P/Q Channels (p + channel)

Distribution by Scientific Domains


Selected Abstracts


Guest-Induced Chirality in the Ferrimagnetic Nanoporous Diamond Framework Mn3(HCOO)6,

ADVANCED FUNCTIONAL MATERIALS, Issue 4 2007
B. Zhang
Abstract Chiral magnets are obtained by inclusion of chiral guest molecules into the channels of an achiral nanoporous ferrimagnet consisting of the Mn3(HCOO)6 (1) framework. Insertion of the R or the S enantiomer of 2-chloropropan-1-ol (CH3C*HClCH2OH) in the chiral pores of the previously emptied framework (space group P21/c) results in the two corresponding chiral solids (1R and 1S, space group P21), while insertion of a racemic mixture of the two enantiomers retains the achirality of the host for the meso solid (1RS, space group P21/c). The R guest is ordered in the M channels while the S guest is ordered in the P channels. In contrast, the R guests in the P channels and the S guests in the M channels are disordered on two crystallographic orientations. For the racemic mixture of the two enantiomers in 1RS, random disorder of guests in both channels is observed. Thus, the localization of the guest molecule depends on the nature of the surface to recognize the guest of a particular chirality. The guest inclusion compounds are thermally stable. The 1R and 1S compounds are optically active. All the compounds adopt a ferrimagnetic ground state. Compared to the host framework of 1 without guest, the Curie temperature decreases for both 1R and 1S but increases for 1RS. The additional interactions between the framework and the inserted guest alcohols strengthen the lattice via hydrogen bonds and other electrostatic forces, and it might account for the significant lowering of the lattice contribution as well as the magnetic component to the specific heat capacity upon guest loading. [source]


Calcium handling in afferent arterioles

ACTA PHYSIOLOGICA, Issue 4 2004
M. Salomonsson
Abstract The cytosolic intracellular calcium concentration ([Ca2+]i) is a major determining factor in the vascular smooth muscle tone. In the afferent arteriole it has been shown that agonists utilizing G-protein coupled receptors recruit Ca2+ via release from intracellular stores and entry via pathways in the plasma membrane. The relative importances of entry vs. mobilization seem to differ between different agonists, species and preparations. The entry pathway might include different types of voltage sensitive Ca2+ channels located in the plasmalemma such as dihydropyridine sensitive L-type channels, T-type channels and P/Q channels. A role for non-voltage sensitive entry pathways has also been suggested. The importance of voltage sensitive Ca2+ channels in the control of the tone of the afferent arteriole (and thus in the control of renal function and whole body control of extracellular fluid volume and blood pressure) sheds light on the control of the membrane potential of afferent arteriolar smooth muscle cells. Thus, K+ and Cl, channels are of importance in their role as major determinants of membrane potential. Some studies suggest a role for calcium-activated chloride (ClCa) channels in the renal vasoconstriction elicited by agonists. Other investigators have found evidence for several types of K+ channels in the regulation of the afferent arteriolar tone. The available literature in this field regarding afferent arterioles is, however, relatively sparse and not conclusive. This review is an attempt to summarize the results obtained by others and ourselves in the field of agonist induced afferent arteriolar Ca2+ recruitment, with special emphasis on the control of voltage sensitive Ca2+ entry. Outline of the Manuscript: This manuscript is structured as follows: it begins with an introduction where the general role for [Ca2+]i as a key factor in the regulation of the tone of vascular smooth muscles (VSMC) is detailed. In this section there is an emphasis is on observations that could be attributed to afferent arteriolar function. We then investigate the literature and describe our results regarding the relative roles for Ca2+ entry and intracellular release in afferent arterioles in response to vasoactive agents, with the focus on noradrenalin (NA) and angiotensin II (Ang II). Finally, we examine the role of ion channels (i.e. K+ and Cl, channels) for the membrane potential, and thus activation of voltage sensitive Ca2+ channels. [source]


Endogenous and exogenous dopamine presynaptically inhibits glutamatergic reticulospinal transmission via an action of D2 -receptors on N-type Ca2+ channels

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2003
Erik Svensson
Abstract In this study, the effects of exogenously applied and endogenously released dopamine (DA), a powerful modulator of the lamprey locomotor network, are examined on excitatory glutamatergic synaptic transmission between reticulospinal axons and spinal neurons. Bath application of DA (1,50 µm) reduced the amplitude of monosynaptic reticulospinal-evoked glutamatergic excitatory postsynaptic potentials (EPSPs). The effect of DA was blocked by the D2 -receptor antagonist eticlopride, and mimicked by the selective D2 -receptor agonist 2,10,11 trihydroxy- N -propyl-noraporphine hydrobromide (TNPA). Bath application of the DA reuptake blocker bupropion, which increases the extracellular level of dopamine, also reduced the monosynaptic EPSP amplitude. This effect was also blocked by the D2 -receptor antagonist eticlopride. To investigate if the action of DA was exerted at the presynaptic level, the reticulospinal axon action potentials were prolonged by administering K+ channel antagonists while blocking l -type Ca2+ channels. A remaining Ca2+ component, mainly dependent on N and P/Q channels, was depressed by DA. When DA (25,50 µm) was applied in the presence of ,-conotoxin GVIA, a toxin specific for N-type Ca2+ channels, it failed to affect the monosynaptic EPSP amplitude. DA did not affect the response to extracellularly ejected d -glutamate, the postsynaptic membrane potential, or the electrical component of the EPSPs. DA thus acts at the presynaptic level to modulate reticulospinal transmission. [source]


Calcium channel subtypes differentially regulate fusion pore stability and expansion

JOURNAL OF NEUROCHEMISTRY, Issue 4 2007
Alvaro O. Ardiles
Abstract Various studies have focused in the relative contribution of different voltage-activated Ca2+ channels (VACC) to total transmitter release. However, how Ca2+ entry through a given VACC subtype defines the pattern of individual exocytotic events remains unknown. To address this question, we have used amperometry in bovine chromaffin cells. L, N, and P/Q channels were individually or jointly blocked with furnidipine, ,-conotoxin GVIA, ,-agatoxin IVA, or ,-conotoxin MVIIC. The three channel types contributed similarly to cytosolic Ca2+ signals induced by 70 mmol/L K+. However, they exhibited different contributions to the frequency of exocytotic events and they were shown to differently regulate the final steps of the exocytosis. When compared with the other VACC subtypes, Ca2+ entry through P/Q channels effectively induced exocytosis, it decreased fusion pore stability and accelerated its expansion. Conversely, Ca2+ entry through N channels was less efficient in inducing exocytotic events, also slowing fusion pore expansion. Finally, Ca2+ entry through L channels inefficiently induced exocytosis, and the individual blockade of this channel significantly modified fusion pore dynamics. The distance between a given VACC subtype and the release sites could account for the differential effects of the distinct VACC on the fusion pore dynamics. [source]


Differential Ca2+ -dependence of transmitter release mediated by P/Q- and N-type calcium channels at neonatal rat neuromuscular junctions

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2002
Marcelo D. Rosato-Siri
Abstract N- and P/Q-type voltage dependent calcium channels (VDCCs) mediate transmitter release at neonatal rat neuromuscular junction (NMJ). Thus the neonatal NMJ allows an examination of the coupling of different subtypes of VDCCs to the release process at a single synapse. We studied calcium dependence of transmitter release mediated by each channel by blocking with ,-conotoxin GVIA the N-type channel or with ,-agatoxin IVA the P/Q-type channel while changing the extracellular calcium concentration ([Ca2+]o). Transmitter release mediated by P/Q-type VDCCs showed steeper calcium dependence than N-type mediated release (average slope 3.6 ± 0.09 vs. 2.6 ± 0.03, respectively). Loading the nerve terminals with 10 µm BAPTA-AM in the extracellular solution reduced transmitter release and occluded the blocking effect of ,-conotoxin GVIA (blockade ,2 ± 9%) without affecting the action of ,-agatoxin IVA (blockade 85 ± 4%). Both VDCC blockers were able to reduce the amount of facilitation produced by double-pulse stimulation. In these conditions facilitation was restored by increasing [Ca2+]o. The facilitation index (fi) was also reduced by loading nerve terminals with 10 µm BAPTA-AM (fi = 1.2 ± 0.1). The control fi was 2.5 ± 0.1. These results show that P/Q-type VDCCs were more efficiently coupled to neurotransmitter release than were N-type VDCCs at the neonatal neuromuscular junction. This difference could be accounted for by a differential location of these channels at the release site. In addition, our results indicate that space,time overlapping of calcium domains was required for facilitation. [source]