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PubMed1984

Radioimmunoassay of pancreatic polypeptide in mammalian and submammalian vertebrates using a carboxyl-terminal hexapeptide antiserum.

Pancreatic polypeptide (PP) immunoreactivity in acid-ethanol extracts of the pancreas of representative species of mammals, birds, reptiles, amphibians, and fish was studied by a radioimmunoassay (RIA) that utilizes an antiserum which cross-reacts exclusively with the COOH-terminal hexapeptide of PP (CTPP). PP immunoreactivity in acid-ethanol extracts of rat nonpancreas tissues (stomach, duodenum, skeletal muscle, brain) was also examined. Significant concentrations of PP immunoreactivity were detected in the pancreatic extracts of all species, except fish. Appreciable quantities of PP immunoreactivity were also found in the stomach and duodenum of rats. In all cases, tissue extracts showed parallelism with reference PP (bovine) in the RIA. Gel chromatography (Sephadex G-50sf) of tissue extracts (rat, turtle) demonstrated a major peak of PP immunoreactivity, which eluted in the region of the reference PP. Salamander PP immunoreactivity eluted after bovine PP. In addition, the CTPP RIA can be applied to measure plasma levels of PP in rats, dogs, and humans. By using this PP RIA, we observed that plasma PP levels increase significantly in dogs (P less than 0.05) after intravenous administration of neurotensin. In rats, administration of intravenous bombesin resulted in a significant elevation of plasma PP.

Animals↗
PubMed1989

Characteristics of the galanin-induced depolarization of mudpuppy parasympathetic postganglionic neurons.

The depolarization of mudpuppy parasympathetic cardiac neurons, produced by pressure application of the neuropeptide galanin, has been characterized. The amplitude and duration of the depolarization were dependent on the duration of the galanin application. The amplitude of the depolarization increased with hyperpolarization and the reversal potential determined by extrapolation was approximately +10 mV. The amplitude and time course of the galanin-induced depolarization were not changed by substitution of either manganese or magnesium for extracellular calcium, but were decreased by exposure to 50-100 microM d-tubocurarine. It is proposed that the galanin-induced depolarization results from a receptor-activated, nonselective, cation channel; and further, that the receptor initiating depolarization differs from the galanin receptor mediating hyperpolarizing responses in these parasympathetic neurons.

Action Potentials↗
PubMed1992

Galanin and bethanechol appear to activate the same inwardly rectifying potassium current in mudpuppy parasympathetic neurons.

Galanin- and bethanechol-activated whole cell currents were studied in dissociated mudpuppy parasympathetic neurons kept in 12.5 mM KCl. The bethanechol-induced current was reduced when generated during a galanin-induced current. The galanin and bethanechol currents reversed at -45 mV and exhibited inward rectification at more negative potentials. Both the galanin- and bethanechol-induced current relaxations recorded during negative voltage steps were fitted best by two exponentials with the averaged time constant values not significantly different for the galanin and bethanechol currents. We conclude that galanin and bethanechol activate a similar membrane potassium conductance which is different from the background potassium conductance.

Animals↗
PubMed1984

A comparison of the effects of isomers of alpha-aminoadipic acid and 2-amino-4-phosphonobutyric acid on the light response of the müller glial cell and the electroretinogram.

Intracellular recordings of the light response of retinal Müller glial cells revealed differential effects of optical isomers of alpha-aminoadipic acid, a putative gliotoxin. L-alpha-aminoadipic acid preferentially abolished the "on" component but not the "off" component of the intracellularly recorded Müller cell light response, abolished the b-wave but not the d-wave of the electroretinogram, and caused histological damage to the Müller cells. D-alpha-aminoadipic acid preferentially reduced the "off" component of the Müller cell light response and the d-wave of the electroretinogram, and did not cause appreciable histological damage to the Müller cells. 2-amino-4-phosphonobutyric acid, which has been shown to act preferentially at the synapse of photoreceptors onto depolarizing bipolar cells in the mudpuppy retina, abolished the "on" response of Müller cells and the b-wave of the electroretinogram, but caused no histological damage to the Müller glial cells. None of the agents caused a significant change in the resting membrane potential of the glial cells. The similarity of the electrical effects of L-alpha-aminoadipic acid and 2-amino-4-phosphonobutyric acid suggests that the initial loss of the b-wave following L-alpha-aminoadipic acid treatment is due to action of the amino acid at a synaptic site via a mechanism distinct from that which causes subsequent histological damage to the glial cells.

2-Aminoadipic Acid↗
PubMed1991

Analysis of the galanin-induced decrease in membrane excitability in mudpuppy parasympathetic neurons.

Previously, we showed that the neuropeptide galanin hyperpolarizes and decreases membrane excitability of mudpuppy parasympathetic neurons [Konopka L. M., McKeon T. W. and Parsons R. L. (1989) J. Physiol. 410, 107-122]. We also demonstrated that membrane excitability remains depressed when the agonist-induced potential change is negated electrotonically. We hypothesized that galanin inhibits the membrane conductances associated with spike generation. However, we cannot rule out the possibility that the decreased excitability is due to a galanin-induced increase in membrane potassium conductance which reduces the effectiveness of subsequent depolarizing stimuli. Therefore, in the present study we tested, with the galanin-induced hyperpolarization negated, whether the galanin-induced increased membrane potassium conductance was responsible for the decreased excitability. The results showed that the galanin-induced decreased excitability was not dependent on the peak amplitude of the galanin-induced hyperpolarization. Furthermore, the decreased excitability occurred in cells in which there was no measurable galanin-induced hyperpolarization. Moreover, in most cells the galanin-induced decrease in input resistance, measured at the peak of the hyperpolarization (3-25 mV), was less than 15% and when the hyperpolarization was negated electronically, the decrease was even less (approximately 2%). These results indicated that when the hyperpolarization was negated, the galanin-induced increase in potassium conductance was not responsible for the decreased excitability. In preparations pretreated with 5 mM tetraethylammonium, galanin decreased excitability which indicated that a galanin-induced decrease in the calcium-dependent potassium current was not necessary for the decreased excitability. Galanin also decreased excitability in preparations exposed to either 1-3 microM tetrodotoxin or 100-200 microM cadmium. Following galanin application, the threshold for initiation of tetrodotoxin-insensitive spikes was shifted to more positive membrane potentials. Galanin also decreased the amplitude and hyperpolarizing afterpotential of barium spikes in the absence of any agonist-induced hyperpolarization. These observations confirmed that galanin decreased the voltage-dependent calcium conductance. In the present study, we showed that when the hyperpolarization was negated, galanin decreased excitability by shifting the threshold for spike generation regardless of whether voltage-dependent sodium or calcium currents were primarily responsible for the depolarizing component of the action potential.

Action Potentials↗
PubMed1991

Characterization of serine's inhibitory action on neurons in the mudpuppy retina.

Experiments were performed in the superfused retina-eyecup of mudpuppies using intracellular electrophysiological techniques to evaluate the effects of serine on amacrine and ganglion cells. Serine was found to have a dose-dependent inhibitory effect mediated by the opening of chloride channels. Serine appears to act on a glycine receptor based on the observations that: (1) serine's effect is blocked by strychnine but not by bicuculline or picrotoxin, (2) in the presence of saturating glycine concentrations serine had no effect on membrane voltage or conductance, and (3) cells inhibited by serine were always sensitive to glycine, but not always sensitive to GABA. High pressure liquid chromatography measurements disclose that there is a high concentration of extracellular serine in the retina. The data indicate that serine could act as an inhibitory neurotransmitter.

Animals↗
PubMed1991

Biogenic amine localization in cardiac ganglion intrinsic neurons: electron microscopic histochemistry of SIF cells.

The parasympathetic cardiac ganglion in the mudpuppy, N. maculosus, contains postganglionic nerve cells and intrinsic neurons, many of which are small intensely fluorescent (SIF) cells. Several bioactive substances have been localized in the intrinsic nerve cells which may have integrative effects at synapses within the ganglion. Ganglionic intrinsic neurons can be identified electron microscopically by the presence of numerous cytoplasmic granular vesicles 80-120 nm in diameter. Throughout the ganglion there are bundles of unmyelinated fibers some of which are filled with granular and agranular vesicles and axosomatic terminals with similar vesicles synapsing on principal parasympathetic nerve cells. To understand the aminergic contribution to ganglionic synaptic circuitry the chromaffin reaction was used. The intrinsic neurons (i.e., SIF cells) were readily identified by their characteristic intracellular granule population. All intrinsic nerve cells identified showed granules which were positively labelled by the chromaffin reaction. Granular vesicles in synaptic profiles on principal cells (P cells) were also labelled indicating a direct aminergic synaptic innervation to these cells. The cell bodies of intrinsic neurons, ensheathed with supportive glial-like cellular processes, rarely received synapses. Elemental microanalysis was used to verify the chromium content of the electron dense product within the granular vesicles. These studies demonstrated direct aminergic synaptic input to at least a subpopulation of principal parasympathetic cells in the cardiac ganglion of mudpuppy.

Animals↗
PubMed2004

The modulation of action potential generation by calcium-induced calcium release is enhanced by mitochondrial inhibitors in mudpuppy parasympathetic neurons.

Previously, we demonstrated that outward currents activated by calcium-induced calcium release (CICR) opposed depolarization-induced action potential (AP) generation in dissociated mudpuppy parasympathetic neurons [J Neurophysiol 88 (2002) 1119]. In the present study, we tested whether AP generation by depolarizing current ramps could be altered by dissipating the mitochondrial membrane potential and thus interrupting mitochondrial Ca2+ buffering. Exposure to the protonophore carbonyl cyanide m-chlorophenylhydrazone (CCCP; 2 microM) alone or in combination with the mitochondrial ATP synthase inhibitor oligomycin (8 microg/ml), increased the latency to AP generation. Exposure to the electron transport chain inhibitor rotenone (10 microM) alone or in combination with oligomycin (8 microg/ml) similarly increased the latency to AP generation. CCCP and oligomycin or rotenone and oligomycin treatment caused rhodamine 123 loss from mitochondria within a few minutes, confirming that the mitochondrial membrane potential was dissipated during drug exposure. Oligomycin alone had no effect on the latency to AP generation and did not cause loss of rhodamine 123 from mitochondria. The increase in latency induced by CCCP and oligomycin was similar when recordings were made with either the perforated patch or standard whole cell patch recording configuration. Exposure to the endoplasmic reticulum Ca-ATPase inhibitor thapsigargin (1 microM), decreased the latency to AP generation. In cells pretreated with thapsigargin to eliminate CICR, CCCP and oligomycin had no effect on AP latency. Pretreatment with iberiotoxin (IBX; 100 nM), an inhibitor of large conductance, calcium- and voltage-activated potassium channels, reduced the extent of the CCCP- and oligomycin-induced increase in latency to AP generation. These results indicate that treatment with CCCP or rotenone to dissipate the mitochondrial membrane potential, a condition which should minimize sequestration of Ca2+ by mitochondria, facilitated the Ca(2+)-induced Ca2+ release activation of IBX-sensitive and IBX-insensitive conductances that regulate AP generation.

Action Potentials↗
PubMed1990

Visualization of transport-related configurations of the nuclear pore transporter.

The transport of macromolecules between the cytoplasm and nucleus of the cell is mediated by the nuclear pore complex (NPC). In this study, details of the central transporter assembly within NPCs have been examined by cryoelectron microscopy, image processing, and classification analysis. The NPC transporter in isolated amphibian nuclei appears to adopt a minimum of four transport-related configurations including: (a) a putative closed form with a 90-100 A diameter central pore, (b) a docked form with material aligned over the pore, (c) an open form with substrates apparently caught "in transit," and (d) an open form with an enlarged pore. This data confirms previous observations on NPC transporters labeled with nucleoplasmin-gold (Akey, C.W., and D.S. Goldfarb. 1989. J. Cell Biol. 109:971-982) and allows a working model of the central NPC transporter to be proposed. The model is comprised of two supramolecular irislike assemblies which open asynchronously to provide an expanded pore for translocation while maintaining transport fidelity.

Animals↗
PubMed1995

Structural plasticity of the nuclear pore complex.

The nuclear pore complex (NPC) is strategically located at continuous junctions of the inner and outer nuclear membranes to catalyze macromolecular transport, without impending the diffusion of small molecules. In this paper, the structural plasticity of 4412 NPCs in isolated nuclear envelopes has been evaluated, utilizing correspondence analysis, classification and difference mapping. The data are grouped into seven clusters comprising two major groups, based on the degree of radial compaction within spokes and the symmetry of the inner spoke ring. The results have been correlated with differences in spoke domain packing observed in two published three-dimensional maps suggesting that symmetrical detergent-extracted NPCs are similar, but not identical to the most probable in vivo structure. A model is proposed in which spoke architecture is responsive to changes in the turgor pressure of the nuclear envelope. For example, detergent extraction may allow the outward facing domains of each spoke to adopt a radially-extended configuration while osmotic swelling may induce an inwards displacement, resulting in a radially compact spoke. Difference maps between approximately 822 symmetric projections of NPCs in membranes and after detergent-extraction have localized the nuclear envelope border. The data place limits on the radial and circumferential dimensions of diffusion channels (approximately 0 to 20 A x 190 A), proposed to reside at the pore periphery. The results confirm the observation that each spoke penetrates the nuclear envelope, linking up with the radial arms to form a "lumenal ring". Finally, putative closed, open and in-transit forms of the transporter are found with the same relative frequency in membrane-associated NPCs with radially compact or extended spokes; hence spoke deformations in isolated envelopes may be induced by experimental factors. However, concerted movements of the spoke domains (if reversible) may be utilized in the biological function of the NPC and some examples are given.

Analysis of Variance↗
PubMed1997

Two phenylglycine derivatives antagonize responses to L-AP4 in ON bipolar cells of the amphibian retina.

Light responses of retinal ON bipolar cells are mediated by metabotropic glutamate receptors selectively activated by L-2-amino-4-phosphonobutyric acid (L-AP4). Antagonists to L-AP4 receptors in ON bipolar cells have not previously been identified. This study examines the electrophysiological effects of (S)-2-amino-2-methyl-4-phosphonobutanoic acid (MAP4), (RS)-4-4-chloro-3,5-dihydroxyphenylglycine (CDHPG) and (RS)-3,4,5-trihydroxyphenylglycine (THPG), at L-AP4 receptors in ON bipolar cells of the amphibian retina. Unlike its actions in spinal cord, in retinal ON bipolar cells MAP4 is a weak agonist which exhibits no detectable antagonism to L-AP4. On the other hand, CDHPG exhibits a mixture of agonist and antagonist properties. Addition of Co2+ and oxygenation of CDHPG turns the solution brown and enhances antagonist effects, suggesting that the antagonism reflects actions of a breakdown product of CDHPG. Although THPG did not prove to be this breakdown product, it also has electrophysiological effects consistent with an L-AP4 receptor antagonist. The results suggest that THPG and breakdown products of CDHPG may be antagonists to L-AP4 receptors in retinal ON bipolar cells, although the possibility that these compounds antagonize effects of L-AP4 by acting at some site in the transduction pathway of L-AP4 receptors cannot yet be excluded.

Aminobutyrates↗
PubMed2001

Localization of neurotransmitters and calcium binding proteins to neurons of salamander and mudpuppy retinas.

We wished to identify the different types of retinal neurons on the basis of their content of neuroactive substances in both larval tiger salamander and mudpuppy retinas, favored species for electrophysiological investigation. Sections and wholemounts of retinas were labeled by immunocytochemical methods to demonstrate three calcium binding protein species and the common neurotransmitters, glycine, GABA and acetylcholine. Double immunostained sections and single labeled wholemount retinas were examined by confocal microscopy. Immunostaining patterns appeared to be the same in salamander and mudpuppy. Double and single cones, horizontal cells, some amacrine cells and ganglion cells were strongly calbindin-immunoreactive (IR). Calbindin-IR horizontal cells colocalized GABA. Many bipolar cells, horizontal cells, some amacrine cells and ganglion cells were strongly calretinin-IR. One type of horizontal cell and an infrequently occurring amacrine cell were parvalbumin-IR. Acetylcholine as visualized by ChAT-immunoreactivity was seen in a mirror-symmetric pair of amacrine cells that colocalized GABA and glycine. Glycine and GABA colocalized with calretinin, calbindin and occasionally with parvalbumin in amacrine cells.

Acetylcholine↗
PubMed1996

Cholinergic modulation of dopamine release and horizontal cell coupling in mudpuppy retina.

The effects of cholinergic agonists and antagonists on electrical coupling between horizontal cells were studied in dark-adapted mudpuppy retinas. Carbachol and the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP) uncoupled horizontal cells, but the muscarinic agonist oxotremorine did not. The uncoupling effects of carbachol and DMPP were blocked by the nicotinic antagonist D-tubocurarine and by the dopamine antagonist fluphenazine, indicating that carbachol uncoupled horizontal cells by stimulating dopamine release via nicotinic receptors. Carbachol also caused an increase in release of [3H]dopamine from retinas. D-Tubocurarine increased horizontal cell coupling, indicating that tonic cholinergic input was present in dark-adapted retinas. D-Tubocurarine did not reduce light-evoked uncoupling of horizontal cells, suggesting that cholinergic neurons are not an essential part of the direct pathway by which light causes an immediate increase in dopamine release.

Acetylcholine↗
PubMed1990

Mechanisms of chemosensory transduction in taste cells.

The application of new techniques to the study of taste cells has revealed much about both the basic physiology of these cells and also about the mechanisms of taste transduction. The taste cells are electrically excitable cells with a variety of voltage-dependent ion currents. These ionic currents have an important role in the transduction of salt taste in mammals and frogs. In mudpuppies different ion channels are involved in the transduction of acidic-sour stimuli. The role of ion currents in the transduction of sweet taste is less clear. Some proposed mechanisms suggest an important role for ion currents and others suggest that the transduction process may be a biochemical event involving cell surface receptors and intracellular second messengers, possibly cAMP. The transduction of bitter taste seems to be a biochemical event involving cell surface receptors and intracellular second messengers in the inositol trisphosphate pathway. Thus, one cannot talk about "the mechanism" of taste transduction. Different taste modalities are transduced by different mechanisms. A corollary to this is that taste cells are not a homogeneous population of cells. In order to provide animals with the ability to discriminate between different taste modalities the taste cells consist of distinct subpopulations of cells based on their primary taste modality. The primary taste modality in a given cell is determined by the receptors and transduction mechanism(s) expressed in that cell. Evidence suggests that modality-specific receptors are expressed in a segregated manner in distinct subpopulations of taste cells. Secondary responses observed in gustatory axons may arise due to a lack of absolute specificity in the transduction processes and nonspecific effects of low pH and high ionic strength and osmolarity on the taste cells. An interesting area for future work will be to elucidate the mechanism(s) by which basal cells become committed to a given taste modality and how the gustatory neurons influence this process of differentiation. The involvement of the gustatory neurons is critical as they must synapse with taste cells of the correct taste modality to preserve the integrity of the information transferred to the CNS. This process of synaptogenesis is presumably mediated by the expression of taste-modality-specific, cell surface antigens on the basolateral domain of a taste cell and receptors on the appropriate neurons, but much work will be necessary to elucidate this process.(ABSTRACT TRUNCATED AT 400 WORDS)

Amiloride↗