). In accordance with our previous conclusions, the present results suggest that direct cardiac action is not involved in the mechanisms of hypotension produced by PAF. It was also shown that high concentrations of PAF and LPC may act nonspecifically as amphiphilic compounds to induce transmitter release from sympathetic nerve endings, which may in turn augment the Ca current channels in the myocardial cell membrane.Key words: platelet-activating factor, cardiac action potential, slow response, Ca2+ channel, sympathetic nerve ending.


1994 ◽  
Vol 11 (3) ◽  
pp. 501-517 ◽  
Author(s):  
Leo Peichl ◽  
Juncal González-Soriano

AbstractRetinal horizontal cells of four rodent species, rat, mouse, gerbil, and guinea pig were examined to determine whether they conform to the basic pattern of two horizontal cell types found in other mammalian orders. Intracellular injections of Lucifer-Yellow were made to reveal the morphologies of individual cells. Immunocytochemistry with antisera against the calcium-binding proteins calbindin D-28k and parvalbumin was used to assess population densities and mosaics.Lucifer-Yellow injections showed axonless A-type and axon-bearing B-type horizontal cells in guinea pig, but revealed only B-type cells in rat and gerbil retinae. Calbindin immunocytochemistry labeled the A-and B-type populations in guinea pig, but only a homogeneous regular mosaic of cells with B-type features in rat, mouse, and gerbil. All calbindin-immunoreactive horizontal cells in the latter species were also parvalbumin-immunoreactive; comparison with Nissl-stained retinae showed that both antisera label all of the horizontal cells. Taken together, the data from cell injections and the population studies provide strong evidence that rat, mouse, and gerbil retinae have only one type of horizontal cell, the axon-bearing B-type, where as the guinea pig has both A-and B-type cells. Thus, at least three members of the family Muridae differ from other rodents and deviate from the proposed mammalian scheme of horizontal cell types.The absence of A-type cells is apparently not linked to any peculiarities in the photoreceptor populations, and there is no consistent match between the topographic distributions of the horizontal cells and those of the cone photoreceptors or ganglion cells across the four rodent species. However, the cone to horizontal cell ratio is rather similar in the species with and without A-type cells.


Author(s):  
Åsa Thureson-Klein ◽  
David J. Dzielak ◽  
Lennart Stjärne

Large and small dense cored vesicles are present in various proportions in the noradrenergic nerve terminals of different species. These vesicles differ not only in size but in chemical composition as well. For example, only the large vesicles contain opioid peptide, a significant amount of matrix dopamine β-hydroxylase and measurable concentrations of chromogranin A. However, while much is known about the composition of isolated large and small vesicles their exact role in transmitter release is controversial. It has not been established to what extent large and small vesicles participate in exocytosis. Moreover, physiological and pharmacological experiments have indicated that there is not always a proportional co-release of noradrenaline and dopamine β-hydroxylase. The present study was performed to find morphological evidence for the hypothesis that both large and small vesicles can release transmitter but only the large vesicles release the enzyme.


2007 ◽  
Vol 97 (1) ◽  
pp. 134-143 ◽  
Author(s):  
Gry Houeland ◽  
Arash Nakhost ◽  
Wayne S. Sossin ◽  
Vincent F. Castellucci

Activation of phosphokinase C (PKC) can increase transmitter release at sensory–motor neuron synapses in Aplysia, but the target of PKC phosphorylation has not been determined. One putative target of PKC at synapses is the synaptosomal-associated protein of 25 kDa (SNAP-25), a member of the SNARE protein complex implicated in synaptic vesicle docking and fusion. To determine whether PKC regulated transmitter release through phosphorylation of SNAP-25, we cloned Aplysia SNAP-25 and expressed enhanced green fluorescent protein (EGFP)–coupled SNAP-25 constructs mutated at the PKC phosphorylation site Ser198 in Aplysia sensory neurons. We found several distinct effects of expression of EGFP–SNAP-25 constructs. First, the rates of synaptic depression were slowed when cells contained SNAP-25 with phosphomimetic residues Glu or Asp. Second, PDBu-mediated increases in transmitter release at naïve synapses were blocked in cells expressing nonphosphorylated-state SNAP-25. Finally, expression of EGFP-coupled SNAP-25 but not uncoupled SNAP-25 inhibited 5-HT–mediated reversal of depression and the ability of EGFP-coupled SNAP-25 to inhibit the reversal of depression was affected by changes at Ser198. These results suggest SNAP-25 and phosphorylation of SNAP-25 by PKC can regulate transmitter release at Aplysia sensory–motor neuron synapses by a number of distinct processes.


1983 ◽  
Vol 61 (10) ◽  
pp. 1197-1201 ◽  
Author(s):  
Stanley Kalsner

The possibility of negative feedback regulation of noradrenaline release was studied in the sympathetically innervated ureters of the guinea pig mounted in vitro. Tissues were transmurally stimulated with 300 pulses at 2 Hz over a range of voltages, from 10 to 60 V. It was determined that the output of transmitter increased with increasing voltage but that the effects of supposed presynaptic antagonism by yohimbine and presynaptic agonism by added noradrenaline did not fulfill the requirements of presynaptic theory governing negative feedback. It is concluded that the presynaptic effects of these drugs is neither linked to the operation of a negative feedback system nor sensitive to the perineuronal concentrations of free and active neurotransmitter.


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