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PubMed1989

Interaction of noradrenergic and cholinergic systems in regulation of ocular dominance plasticity.

We studied interactions among the noradrenergic (NA) and the muscarinic cholinergic (ACh) systems in the regulation of ocular dominance plasticity in kitten visual cortex. The cortex was bilaterally infused with 6-hydroxydopamine (6-OHDA) for a week. Upon termination of the 6-OHDA infusion, one hemisphere was infused with a muscarinic ACh agonist, bethanechol, through the same, chronically implanted cannula for the second week together with monocular lid suture. The other hemisphere received an infusion of the vehicle solution alone. (1) Only in the hemisphere infused with bethanechol at relatively high concentrations did we obtain a clear shift in ocular dominance. We also found that the effect of bethanechol was concentration-dependent. (2) By comparing necessary concentrations of bethanechol and NA for the respective maximal effects, we noted that the former was at least 100-fold less effective than the latter in restoring the plasticity. (3) The cortical infusion of bethanechol did not restore the plasticity to the propranolol-pretreated cortex; the ocular dominance distribution remained virtually unchanged. This result was interpreted as suggesting that functioning beta-adrenoreceptors are needed for the cortical effect of activating the muscarinic ACh receptors to become detectable. (4) The expected shift in ocular dominance following monocular deprivation was partially suppressed, when highly concentrated scopolamine, a muscarinic ACh antagonist, was used, indicating that the involvement of the ACh system in this matter was indirect. The concentration of scopolamine needed for the half-maximum effect was 172-fold higher than that of propranolol. We thus conclude that the involvement of the muscarinic ACh system in ocular dominance plasticity is secondary to that of the NA-beta-adrenoreceptor system.

Aging↗
PubMed1994

Urinary bladder dysfunction in spontaneously diabetic Chinese hamsters.

Urinary bladder dysfunction was investigated in spontaneously diabetic Chinese hamsters of the Asahikawa colony (CHAD). The wet weight of the urinary bladder was significantly increased in CHAD when compared with non-diabetic controls. In response to continuous infusion of physiological saline into the bladder under anesthesia, regular micturition was observed in controls. However, the threshold volume (i.e. the minimum volume at which rhythmic contraction appeared) was significantly increased and the amplitude of bladder contractions during micturition was decreased in CHAD aged 3-5 months (duration of diabetes, 0.6-2.2 months), leading to incomplete micturition. The frequency of micturition was also increased. Overflow incontinence was observed in all CHAD aged 13-15 months (duration of diabetes, 10-14 months). Acetylcholinesterase staining and activity in the urinary bladder walls were both significantly decreased in CHAD compared with controls. The in vitro increment of urinary bladder pressure caused by stimulation with bethanechol was not different between CHAD and controls. These findings suggest that CHAD have urinary bladder dysfunction which is caused by autonomic neuropathy and not by detrusor myopathy.

Acetylcholinesterase↗
PubMed1980

Gastrin release after truncal vagotomy in fistula dogs: hypersensitivity to bombesin but not bethanechol.

Integrated gastrin response was measured by the serial changes in serum immunoreactive gastrin after various stimuli in three dogs with gastric fistula and highly selective fundic vagotomy, who were then subjected to truncal vagotomy. Truncal vagotomy eliminated the gastrin as well as the gastric acid response to vagal excitation by 2-deoxy-glucose, but did not significantly changes the responses to bethanechol (20 or 120 micrograms/kg/hr by IV infusion). Acid output was the same with bombesin or its nonapeptide in the dogs with fundic vagotomy as it was after subsequent truncal vagotomy, but gastrin release was very much increased by truncal vagotomy. For a 3-hour infusion of bombesin integrated gastrin release was 65 and 143 ng/ml/min and for its nonapeptide 43 and 109 ng/ml/min in the dogs with fundic and truncal vagotomy respectively. The marked hypersensitivity of the gastrin response after truncal vagotomy to bombesin but not to a cholinergic agonist suggests that the antral denervation led to a post-denervation hyper-response to the putative transmitter, bombesin, and that the vagal release of antral gastrin may thus represent a peptidergic neurohormonal mechanism. Also, a long half-life of effect suggests that bombesin binds avidly to its receptors.

Animals↗
PubMedDate not supplied

Analysis of food stimulation of gastrin release in dogs by a panel of inhibitors.

The release of gastrin into the serum of five conscious gastric fistula dogs after a meat meal was monitored for 2 hours. Neither the rate of increase in serum gastrin nor the 2 hour cumulative integrated gastrin response was changed by administration of small doses of somatostatin tetradecapeptide (0.5 microgram/kg.hr IV for 2 hr), 16-16 dimethyl prostaglandin E2 (0.25 microgram/kg.hr IV for 2 hr or 1 microgram/kg intragastrically), or bethanechol (20 micrograms/kg.hr IV for 2 hr). Acidification of the food in the antrum to pH 1.2 to 1.4 eliminated serum gastrin release in response to food. In control studies, serum gastrin levels were not altered by IV administration of saline for 2 hr with no food or when a plate of food was held just out of the dogs' reach (teasing). Food-stimulated gastrin release was contrasted with that stimulated by bombesin under identical laboratory conditions [17]. In each case, antral acidification, somatostatin, prostaglandin E2 and bethanechol affected bombesin-stimulated gastrin release differently from that stimulated by food. We conclude that food and bombesin release gastrin by different pathways.

Animals↗
PubMedDate not supplied

Sauvagine: effects on gastric acid secretion in rats.

Intracerebroventricular (ICV) and subcutaneous (SC) injections of sauvagine powerfully inhibited gastric acid secretion stimulated by gastric distension and by 2-deoxy-D-glucose, but not by histamine in pylorus-ligated rats. Naloxone failed to antagonize the antisecretory effects of SC and ICV sauvagine. Intravenous infusion of sauvagine completely suppressed bethanechol-stimulated gastric secretion, significantly decreased pentagastrin-stimulated gastric secretion and did not modify histamine-stimulated gastric secretion in gastric-perfused rats. The inhibitory effect of sauvagine on gastric secretory response is not mediated through opioid or histamine receptors. It appears to be dependent on a vagal mechanism as well as other mechanisms that await further elucidation.

Amphibian Proteins↗
PubMedDate not supplied

Inhibitory role on gastric secretion of a central NK-3 tachykinin receptor agonist, senktide.

When administered intracerebroventricularly, the highly selective NK-3 tachykinin receptor agonist senktide possesses a potent and dose-related inhibitory effect on gastric acid secretion. The central mechanism governing the antisecretory effect of senktide was examined in perfused-stomach rats by studying its influence on gastric acid secretion elicited by the secretagogues histamine, pentagastrin and bethanechol. Given intracerebroventricularly, senktide reduced the acid response to histamine, but not that to pentagastrin or bethanechol. Stimulation of NK-3 receptors in rat brain thus appears to inhibit gastric acid secretion through histaminergic pathways.

Animals↗
PubMedDate not supplied

Galanin inhibits rat pancreatic amylase release via cholinergic suppression.

The effects of galanin on pancreatic exocrine function were examined using rat pancreatic tissues. In anesthetized rats, galanin (40 micrograms/kg/h) decreased amylase secretion stimulated by 2-deoxy glucose (5.8 +/- 0.1 vs. 3.1 +/- 0.1 times basal) and cholecystokinin octapeptide (21.5 +/- 0.6 vs. 16.8 +/- 0.5), while not inhibiting bethanechol-stimulated secretion. In dispersed acini, there was no effect of galanin alone (10(-8) to 10(-13) M) on amylase release, nor did galanin (10(-6) or 10(-8) M) coincubation affect amylase release stimulated by bethanechol (10(-3) to 10(-7) M) or CCK-8 (10(-8) to 10(-13) M). Using pancreatic lobules, coincubation with galanin (10(-6) M) suppressed 75 mM KCl-stimulated amylase secretion and ACh release (10.1 +/- 0.6% vs. 7.3 +/- 0.4%). Veratridine-stimulated (10(-4) M) amylase secretion and ACh release (12.4 +/- 1.7% vs. 8.5 +/- 0.7%) were similarly diminished.

Acetylcholine↗
PubMed1992

Involvement of Ca2+ entry and inositol trisphosphate-induced internal Ca2+ mobilization in muscarinic receptor-mediated catecholamine release in dog adrenal chromaffin cells.

Catecholamine (CA) release from adrenal medulla evoked by muscarinic receptor stimulation has been studied using isolated perfused adrenal gland and cultured chromaffin cells from dogs. Muscarine and oxotremorine (1-100 microM), and bethanechol (0.1-1 mM) dose-dependently stimulated CA release. Muscarine-evoked CA release was antagonized with M1-antagonist, pirenzepine and, to a lesser extent, with atropine; and was reduced either by removal of extracellular Ca2+ or treatment with Ca2+ channel blockers. Muscarine caused an increase of 45Ca uptake and 22Na uptake. Tetrodotoxin (TTX) did not affect muscarine-evoked increase of 22Na uptake and CA release. Under the absence of extracellular Ca2+, muscarine stimulated a 45Ca efflux. Muscarine-induced CA release was attenuated by treating the cells with 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate-HCl (TMB-8) which blocks Ca2+ release from the intracellular store. A phospholipase C inhibitor, neomycin, markedly reduced muscarine-induced CA release but not nicotine- and high K(+)-evoked release. Cinnarizine, a Ca2+ channel blocker, attenuated muscarine-evoked but not caffeine-induced CA release and 45Ca efflux in the absence of extracellular Ca2+. Muscarine caused an increase in intracellular free Ca2+ concentration ([Ca2+]i) in the presence of extracellular Ca2+. It caused a similar increase, but to a lesser extent, in the absence of extracellular Ca2+. The increase of [Ca2+]i induced by muscarine without extracellular Ca2+ was reduced by neomycin and cinnarizine. Polymixin B and retinal, which reduced 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced CA release, had little effect on muscarine-induced CA release. Muscarine increased cellular Ins(1,4,5)P3 production, and atropine inhibited this increase.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMedDate not supplied

Novel CNS-directed drug delivery systems in Alzheimer's disease and other neurological disorders.

Increasing knowledge of the neurochemical aspects of central nervous system function raises the possibility of treating Alzheimer's disease (AD) and other neurological diseases by the appropriate manipulation of neurotransmitters, neuromodulators, neurohormones or neurotrophic factors. Clinical application of this knowledge may, however, be inhibited by long standing problems with drug delivery to the central nervous system (CNS). Novel, CNS-directed, drug delivery systems might be used to overcome many of these problems. The problems encountered in drug delivery to the brain, present experience with the clinical use of some novel drug delivery systems and the advantages and disadvantages of these systems will be discussed.

Alzheimer Disease↗
PubMedDate not supplied

The necessity of human trials of putative therapies for Alzheimer's disease.

The absence of a suitable animal model for Alzheimer's disease leaves therapeutic trials in human subjects as a necessity. Reasonable criteria can be formulated for deciding which therapies should be tested. Scientific rationale and likelihood of success should be major considerations. Novel approaches of delivering drugs to the central nervous system should not be discouraged so long as complication rates can be shown to be low.

Alzheimer Disease↗
PubMedDate not supplied

Methodological considerations in cognitive disorders or: "the baby needs enough bath water".

Establishing treatment efficacy for neuropsychiatric disorders is an often protracted process due to vagaries of symptoms, course, and probably the inherent variability of the central nervous system. No single study design is likely to be definitive. Thorough evaluation of intracranial drug infusion for illnesses such as Alzheimer's Disease will require extended, multidisciplinary work before true evaluation can confidently be made.

Alzheimer Disease↗
PubMedDate not supplied

Pathological changes in frontal cortex from biopsy to autopsy in Alzheimer's disease.

We evaluated the change in density of total senile plaques, plaque subtypes, and neurofibrillary tangles, from biopsy to autopsy in left frontal cortical sections from four patients with clinically typical Alzheimer's disease (AD). Comparisons were made on sections stained with modified Bielschowsky and Thioflavin S. In two cases, comparisons were also made on tissue stained with a monoclonal Alz-50 antibody and an antiserum to A beta (beta-amyloid protein). Despite a marked decline in mental status over several years of follow-up clinical evaluations, there was no consistent significant change in numerical density of plaques or tangles among the four cases. However, we did find fewer primitive plaques in the autopsy specimens. These results from longitudinally evaluated persons with typical AD suggest that although plaques and tangles may serve as adequate markers of the presence of AD, their numerical density within a single neocortical region may not reflect dementia severity. This conclusion supports the results of recent cross-sectional studies on the progression of pathology among persons with AD.

Alzheimer Disease↗
PubMed1982

Gastrointestinal propulsion measurement with radiopaque capsules during 16,16-dimethyl PGE2 infusion.

A method to quantitate gastric emptying (GE) and small intestinal transit (SIT) by obtaining serial abdominal x-rays after administration of radiopaque capsules was developed. The technique was verified by studying gastric emptying and small intestinal transit in healthy volunteers treated with subcutaneous injections of 0.4 or 0.8 mgs of atropine, 2.5 mg bethanechol, or saline placebo. Atropine decreased gastric emptying and small intestinal transit, and bethanechol only increased gastric emptying. The suitability of this technique for measuring gastrointestinal propulsion in post-operative patients was demonstrated in females undergoing hysterectomy. The small intestine recovered propulsive ability at least six hours sooner than the stomach. This technique was also used while performing a single dose, intravenous tolerance study of 16,16-dimethyl prostaglandin E2 (DmPGE2) in normal volunteers. DmPGE2 was administered over five minutes at a dose of 7 to 140 ng/kg. DmPGE2 was well tolerated producing only minor side effects that were not dose related. In doses up to 70 ng/kg, DmPGE2 increased gastric emptying and inhibited small intestinal transit. The delayed small intestinal transit may make DmPGE2 an inappropriate choice for treatment of post-operative or paralytic ileus.

Adolescent↗
PubMed1990

Injection of a cholinergic agonist in the dorsolateral pontine tegmentum of cats affects the posturokinetic responses to cortical stimulation.

Microinjection into the dorsolateral pontine tegmentum of the muscarinic agonist bethanechol, leading to activation of cholinoceptive pontine reticular formation (pRF) neurons and the related medullary inhibitory reticulospinal system, did not modify the threshold, latency and amplitude of the forelimb flexion elicited by unilateral stimulation of the corresponding motor cortex. However, the remaining limbs which displayed a diagonal pattern of postural adjustments showed a dissociation of their postural responses in 2 components: the early component of central origin greatly decreased in amplitude, while the late component attributed to reflex mechanism triggered by the unbalance brought about by the flexion movement increased. Further evidence indicated that the pRF system intervenes in the gain regulation of the early postural responses during the cortically induced limb movement.

Animals↗
PubMed1991

Muscarinic agonists block a late-afterhyperpolarization in medial septum/diagonal band neurons in vitro.

Intracellular recordings were made from neurons located in the medial septum (MS), and nucleus of the diagonal band (nDB) from slices of guinea pig brain. These forebrain nuclei contain both cholinergic and noncholinergic neurons that project to the cortex and hippocampus and are involved in many cortical functions. Muscarinic agonists (bethanechol, 2-30 microM) had the specific action to reduce a long-duration afterhyperpolarization (long-AHP) while leaving other shorter duration AHPs intact. Since the long-AHP was observed in both cholinergic and non-cholinergic neurons, muscarinic agonists were not selective for any one cell type. Block of a long-AHP was not associated with a consistent increase in cell excitability and therefore can not fully explain the excitatory actions of acetylcholine (ACh) observed in vivo within the MS/nDB.

Animals↗
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↗
PubMed1982

The role of calcium in agonist-stimulated hydrolysis of phosphatidylinositol in mouse pancreas.

The effects of Ca2+ on agonist-stimulated hydrolysis of myo-[2-3H]inositol-labelled phosphatidylinositol in mouse pancreas in vitro, were studied. The increase in cytosol Ca2+ concentration produced by the ionophore A23187 did not stimulate the breakdown of phosphatidylinositol. Cholecystokinin-octapeptide (CCK-8) stimulated the hydrolysis of phosphatidylinositol under conditions in which intracellular calcium stores were depleted. The breakdown of phosphatidylinositol was stimulated by bethanechol and CCK-8 in Ca2+ -free Krebs solution, and the addition of Ca2+ to the medium potentiated the effects of these agonists. Lanthanum significantly reduced bethanechol and CCK-8-stimulated hydrolysis of phosphatidylinositol in Krebs solution, but was without effect in Ca2+ -free Krebs solution. The results of this study support the proposal that hydrolysis does not occur as a result of Ca2+ mobilization and may be involved in Ca2+ gating in the pancreas.

Animals↗