Colchicine affects protein kinase C‐induced modulation of synaptic transmission in cultured hippocampal pyramidal cells

Bouron, Alexandre

doi:10.1016/s0014-5793(97)00135-x

Cited by 15 publications

(11 citation statements)

References 25 publications

(16 reference statements)

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“…Since Ca 2ϩ channels were blocked with Cd 2ϩ , the carbachol action was independent of the entry of Ca 2ϩ through presynaptic voltage-gated Ca 2ϩ channels. This is in agreement with previous reports showing that phorbol esters increase excitatory and inhibitory synaptic transmission in the presence of Cd 2ϩ in hippocampal cells (14,29). However, the exact molecular mechanism of action of PKC activators on neurotransmission is unknown.…”

Section: Physiology: Bouron and Reutersupporting

confidence: 93%

“…However, the modulatory effect was still observed after treating the cells with the inactive analogue 4␣-PMA. It is worth mentioning that carbachol (200 M) and acute applications of PMA (100 nM) increased the sEPSC frequency to the same extent (14), but these effects were not additive, suggesting a common site of action (not shown). In contrast, 4␤-PMA and activation of adenylate cyclase by forskolin did act additively (not shown) (29).…”

Section: Resultsmentioning

confidence: 97%

“…A similar effect was also observed with acetylcholine (50 M, 2.5 Ϯ 0.07-fold increase, P Ͻ 0.05, n ϭ 4, not shown). The ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type channel blocker 6-cyano-nitroquinoxaline-2,3-dione (10 M) reversibly suppressed the sEPSCs in control solution and in carbachol-containing solutions (14).…”

Section: Resultsmentioning

confidence: 99%

“…The experimental procedures for the electrophysiological measurements and analyses have been described (13,14). Briefly, the sEPSCs were recorded at a holding potential of Ϫ50 mV by means of the whole-cell configuration of the patch-clamp technique (15).…”

Section: Methodsmentioning

confidence: 99%

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Muscarinic stimulation of synaptic activity by protein kinase C is inhibited by adenosine in cultured hippocampal neurons

Bouron

Réuter²

1997

Proc. Natl. Acad. Sci. U.S.A.

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We have studied the effect of the cholinergic agonist carbachol on the spontaneous release of glutamate in cultured rat hippocampal cells. Spontaneous excitatory postsynaptic currents (sEPSCs) through glutamatergic ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type channels were recorded by means of the patch-clamp technique. Carbachol increased the frequency of sEPSCs in a concentration-dependent manner. The kinetic properties of the sEPSCs and the amplitude distribution histograms were not affected by carbachol, arguing for a presynaptic site of action. This was confirmed by measuring the turnover of the synaptic vesicular pool by means of the f luorescent dye FM 1-43. The carbachol-induced increase in sEPSC frequency was not mimicked by nicotine, but could be blocked by atropine or by pirenzepine, a muscarinic cholinergic receptor subtype M1 antagonist. Intracellular Ca 2؉ signals recorded with the f luorescent probe Fluo-3 indicated that carbachol transiently increased intracellular Ca 2؉ concentration. Since, however, carbachol still enhanced the sEPSC frequency in bis(2-aminophenoxy)ethane-N,N,N ,N -tetra-acetate-loaded cells, this effect could not be attributed to the rise in intracellular Ca 2؉ concentration. On the other hand, the protein kinase inhibitor staurosporine as well as a down-regulation of protein kinase C by prolonged treatment of the cells with 4␤-phorbol 12-myristate 13-acetate inhibited the carbachol effect. This argues for an involvement of protein kinase C in presynaptic regulation of spontaneous glutamate release. Adenosine, which inhibits synaptic transmission, suppressed the carbachol-induced stimulation of sEPSCs by a G proteindependent mechanism activated by presynaptic A1-receptors.The occurrence of memory deficits in neurodegenerative disorders, such as Alzheimer disease, or the effects of cholinergic drugs on learning and memory have revealed an important role of the central cholinergic system in human cognitive functions (1-4). The hippocampus, which is known to be involved in memory formation (1, 4), receives cholinergic neurons from the basal forebrain. The cholinergic septohippocampal pathway modulates the activity of the hippocampus. For instance it is involved in the control of the theta rhythmic activity (5).Hippocampal cells express cholinergic nicotinic and muscarinic receptors with a predominance of the latter (5). Five muscarinic cholinergic receptor subtypes (M1-M5) have been identified (6). M1, M3, and M5 are coupled to phospholipase C activation resulting in the production of the second messengers inositol trisphosphate (IP 3 ) and diacylglycerol, whereas M2 and M4 inhibit adenylate cyclase activity (6). Immunoprecipitation studies, measurements of mRNA levels and of ligand binding sites indicate that the M1-subtype is the most abundant muscarinic receptor in the hippocampus (7).However, the role of M1-receptor activation and the subsequent signaling pathway in neurotransmitter release are only poorly understood. We have studied the effect of ...

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Section: Physiology: Bouron and Reutersupporting

confidence: 93%

Section: Resultsmentioning

confidence: 97%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Muscarinic stimulation of synaptic activity by protein kinase C is inhibited by adenosine in cultured hippocampal neurons

Bouron

Réuter²

1997

Proc. Natl. Acad. Sci. U.S.A.

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“…Brighter fluorescence in light-adapted terminals indicates higher concentrations of PKC and the more cytosolic localisation may be linked to increased dynamics of vesicle translocation and a stronger involvement of the actin and microtubular cytoskeleton. Notably, the organisation of both cytoskeletal components is regulated by PKC-dependent signalling mechanisms (Bouron 1997;Komoly et al 1991;Li and Aderem 1992). Other patterns of PKC immunoreactivity reported for bipolar cell terminals may be related to various degrees of ischemia, which is known to affect the activity and concentration of this enzyme (Osborne et al 1995;Wood et al 1997).…”

Section: Discussionmentioning

confidence: 95%

Adaptation-dependent plasticity of rod bipolar cell axon terminal morphology in the rat retina

Behrens

Kasten

Wagner

1998

Cell and Tissue Research

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We chose synaptic terminals of rat rod bipolar cells as a model system to study activity-related changes in the overall morphology and the fine structure of synaptic sites. Using confocal laser scanning microscopy in conjunction with three-dimensional reconstruction and electron microscopy, we examined the effect of light and dark adaptation on axon terminals identified by protein kinase C (PKC) immunoreactivity. Rod bipolar cell axon terminals consisted of 2-3 polymorphic boutons situated close to the ganglion cell layer and a single ovoid swelling located more distally. Both components of the terminal complex showed adaptation-dependent differences in the distribution of PKC immunoreactivity and in their morphology. In light-adapted rod bipolar cell axon terminals, PKC immunoreactivity was homogeneously distributed throughout the cytoplasm, whereas terminals from dark-adapted animals showed PKC immunoreactivity preferentially localised in the submembrane compartment and a reduced staining of the more central cytoplasm. In three-dimensional reconstructions of optical sections and at the ultrastructural level, the shape of light-adapted axon terminals was round and smooth and exhibited more convexly curved synaptic membranes. In contrast, dark-adapted terminals had irregular contours, numerous dimples and a concave synaptic curvature. No spinules of bipolar cell terminals were observed in dark-adapted material. These observations are discussed in the context of activity-related morphological plasticity of central nervous system synapses and of the functions of PKC in the cycle of vesicle fusion and retrieval at the tonically active ribbon synapses of the rod bipolar axon terminal.

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Contractile and Electrical Activity of Neurons on Exposure to Colchicine

Sergeeva

Vasyagina

et al. 2013

Neurosci Behav Physi

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Colchicine affects protein kinase C‐induced modulation of synaptic transmission in cultured hippocampal pyramidal cells

Cited by 15 publications

References 25 publications

Muscarinic stimulation of synaptic activity by protein kinase C is inhibited by adenosine in cultured hippocampal neurons

Muscarinic stimulation of synaptic activity by protein kinase C is inhibited by adenosine in cultured hippocampal neurons

Adaptation-dependent plasticity of rod bipolar cell axon terminal morphology in the rat retina

Contractile and Electrical Activity of Neurons on Exposure to Colchicine

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