PubMed · 4707957
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N A Buchwald, C D Hull. 1973. Neuronal processes underlying rhythmic brain activity.. https://pubmed.ncbi.nlm.nih.gov/4707957/
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The electromechanical activity of the common bile duct (CBD) was studied in 11 dogs aiming at elucidating the mechanism of bile transport through the CBD as well as at characterizing a normal electrocholedochogram that could act as a standard for the pathologic conditions. After opening the abdomen under anesthesia and exposing the CBD, the electric activity of the CBD was recorded by 2 electrodes sutured to its serosa and the pressure registered by a perfused catheter introduced into the CBD. The effect of CBD distention and myotomy on its EMG activity was tested. Slow waves or pacesetter potentials (PPs) were recorded exhibiting the same frequency, amplitude, and velocity of conduction from the 2 electrodes of each dog on all test days. They were followed by action potentials (APs) which were inconsistent and associated with a rise in the CBD pressure. These variables were higher postcibally than in the fasting state (p < 0.05). They increased on balloon-produced distention of the CBD. The caudad direction of PPs and APs was evident when, following the CBD myotomies, the signals appeared from the segment proximal but not distal to the cut. The study demonstrated that the CBD possesses an electric activity which seems to be responsible for the motile activity of the duct. Furthermore a normal "electrocholedochogram" was characterized which is expected to exhibit changes in pathologic conditions of the CBD. It is proposed that the electrocholedochogram could act as an investigative tool in the diagnosis of CBD disorders, provided it could be performed transcutaneously.
The neurotransmitter glutamate, in addition to activating ligand-gated ion channels, also stimulates phosphoinositide (PI) hydrolysis in neurons by activating a group of G-protein-coupled metabotropic glutamate receptors (mGluRs). A role for mGluRs in synaptic plasticity originally was hypothesized based on the observation that the developmental decline in glutamate-stimulated PI turnover is well correlated with the decline in experience-dependent synaptic plasticity in visual cortex. Over the past few years, the compound alpha-methyl-4-carboxyphenylglycine (MCPG) has been widely used to test the role of PI-coupled mGluRs in a number of types of synaptic plasticity, including long-term potentiation (LTP), long-term depression (LTD), ocular dominance plasticity in visual cortex, and the neural plasticity underlying learning and memory. The conclusions of most of these studies were based on the assumption that MCPG blocks the actions of glutamate at PI-coupled mGluRs in the cerebral cortex. Here we show that this assumption is not valid in visual cortex. Although MCPG does antagonize the actions of the synthetic mGluR agonist 1S, 3R-aminocyclopentane-1,3-dicarboxylic acid, it fails to block PI turnover and changes in spike adaptation stimulated by glutamate, the endogenous mGluR ligand. In addition, we find that MCPG fails to block the NMDA receptor-dependent forms of LTP, LTD, and depotentiation in visual cortex.
Melanotropic cells release predocked, large, dense-cored vesicles containing alpha-melanocyte stimulating hormone in response to calcium entry through voltage-gated calcium channels. Our first objective was to study the relationship between exocytosis, rapid endocytosis, and calcium entry evoked by short step depolarizations in the order of duration of single action potentials (APs). Exocytosis and rapid endocytosis were monitored by capacitance measurements. We show that short step depolarizations (40 msec) evoke the fast release of only approximately 3% of the predocked release-ready vesicle pool. Second, we asked what the distance is between voltage-gated calcium channels and predocked vesicles in these cells by modulating the intracellular buffer capacity. Exocytosis and rapid endocytosis were differentially affected by low concentrations of the calcium chelator EGTA. EGTA slightly attenuated exocytosis at 100 microM relative to 50 microM, but exocytosis was strongly depressed at 400 microM, showing that calcium ions have to travel a large distance to stimulate exocytosis. Nevertheless, the efficacy of calcium ions to stimulate exocytosis was constant for pulse durations between 2 and 40 msec, indicating that in melanotropes, exocytosis is related linearly to the amount and duration of calcium entry during a single AP. Rapid endocytosis was already strongly depressed at 100 microM EGTA, which shows that the process of endocytosis itself is calcium dependent in melanotropic cells. Furthermore, rapid endocytosis proceeded with a time constant of approximately 116 msec at 33 degrees C, which is three times faster than at room temperature. There was a strong correlation between the amplitude of endocytosis and the amplitude of exocytosis immediately preceding endocytosis. Both this correlation and the fast time constant of endocytosis suggest that the exocytotic vesicle is retrieved rapidly.