Synaptic excitation may activate a calcium-dependent potassium conductance in hippocampal pyramidal cells

In hippocampal CAl pyramidal cells, orthodromic synaptic excitation is followed by an early hyperpolarization mediated by gamma-aminobutyric acid (GABA) and a late non-GABA-mediated hyperpolarization that has properties consistent with an increase in potassium conductance. Depolarizations produced by iontophoretically applied glutamate are followed by hyperpolarizations that have features in accordance with an increase in potassium conductance. The hyperpolarizations are independent of chloride and resistant to tetradotoxin but are blocked by a low-calcium, high-cobalt medium. Voltage clamping the glutamate depolarization does not reduce the subsequent hyperpolarization, indicating that the hyperpolarization results from a direct increase in calcium conductance produced by glutamate, rather than from activation of voltage-sensitive calcium channels. A single transmitter, possibly acting on one type of receptor and channel, may initiate both excitation and inhibition in the same postsynaptic cell.     

Depolarization and muscarinic excitation induced in a sympathetic ganglion by vasoactive intestinal polypeptide

The effects of vasoactive intestinal polypeptide (VIP) in the superior cervical ganglion of the cat were studied in vitro and in vivo with sucrose gap and multiunit recording, respectively. At a dose of 0.03 to 0.12 nanomole, VIP produced a dose-dependent, prolonged (3 to 15 minutes) depolarization of the ganglion and enhanced the ganglionic depolarization elicited by the muscarinic agonist acetyl-beta-methylcholine. At a dose of 1.8 to 10 nanomoles, the peptide enhanced and prolonged the postganglionic discharge elicited by acetyl-beta-methylcholine, enhanced muscarinic transmission in ganglia treated with an anticholinesterase agent, and enhanced the late muscarinic discharge elicited by acetylcholine. VIP did not affect the early nicotinic discharge elicited by acetylcholine or by electrical stimulation of the preganglionic nerve. It is concluded that VIP has a selective facilitatory action on muscarinic excitatory mechanisms in the superior cervical ganglion of the cat.     

Generation of adrenergic and cholinergic potentials in sympathetic ganglion cells

Norepinephrine elicited a hyperpolarizing response, and acetylcholine (during nicotinic blockade) elicited a depolarizing one. Both responses showed no increase in membrane conductance. The norepinephrine response was suppressed by initial depolarization; the acetylcholine response (frog cells); by hyperpolarization. These neurotransmitters apparently can activate electrogenic mechanisms which do not involve movement of ions down their electrochemical gradients.     

Role for ganglionic norepinephrine in sympathetic synaptic transmission

Transmission of nerve impulses in superior cervical sympathetic ganglia of cats and rabbits is markedly enhanced after reserpine-induced depletion of ganglionic norepinephrine. Transmission is also enhanced by administration of adrenergic blocking agents. In contrast, reserpine-induced release of ganglionic norepinephrine in animals pretreated with a monoamine oxidase inhibitor results in a pronounced depression of ganglionic transmission, which lasts until the ganglionic norepinephrine disappears. These results support the concept that norepinephrine in ganglia modulates the action of acetylcholine.     

Mediation of responses to calcium in taste cells by modulation of a potassium conductance

Calcium salts are strong taste stimuli in vertebrate animals. However, the chemosensory transduction mechanisms for calcium are not known. In taste buds of Necturus maculosus (mud puppy), calcium evokes depolarizing receptor potentials by acting extracellularly on the apical ends of taste cells to block a resting potassium conductance. Therefore, divalent cations elicit receptor potentials in taste cells by modulating a potassium conductance rather than by permeating the cell membrane, the mechanism utilized by monovalent cations such as sodium and potassium ions.     

Dopamine-beta-hydroxylase: evidence for increased activity in sympathetic neurons during psychotic states

Tritiated dopamine was infused into psychiatric patients during acute psychotic episodes and in remission. An index of the activity of dopamine-beta-hydroxylase of salivary gland sympathetic neurons was determined by measuring the distribution of tritiated metabolites in salivary fluid. Increased synthesis of norepinephrine occurred in acute schizophrenia and in the manic state of manic-depressive psychosis but not in the depressed phase.     

Sleep and synaptic homeostasis: structural evidence in Drosophila

The functions of sleep remain elusive, but a strong link exists between sleep need and neuronal plasticity. We tested the hypothesis that plastic processes during wake lead to a net increase in synaptic strength and sleep is necessary for synaptic renormalization. We found that, in three Drosophila neuronal circuits, synapse size or number increases after a few hours of wake and decreases only if flies are allowed to sleep. A richer wake experience resulted in both larger synaptic growth and greater sleep need. Finally, we demonstrate that the gene Fmr1 (fragile X mental retardation 1) plays an important role in sleep-dependent synaptic renormalization.     

Adenosine 3',5'-monophosphate: electrophysiological evidence for a role in synaptic transmission

Synaptic potentials and changes in resting membrane potentials of superior cervical ganglia of the rabbit were measured in the presence of adenosine 3',5'-monophosphate and agents that affect its metabolism. Adenosine 3',5'-monophosphate and its mono- and dibutyryl derivatives caused a hyperpolarization of the postganglionic neurons. Theophylline potentiated the slow inhibitory postsynaptic potential that follows synaptic transmission, as well as the hyperpolarization of postganglionic neurons caused by exogenous dopamine. Conversely, prostaglandin E(1) inhibited both the slow inhibitory postsynaptic potential and the dopamine-induced hyperpolarization. We hypothesize that the slow inhibitory postsynaptic potential as well as the dopamine-induced hyperpolarization result from increased amounts of adenosine 3'5'-monophosphate in the postganglionic neurons. The dibutyryl derivative of guanosine 3'5'-monophosphate caused a depolarization of the postganglionic neurons, which is consistent with the possibility that guanosine 3'5'-monophosphate mediates synaptic transmission at muscarinic cholinergic synapses.     

Guanosine 3',5'-monophosphate in sympathetic ganglia: increase assoicated with synaptic transmission

Brief stimulation of cholinergic preganglionic nerve fibers resulted in an increase in guanosine 3',5'-monophosphate (cyclic GMP) in the bullfrog sympathetic ganglion. When the release of synaptic transmitter was prevented by a high-magnesium, low-calcium Ringer solution, stimulation of preganglionic nerve fibers did not increase cyclic GMP in the ganglion. The increase in cyclic GMP caused by preganglionic stimulation was also blocked by the muscarinic antagonist, atropine. The data indicate that the increase in cyclic GMP is associated with synaptic transmission and support the possibility that cyclic GMP may mediate the postsynaptic action of acetylcholine at muscarinic cholinergic synapses.     

Reactivation of an inactive human X chromosome: evidence for X inactivation by DNA methylation

A mouse-human somatic cell hybrid clone, deficient in hypoxanthine-guanine phosphoribosyltransferase (HPRT) and containing a structurally normal inactive human X chromosome, was isolated. The hybrid cells were treated with 5-azacytidine and tested for the reactivation and expression of human X-linked genes. The frequency of HPRT-positives clones after 5-azacytidine treatment was 1000-fold greater than that observed in untreated hybrid cells. Fourteen independent HPRT-positive clones were isolated and analyzed for the expression of human X markers. Isoelectric focusing showed that the HPRT expressed in these clones is human. One of the 14 clones expressed human glucose-6-phosphate dehydrogenase and another expressed human phosphoglycerate kinase. Since 5-azacytidine treatment results in hypomethylation of DNA, DNA methylation may be a mechanism of human X chromosome inactivation.     

Authigenic potassium feldspar in cambrian carbonates: evidence of alleghanian brine migration

The shallow-water limestones and dolostones of the Conococheague Limestone (Upper Cambrian) of western Maryland contain large amounts of authigenic potassium feldspar. The presence of halite daughter crystals in breached fluid inclusions, low whole-rock ratios of chlorine to bromine, and thermochemical data suggest that the potassium feldspar formed at low temperature by the reaction of connate brines with intercalated siliciclastic debris. Analyses of argon age spectra indicate that the authigenic feldspar probably formed during Late Pennsylvanian to Early Permian time. These results may indicate mobilization and migration of connate brines brought about by Alleghanian folding. The widespread occurrence of authigenic potassium feldspar in Cambrian and Ordovician carbonate rocks throughout the Appalachians suggests that this may have occurred throughout the entire basin.     

Goldfish retina: sign of the rod input in opponent color ganglion cells

After light adaptation, all "on-center" ganglion cells in the dark became "red on-center," and all "off-center" cells turned into "red off-center" cells. On a chance basis, this similitude of effect between the rods and the red cones in opponent color cells was not expected. These findings indicate that in the goldfish there is some similarity between the connections of the rods and of the long-wavelength cones.     

Restoration of inactivation in mutants of Shaker potassium channels by a peptide derived from ShB

Site-directed mutagenesis experiments have suggested a model for the inactivation mechanism of Shaker potassium channels from Drosophila melanogaster. In this model, the first 20 amino acids form a cytoplasmic domain that interacts with the open channel to cause inactivation. The model was tested by the internal application of a synthetic peptide, with the sequence of the first 20 residues of the ShB alternatively spliced variant, to noninactivating mutant channels expressed in Xenopus oocytes. The peptide restored inactivation in a concentration-dependent manner. Like normal inactivation, peptide-induced inactivation was not noticeably voltage-dependent. Trypsin-treated peptide and peptides with sequences derived from the first 20 residues of noninactivating mutants did not restore inactivation. These results support the proposal that inactivation occurs by a cytoplasmic domain that occludes the ion-conducting pore of the channel.     

Stomatal opening: role of potassium uptake by guard cells

Stomata in isolated epidermal strips open in response to light plus air free of carbon dioxide when the strips are floated on potassium chloride solutions of low concentrations. This opening depends on the stimulation of active accumulation of potassium in quantities sufficient to account for the observed changes in solute potential of the guard cells.     

Electron microscopic evidence for plasmodesmata in dicotyledonous guard cells

In Nicotianna tobaccum and Vicia faba leaves, plasmodesmata were observed by electron microscopy in walls between sister guard cells and walls between guard and epidermal cells. The latter were found primarily in pit fields of anticlinal walls and showed considerable complexity as evidenced by branching. Cytologically, the plasmodesmata appear functional in operative guard cells and should be considered in the mechanism of stomatal movements.     

Slow transport of tubulin in the neurites of differentiated PC12 cells

In order to study the rate and form of tubulin transport in cultured neuronal cells, the fluorescence recovery after the photobleaching of a fluorescent tubulin analog has been followed within the neuritic processes of differentiated PC12 cells. In these cells, as in peripheral axons, tubulin is transported in coherent, nondiffusing waves at two different slow rates that are within the range of the slow components a and b of axonal transport measured in vivo. Finally, it appears that most, if not all, of the tubulin analog is moving out these processes. Thus, slow neuroplasmic transport in cultured neuron-like cells is a good model of axonal transport, in which experimental manipulations of the system can be performed that would be difficult in the whole animal.     

Spontaneous impulse activity of rat retinal ganglion cells in prenatal life

The existence of spontaneous neural activity in mammalian retinal ganglion cells during prenatal life has long been suspected. This activity could play a key role in the refinement of retinal projections during development. Recordings in vivo from the retinas of rat fetuses between embryonic day 17 and 21 found action potentials in spontaneously active ganglion cells at all the ages studied.     

Biochemical evidence for keratinization by mouse epidermal cells in culture

More than 70 percent of the urea-extractable proteins from mouse stratum corneum or from differentiated cells of mouse epidermis grown in culture are two proteins of molecular weight 68,000 (keratin I) and 60,000 (kerae are two proteins of molecular weight 68,000 (keratin 1) and 60,000 (keratin 2), which are present in equimolar amounts on polyacrylamide gels. These proteins are the subunits of the keratin filaments, because when isolated from stratum corneum or cells grown in culture they form native-type epidermal keratin filaments in vitro. These observations provide biochemical evidence that epidermal cells grown in culture synthesize the major differentiation products of the epidermis.