53 research outputs found
Characterization of Voltage-Gated Ca2+ Conductances in Layer 5 Neocortical Pyramidal Neurons from Rats
Neuronal voltage-gated Ca2+ channels are involved in electrical signalling and in converting these signals into cytoplasmic calcium changes. One important function of voltage-gated Ca2+ channels is generating regenerative dendritic Ca2+ spikes. However, the Ca2+ dependent mechanisms used to create these spikes are only partially understood. To start investigating this mechanism, we set out to kinetically and pharmacologically identify the sub-types of somatic voltage-gated Ca2+ channels in pyramidal neurons from layer 5 of rat somatosensory cortex, using the nucleated configuration of the patch-clamp technique. The activation kinetics of the total Ba2+ current revealed conductance activation only at medium and high voltages suggesting that T-type calcium channels were not present in the patches. Steady-state inactivation protocols in combination with pharmacology revealed the expression of R-type channels. Furthermore, pharmacological experiments identified 5 voltage-gated Ca2+ channel sub-types – L-, N-, R- and P/Q-type. Finally, the activation of the Ca2+ conductances was examined using physiologically derived voltage-clamp protocols including a calcium spike protocol and a mock back-propagating action potential (mBPAP) protocol. These experiments enable us to suggest the possible contribution of the five Ca2+ channel sub-types to Ca2+ current flow during activation under physiological conditions
Physiology and pathophysiology of the vasopressin-regulated renal water reabsorption
To prevent dehydration, terrestrial animals and humans have developed a sensitive and versatile system to maintain their water homeostasis. In states of hypernatremia or hypovolemia, the antidiuretic hormone vasopressin (AVP) is released from the pituitary and binds its type-2 receptor in renal principal cells. This triggers an intracellular cAMP signaling cascade, which phosphorylates aquaporin-2 (AQP2) and targets the channel to the apical plasma membrane. Driven by an osmotic gradient, pro-urinary water then passes the membrane through AQP2 and leaves the cell on the basolateral side via AQP3 and AQP4 water channels. When water homeostasis is restored, AVP levels decline, and AQP2 is internalized from the plasma membrane, leaving the plasma membrane watertight again. The action of AVP is counterbalanced by several hormones like prostaglandin E2, bradykinin, dopamine, endothelin-1, acetylcholine, epidermal growth factor, and purines. Moreover, AQP2 is strongly involved in the pathophysiology of disorders characterized by renal concentrating defects, as well as conditions associated with severe water retention. This review focuses on our recent increase in understanding of the molecular mechanisms underlying AVP-regulated renal water transport in both health and disease
Transmembrane signalling in eukaryotes: a comparison between higher and lower eukaryotes
Transmembrane signalling in eukaryotes: a comparison between higher and lower eukaryotes
Covalent attachment of a progestational steroid to chick oviduct progesterone receptor by photoaffinity labelling
Antisense oligodeoxynucleotides to Gs protein α-subunit sequence accelerate differentiation of fibroblasts to adipocytes
The effect of vasoactive intestinal polypeptide (VIP) on forskolin stimulated adenylate cyclase in the caudate-putamen of the rat
Hormonal Inhibition of the Liver Plasma Membrane (Ca2+ —Mg2+ ) ATPase is Mediated by a Gs-like Protein
Chronic ethanol causes heterologous desensitization of receptors by reducing αsmessenger RNA
The effects of hydrostatic pressure on the low-K m GTPase in brain membranes from two congeneric marine fishes
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