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G T Pearson

Publications and source records attributed to G T Pearson.

At least 37 records · Page 2Linked to original sources
PubMed1992

Complex correlations between the morphology, electrophysiology and peptide immunohistochemistry of guinea-pig enteric neurones.

Neuroanatomical, electrophysiological and immunohistochemical techniques were used to describe correlations between soma morphology and electrophysiological properties in two groups of guinea-pig enteric neurones posing particular challenges. Lucifer Yellow-staining of 542 myenteric plexus neurones of duodenum revealed a great diversity of neuronal morphology. The distribution was: Dogiel Type I 27%, Dogiel Type II 54%, Stach Type IV 9%; 10% were unclassified. Correlations were sought in 59 of these cells between morphology and electrophysiological properties but no particular association was recognised. Dynorphin A(1-8)-like immunoreactivity (Dyn A(1-8)-IR) was found in up to 90% of identified submucous neurones of guinea-pig ileum. Of 62 S-neurones, 41 showed 'weak' and 19 had 'intense' Dyn A (1-8)-IR. There was no evidence of Dyn A(1-8)-IR in 2 S-neurones, nor in 8/8 AH-neurones. As for 11/16 vasoactive intestinal peptide- (VIP-) IR neurones, there was a strong correlation between the presence of 'weak' Dyn A(1-8)-IR and the occurrence of inhibitory (IPSPs) and slow excitatory synaptic potentials (EPSPs) (13/16 cells tested), which were never observed in neurones with 'intense' Dyn A(1-8)-IR (16/16) or neuropeptide Y (NPY)-IR (8/8). Similarly, 7/7 neurones with 'weak' Dyn A(1-8)-IR, but not those (7/7) with 'intense' Dyn A(1-8)-IR, hyperpolarised or showed a conductance change to noradrenaline. It was concluded that dynorphin A(1-8)-like-IR was contained in two populations of submucous neurone that are anatomically, immunohistochemically, electrophysiologically and pharmacologically distinct and closely related to those containing VIP and NPY. Furthermore, as in the myenteric plexus throughout the small intestine, opioid peptides are not expressed in Dogiel Type II cells.

Animals↗
PubMed1989

The hyperactive child: an update.

The physician is uniquely qualified to manage the multiple facets of attention-deficit hyperactivity disorder. This clinically oriented update reviews the current state of the art regarding diagnosis and management of hyperactive children. Three case reports emphasize the wide variation of clinical problems presented by this frequently occurring disorder of childhood. Epidemiology, differential diagnosis, associated features, neurobiologic mechanisms, treatment, long-term outcome, and attention-deficit disorder in adults are addressed. Although medication is an important tool in the treatment of this condition, follow-up studies confirm the importance of a multimodal treatment approach.

Adolescent↗
PubMed1986

Electrophysiology and morphology of vasoactive-intestinal-peptide-immunoreactive neurones of the guinea-pig ileum.

Simultaneous intracellular staining and electrophysiological recording techniques have been applied to neurones of guinea-pig myenteric plexus-longitudinal muscle preparations. With micro-electrodes filled with a solution of the fluorescent dye Lucifer Yellow, neurones were first characterized morphologically and electrophysiologically, and subsequently subjected to an indirect immunohistochemical method for the detection of vasoactive intestinal peptide (VIP)-like immunoreactivity. Cross-correlations of morphology, electrophysiology and VIP immunoreactivity were successfully achieved in a total of 164 neurones. Sixty-three had the slow after-hyperpolarization characteristic of AH neurones; 101 cells displayed fast excitatory post-synaptic potentials (e.p.s.p.s) in response to transmural or focal stimulation and were therefore, by definition, S neurones. Unequivocal VIP immunoreactivity was observed in 25 (25%) S neurones, which, with only one exception, had Dogiel Type I morphology (i.e. many short soma processes and a single long process). In contrast, AH neurones had Dogiel Type II morphology (i.e. smooth soma with several long processes) and none showed VIP immunoreactivity. In addition to cholinergic fast e.p.s.p.s., non-cholinergic slow synaptic inputs were evoked in seventeen of the twenty-two VIP-immunoreactive S neurones tested. Both the fast and slow e.p.s.p.s could be elicited by stimulation of the preparation, oral or aboral to the site of recording. These observations demonstrate that, in the guinea-pig ileum, myenteric plexus neurones showing VIP immunoreactivity are of a single electrophysiological type (S neurones) and belong to essentially one morphological class (Dogiel Type I).

Action Potentials↗
PubMed1985

Human pancreatic acinar cells: studies of stimulus-secretion coupling.

Elements of stimulus-secretion coupling were studied in human pancreatic acinar cells by using tissue samples obtained from cadaver organ donors. In pancreatic fragments, acetylcholine evoked amylase secretion as well as potassium release and increased the outflux of 45Ca and 86Rb from the prelabeled tissue. In patches of basolateral plasma membrane excised from acinar cell clusters, single-channel potassium currents were recorded. The inside of the plasma membrane faced the bath solution, allowing the effects of changes in the free ionized calcium concentration in contact with the membrane interior to be tested. Two types of calcium-activated potassium-selective channels were found with unit conductances of about 250 and 50 picosiemens (pS), respectively. In both cases channel opening was determined by the electrical potential difference across the plasma membrane and the free ionized calcium concentration in the bath solution. The probability of channel opening was markedly increased by elevation of the free ionized calcium concentration in contact with the membrane inside. The results suggest that the acetylcholine-evoked cellular potassium release occurs via selective membrane potassium channels opened by calcium released intracellularly after the action of the secretagogue.

Acetylcholine↗
PubMed1984

Effects of nerve stimulation on enzyme secretion from the in vitro rat pancreas and 3H-release after preincubation with catecholamines.

In the presence of the cholinergic antagonist atropine, electrical field stimulation (FS) (5-20 Hz) caused a marked, reversible increase in the amylase output from superfused rat pancreatic segments. Adrenaline and noradrenaline evoked dose-dependent increases in amylase output which were similar to those produced by FS. The FS- and catecholamine-evoked amylase secretions were abolished by the beta-adrenergic antagonist propranolol. The FS-evoked secretion could be abolished by either the removal of external Ca2+ or the application of tetrodotoxin (TTX, 2 X 10(-6) M). FS also resulted in a reversible increase in the fractional efflux of tritium (3H) from rat pancreatic tissues preincubated with either 3H-noradrenaline or 3H-adrenaline. The effects of FS (5-20 Hz) on 3H efflux were abolished by TTX (2 X 10(-6) M). TTX had no effect on the enhancement of 3H efflux caused by elevation of external potassium concentration (high K+, 75 mM). Removal of superfusate Ca2+ completely abolished both the FS- and high K+-induced increases in 3H efflux. These observations suggest that intrinsic nerve stimulation (i.e. FS) results in the Ca2+-dependent release of sympathetic neurotransmitter, noradrenaline, which has a direct secretory action on the rat pancreas. Furthermore, the findings suggest that adrenaline can be taken up by nervous elements. This raises the possibility that uptake and re-release of circulating adrenaline might contribute to the control of rat pancreatic enzyme secretion by the adrenergic nervous system.

Amylases↗
PubMed1984

Nervous control of membrane conductance in mouse lacrimal acinar cells.

Intracellular microelectrode recordings were made from superfused in vitro preparations of mouse lacrimal gland. The lacrimal acinar cell had a mean resting membrane potential of -44.1 +/- 0.5 mV and a mean input resistance of 3.5 +/- 0.15 M omega. Electrical field stimulation (FS) had similar effects to ACh applied by microionophoresis, both evoking a biphasic membrane hyperpolarization (up to 15 mV) accompanied by a reduction in input resistance. The equilibrium potential values (EFS and EACh) for the responses to brief duration FS and ACh ionophoresis ranged between -45 and -75 mV and depended on the time at which measurements were made following the onset of stimulation. Superfusion of ACh or adrenaline also caused membrane hyperpolarization and increased membrane conductance. Estimations of EFS and EACh made during prolonged periods of FS and ACh superfusion yielded mean values of -53.9 +/- 1.9 mV and -53.4 +/- 1.5 mV respectively. FS evoked a response in all preparations tested with maximal effects seen at 40 Hz frequency. The mean latency of the FS-evoked hyperpolarization (40 Hz) was 270 +/- 21 ms and that for the ACh ionophoretic response was 400 +/- 65 ms. Low frequency FS (0.5-5 Hz) also induced membrane hyperpolarization and responses to single shock stimuli were occasionally observed. The FS-evoked hyperpolarization was abolished following the blockade of nerve conduction by superfusion of either Na-free or tetrodotoxin-containing media. Effects of FS were not seen in the presence of atropine. Neostigmine potentiated the FS- and ACh-evoked hyperpolarizations.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1984

Adrenergic nervous control of cAMP-mediated amylase secretion in the rat pancreas.

In this study of nervous control of exocrine secretion, electrical field stimulation (FS) evoked a marked, tetrodotoxin-sensitive increase in the amylase output from in vitro segments of rat pancreas. Blockade of the large cholinergic component of the response by atropine revealed a smaller noncholinergic nerve-mediated secretion. This noncholinergic secretion was unaffected by phentolamine but abolished by propranolol, as were the secretory responses to norepinephrine and other beta-adrenergic agonists. FS also produced an increase in the efflux of radiolabeled norepinephrine from preloaded tissue that was tetrodotoxin sensitive and calcium dependent. Although FS and the adrenergic secretagogues had no effect on 45Ca2+ metabolism or acinar cell electrical properties of atropine-treated rat pancreas, they both evoked increases in tissue cAMP levels. These increases in cAMP concentration were also blocked by propranolol. The phosphodiesterase inhibitor isobutylmethylxanthine potentiated both the elevation of cAMP levels and the amylase secretion evoked by adrenergic stimulation. Since both specific beta 1- and beta 2-adrenergic agonists elevated cAMP levels and caused amylase secretion, it appears that both beta-receptor subtypes are present in the rat pancreas. Of the selective beta 1- and beta 2-antagonists used, the most pronounced reduction, but not complete blockade, of the FS- and norepinephrine-induced cyclic nucleotide and secretory effects was obtained with the beta 1-antagonist metoprolol. It is concluded that stimulation of adrenergic nerves in the rat pancreas evokes an amylase secretion that is mediated via the activation of mainly beta 1-type adrenergic receptors and the utilization of cAMP as an intracellular second messenger.

Acetylcholine↗
PubMed1984

Neural and hormonal control of membrane conductance in the pig pancreatic acinar cell.

Intracellular microelectrode recordings from superfused segments of pig pancreas have shown the resting acinar cell membrane potentials to range widely, with a mean value of -30.5 +/- 1.3 mV. Electrical field stimulation (FS) of the intrinsic pancreatic nerves induced frequency-dependent membrane hyperpolarization (10-15 mV) accompanied by a concomitant reduction in input resistance. Similar effects could be evoked by the superfusion or electroionophoresis of acetylcholine, amphibian or mammalian bombesin [gastrin-releasing peptide (GRP)], and pentagastrin. In normal Ca2+-containing solutions sustained secretagogue superfusion resulted in sustained hyperpolarization. In the absence of external Ca2+, similar stimulation caused only a transient hyperpolarizing response, with subsequent periods of secretagogue application having no effect. Atropine completely abolished the FS-evoked hyperpolarizations but had no effect on the responses evoked by bombesin, GRP, and pentagastrin. The present findings support the contention that neural and hormonal stimulation of the pig pancreas evokes Ca2+-dependent acinar cell hyperpolarization by causing a selective increase in membrane K+ permeability. A hypothesis is proposed that cellular K+ release through the opened conductance pathway promotes a K+-Na+-Cl- cotransport into the cell that serves a key function in the generation of acinar salt secretion.

Acetylcholine↗
PubMed1981

Ionic currents across pancreatic acinar cell membranes and their role in fluid secretion.

Fluid and enzyme secretion from a number of mammalian exocrine glands is controlled by the action of neurotransmitters and hormones on acinar cell membranes. Sustained stimulation evoking sustained fluid and enzyme secretion also evokes sustained membrane depolarization and increase in conductance. Mouse and rat pancreatic fluid and enzyme secretion, as well as membrane depolarization and conductance increase evoked by sustained stimulation with acetylcholine or cholecystokinin-gastrin peptides, are acutely dependent on extracellular calcium. However, the initial stimulant-evoked conductance increase and secretion appear to be triggered by calcium released from inside the cells. Direct measurement of membrane current during sustained stimulation in voltage-clamp experiments with resolution of the total current into its Na, Cl and K components has allowed calculations of stimulant-evoked Na and Cl uptake into the acinar cells. The NaCl uptake is quantitatively sufficient to account for the stimulant-evoked fluid secretion. The role of the stimulant-evoked transmembrane ionic current appears to be the supply of salt for the fluid secretion. Calcium derived from intracellular sources in the initial phase of secretion, and from the extracellular fluid in the sustained phase, couples fluid and enzyme secretion to hormone-receptor interaction.

Bicarbonates↗
PubMed1981

Control of enzyme secretion by non-cholinergic, non-adrenergic nerves in guinea pig pancreas.

Depolarization of pancreatic cells by exposure to high potassium solutions is associated with release of amylase. In the guinea pig, but not the mouse or cat, this Ca-dependent amylase secretion is resistant to atropine blockade, thus Scheele and Haymovits concluded that the enzyme secretion evoked by K depolarization does not involve release of transmitter from intrapancreatic nerves but is a consequence of Ca uptake into acinar cells mediated by the membrane depolarization. This hypothesis is inconsistent with current concepts of stimulus--secretion coupling in electrically non-excitable cells. The observation of Scheele and Haymovits could, however, also be explained by the release of a non-cholinergic, secretomotor transmitter as a consequence of the depolarization of intrapancreatic nerves. By adapting the technique of electrical field stimulation of isolated pancreatic segments to our studies of amylase secretion, we have now been able to demonstrate both cholinergic and non-cholinergic, non-adrenergic secretomotor nerves in the guinea pig pancreas. Excitation of the non-cholinergic nerves stimulates amylase secretion by a different intracellular coupling mechanism from that activated by cholinergic nerves or by peptides belonging to the cholecystokinin, gastrin or bombesin families.

Acetylcholine↗
PubMed1980

Mouse pancreatic acinar cells: effects of electrical field stimulation on membrane potential and resistance.

1. Intracellular micro-elctrode recordings of acinar cell membrane potential and resistance were made from the mouse pancreas superfused in vitro. The acinar cells under investigation were stimulated by electrical field stimulation using two platinum wire electrodes and by micro-ionophoretic acetylcholine (ACh) application from an extracellular AChCl-filled micro-electrode. 2. Field stimulation evoked membrane depolarization and reduction in input resistance. Maximal effects were observed at 20-40 Hz frequency, 1-2 msec pulse width and 8-20 V amplitude. The mean latency for the field stimulation-evoked depolarization was 900 msec. Field stimulation responses were seen at low frequency levels of stimulation, the majority of cells responding at 5 Hz and some at 2 Hz. The physiological significance of the low frequency stimulation is discussed. 3. The field stimulation effects resembled those induced by ACh ionophoresis and were abolished by atropine. The equilibrium potentials for both field stimulation and ACh ionophoresis were identical at about -15 mV. The field stimulation response was selectively abolished by tetrodotoxin and by superfusion with Na-free or Ca-free media, while the ACh ionophoretic response persisted. Field stimulation therefore initiated nerve action potentials and consequent ACh release. 4. Spontaneous miniature depolarizations observed in some preparations were not abolished by tetrodotoxin and woult therefore seem to be a result of quantal release of ACh from nerve terminals. 5. There is no indication from the present studies of the existence of neurotransmitters other than ACh. No inhibitory effects have been observed. 6. All preparations studied to date have responded to field stimulation and it is concluded that all acinar cells are potentially under cholinergic neural influence.

Acetylcholine↗
PubMed1979

The role of intrinsic, non-adrenergic, non-cholinergic inhibitory nerves in the regulation of distensibility of the guinea-pig colon.

1. The lengthening responses of segments of distal colon of guinea-pigs to applied weights were measured. 2. Distensibility was reduced by tetrodotoxin and quinidine; increased by atropine and hyoscine, and unaffected by guanethidine and phentolamine. 3. Tension changes produced by controlled stretches were increased by tetrodotoxin. 4. These results suggest that there is a net, inhibitory, non-adrenergic, non-cholinergic influence acting on the muscle during stretch against a background of cholinergic excitatory tone. This inhibitory activity may be activated reflexly by stretch.

Animals↗