Maintenance of resting potential in anoxic guinea pig ventricular muscle: electrogenic sodium pumping

Anoxic ventricular muscle maintained a normal resting potenitial despite a large loss of potassium. The resting potential was separated into two components: one that depended on the potassium distribution, and one that depended on the activity of an electrogenic sodium pump.     

Electrogenic sodium pump in squid giant axon

Squid giant axon possesses a hyperpolarizing electrogenic sodium pump which is stimulated by internal sodium and by external potassium. This conclusion is based on the following observations: strophanthidin depolarizes the membrane and enhances the depolarizing effect of 5 or 10 millimolar external potassium; the magnitude of these effects is directly related to the internal sodium concentration; both effects are abolished by cyanide.     

A role for the sodium pump in photoreception in Limulus

The membranes of photoreceptor cells in Limulus have an electrogenic sodium pump which contributes directly to membrane potential and whose activity is changed by light. These light-induced changes in pump activity underlie the receptor potential.     

Electrogenic sodium pump and high specific resistance in nerve cell bodies of the squid

An electrogenic sodium pump contributes to the membrane potential in squid nerve cell bodies, imparting a temperature dependence to the resting potential that is abolished by strophanthidin. The existence of a potential produced by the pump in the soma but not the axon is correlated with a higher membrane resistance in the soma. Thus, membranes from different parts of a neuron may have functionally significant differences in resistance.     

Calmodulin activation of calcium-dependent sodium channels in excised membrane patches of Paramecium

Calmodulin is a calcium-binding protein that participates in the transduction of calcium signals. The electric phenotypes of calmodulin mutants of Paramecium have suggested that the protein may regulate some calcium-dependent ion channels. Calcium-dependent sodium single channels in excised patches of the plasma membrane from Paramecium were identified, and their activity was shown to decrease after brief exposure to submicromolar concentrations of calcium. Channel activity was restored to these inactivated patches by adding calmodulin that was isolated from Paramecium to the cytoplasmic surface. This restoration of channel activity did not require adenosine triphosphate and therefore, probably resulted from direct binding of calmodulin, either to the sodium channel itself or to a channel regulator that was associated with the patch membrane.     

Synaptic theory of working memory

It is usually assumed that enhanced spiking activity in the form of persistent reverberation for several seconds is the neural correlate of working memory. Here, we propose that working memory is sustained by calcium-mediated synaptic facilitation in the recurrent connections of neocortical networks. In this account, the presynaptic residual calcium is used as a buffer that is loaded, refreshed, and read out by spiking activity. Because of the long time constants of calcium kinetics, the refresh rate can be low, resulting in a mechanism that is metabolically efficient and robust. The duration and stability of working memory can be regulated by modulating the spontaneous activity in the network.     

Voltage-dependent sodium channels in an invertebrate striated muscle

Striated skeletal muscles from the planktonic arrowworm Sagitta elegans (phylum Chaetognatha) were voltage-clamped. The muscles displayed classical voltage-dependent sodium channels that (i) showed peak transient currents when the membrane was depolarized 90 millivolts from rest, (ii) opened rapidly with peak currents flowing within 0.4 milliseconds at 4 degrees C, (iii) showed voltage-dependent inactivation with 50 percent inactivation at +25 millivolts from rest, and (iv) were blocked by 500 nanomolar tetrodotoxin.     

Glucuronidase activation: enzyme action at an interface

Although the rate of hydrolysis by mammalian beta-glucuronidase appears to be inhibited by methylene chloride or carbon tetrachloride with the standard technique (phenolphthalein glucuronide as a substrate), the release of steroidal conjugates under conditions generally employed does not appear to be affected.     

Identification of an intracellular peptide segment involved in sodium channel inactivation

Antibodies directed against a conserved intracellular segment of the sodium channel alpha subunit slow the inactivation of sodium channels in rat muscle cells. Of four site-directed antibodies tested, only antibodies against the short intracellular segment between homologous transmembrane domains III and IV slowed inactivation, and their effects were blocked by the corresponding peptide antigen. No effects on the voltage dependence of sodium channel activation or of steady-state inactivation were observed, but the rate of onset of the antibody effect and the extent of slowing of inactivation were voltage-dependent. Antibody binding was more rapid at negative potentials, at which sodium channels are not inactivated; antibody-induced slowing of inactivation was greater during depolarizations to more positive membrane potentials. The peptide segment recognized by this antibody appears to participate directly in rapid sodium channel inactivation during large depolarizations and to undergo a conformational change that reduces its accessibility to antibodies as the channel inactivates.     

Receptor-coupled activation of phosphoinositide-specific phospholipase C by an N protein

Cleavage of phosphatidylinositol 4,5-bisphosphate by phospholipase C results in the production of two important second messengers: inositol-1,4,5-trisphosphate and 1,2-diacylglycerol. Although several receptors promote this cleavage, the molecular details of phospholipase C activation have remained unresolved. In this study, occupancy of a Ca2+-mobilizing receptor, the oligopeptide chemoattractant receptor on human polymorphonuclear leukocyte plasma membranes, was found to lead to the activation of a guanine nucleotide regulatory (N) protein by guanosine 5'-triphosphate. The activated N protein then stimulated a polyphosphoinositide-specific phospholipase C by reducing the Ca2+ requirement for expression of this activity from superphysiological to normal intracellular concentrations. Therefore, the N protein-mediated activation of phospholipase C may be a key step in the pathway of cellular activation by chemoattractants and certain other hormones.     

Synaptic transmission depressed by colchicine blockade of axoplasmic flow

Colchicine, which inhibits axoplasmic transport and induces organelle alterations in nerve terminals, was injected intraocularly in pigeons. Electrical stimulation of the optic nerve yielded normal evoked potentials in retinotectal fibers, whereas postsynaptic responses recorded in the tectum were reduced. Postsynaptic depression suggests a deficit of synaptic transmission, presumably dependent on colchicine interference with migrating material.     

Synaptic protein degradation underlies destabilization of retrieved fear memory

Reactivated memory undergoes a rebuilding process that depends on de novo protein synthesis. This suggests that retrieval is dynamic and serves to incorporate new information into preexisting memories. However, little is known about whether or not protein degradation is involved in the reorganization of retrieved memory. We found that postsynaptic proteins were degraded in the hippocampus by polyubiquitination after retrieval of contextual fear memory. Moreover, the infusion of proteasome inhibitor into the CA1 region immediately after retrieval prevented anisomycin-induced memory impairment, as well as the extinction of fear memory. This suggests that ubiquitin- and proteasome-dependent protein degradation underlies destabilization processes after fear memory retrieval. It also provides strong evidence for the existence of reorganization processes whereby preexisting memory is disrupted by protein degradation, and updated memory is reconsolidated by protein synthesis.     

Synaptic vesicles in electron micrographs of freeze-etched nerve terminals

Freeze-etched neuropil of the cat subfornical organ was examined with the electron microscope for synaptic vesicles. Round vesicles were found exclusively in both unfixed and aldehyde-fixed specimens. Range of diameters and histograms failed to differ significantly between freeze-etched and conventionally prepared material. The mnode of distribution of diameters was approximately 500 angstroms. Round stomata (approximately 350 angstromns in diameter) were found at the outer surface of the plasmalemma of nerve terminials; they are interpreted as pinocytotic vesicles.     

Viviparous leaves produced by somatic activation of an inactive cytokinin-synthesizing gene

Tobacco plants that are somatic mosaics for expression of a cytokinin-synthesizing gene have viviparous leaves. Such a formation of shoots in an abnormal position represents a significant deviation from the usual organization of the plant body where a central axis produces shoots only in the axils of lateral leaf appendages and according to a precise phyllotactic pattern. This report links vivipary to the expression of a gene whose product is involved in the synthesis of the phytohormone cytokinin.     

Synaptic vesicles of inhibitory and excitatory TERMINALS IN THE CEREBELLUM

Populations of synaptic vesicles within cerebellar terminals considered excitatory or inhibitory on the basis of physiological evidence differ with respect to size and shape. Size rather than shape appears to be the main morphological difference between these populations. Elongation of vesicles is depenident on fixation with aldehyde fixatives, and both size and elongation change with age mainly during maturation.     

Synaptic potentials recorded in cell cultures of nerve and muscle

Initially dissociated spinal cord and muscle cells derived from chick embryos differentiate sufficiently in tissue culture to form functional synaptic contacts. Spontaneous and evoked potentials recorded with intracellular microelectrodes resemble synaptic responses of adult spinal cord and neuromuscular junctions.     

Synaptic amplifier of inflammatory pain in the spinal dorsal horn

Inflammation and trauma lead to enhanced pain sensitivity (hyperalgesia), which is in part due to altered sensory processing in the spinal cord. The synaptic hypothesis of hyperalgesia, which postulates that hyperalgesia is induced by the activity-dependent long-term potentiation (LTP) in the spinal cord, has been challenged, because in previous studies of pain pathways, LTP was experimentally induced by nerve stimulation at high frequencies ( approximately 100 hertz). This does not, however, resemble the real low-frequency afferent barrage that occurs during inflammation. We identified a synaptic amplifier at the origin of an ascending pain pathway that is switched-on by low-level activity in nociceptive nerve fibers. This model integrates known signal transduction pathways of hyperalgesia without contradiction.