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M L Epstein

Publications and source records attributed to M L Epstein.

At least 55 records · Page 3Linked to original sources
PubMed1987

Trigeminal ganglion cells cocultured with gut express vasoactive intestinal peptide.

The plasticity of neural crest cells for the expression of adrenergic and cholinergic transmitter phenotypes has been well studied. The object of this study was to determine if cells of a sensory ganglion are capable of neuropeptide transmitter plasticity. We studied whether cells of the trigeminal ganglion, which do not express the neuropeptide vasoactive intestinal peptide (VIP) in vivo, would express this peptide when grown with a tissue the gut, that contains large numbers of VIP neurons. Embryonic aneural chick rectum was explanted with the embryonic quail trigeminal ganglion on the chorioallantoic membrane of chick hosts for 7-8 days. The explants were fixed, sectioned, and stained for VIP immunoreactivity (IR), for neurofilament protein immunoreactivity, and for the quail nucleolar marker. In sections of the explants we observed two populations of quail neurons: small (10-13 microns) VIP-IR cells and large (25-32 microns) cells lacking VIP-IR and resembling native trigeminal neurons. Trigeminal ganglia explanted with embryonic heart or trigeminal ganglia explanted alone lacked small VIP-IR cells but contained large VIP-negative neurons. These results show that cells of the trigeminal ganglion grown with the gut can express a neuropeptide they do not express in the absence of the gut or in vivo. Thus the embryonic trigeminal ganglion contains cells that are plastic with respect to neuropeptide expression.

Animals↗
PubMed1987

Effect of chemical ablation of myenteric neurons on neurotransmitter levels in the rat jejunum.

We have quantified neurotransmitter changes in the rat jejunum in which the myenteric neurons were ablated by serosal application of benzalkonium chloride. Within 2 days after benzalkonium chloride treatment, there was a 40% reduction in the activity of choline acetyltransferase, a specific marker for cholinergic neurons, and a 25% reduction in the amount of vasoactive intestinal peptide per centimeter length of jejunum. By 15 days, levels were comparable to those in control segments, and by 45 days after myenteric neuronal ablation, levels in treated tissues were twice those in controls. In contrast, we observed no reduction in the amount of leucine-enkephalin per centimeter length of jejunum at early times after benzalkonium chloride treatment, although by 45 days, levels of this neurotransmitter in treated segments of jejunum were more than twice those in controls. Significant increases in muscle thickness and tissue weight were also observed at 15, 30, and 45 days after myenteric neuronal ablation. Thus we have observed that in response to chemical ablation of myenteric neurons in the rat jejunum, there is a thickening of the smooth muscle layers and a compensatory increase in the production of certain neurotransmitters by the surviving neuronal elements in the gut.

Animals↗
PubMed1987

Cholinergic amacrine cells of the chicken retina: a light and electron microscope immunocytochemical study.

Cholinergic amacrine cells of the chicken retina were detected by immunohistochemistry using an antiserum against affinity-purified chicken choline acetyltransferase. Three populations of cells were detected: type I cholinergic amacrine cells had cell bodies on the border of the inner nuclear and inner plexiform layers and formed a prominent laminar band in sublamina 2 of the inner plexiform layer, while type II cholinergic amacrine cells had cell bodies in the ganglion cell layer, and formed a prominent laminar band in sublamina 4 of the inner plexiform layer. Type III cholinergic amacrine cell bodies were located towards the middle of the inner nuclear layer, and their processes were more diffusely distributed in sublaminas 1 and 3-5 of the inner plexiform layer. Type I and type II cells were present at densities of over 7000 cells/mm2 in central areas declining to less than 2000 cells/mm2 in the temporal retinal periphery. The cells were organized locally in a non-random mosaic, with regularity indices ranging from 3 peripherally to over 5 centrally. Neither at the light nor electron microscopic levels was a lattice of cholinergic dendrites of the kind reported by Tauchi and Masland [J. Neurosci. 5, 2494-2501 (1985)] detectable. Within the two prominent dendritic plexuses, a major feature of the synaptic interactions of the type I and type II cholinergic cells was extensive synaptic interaction between cholinergic processes. Apart from this, there was little, if any, input to cholinergic processes from non-cholinergic amacrine cells, but there was input from bipolar cells. Output from the cholinergic amacrine cell processes was directed towards non-cholinergic amacrine cells as well as other cholinergic amacrine cells, and ganglion cells.

Animals↗
PubMed1987

The toxic effects of ethylcholine mustard aziridinium ion on cholinergic cells in the chicken retina.

The chicken retina has been used to examine the toxicity of a highly reactive chemical analog of choline, ethylcholine mustard aziridinium ion (ECMA). Following a single intravitreal injection, retinas were analyzed biochemically for CAT and AChE activities, and GABA, glycine, and dopamine levels. Retinas were also examined using histofluorescence for dopamine histochemistry, for AChE, and immunohistochemistry with antibodies to CAT, tyrosine hydroxylase, GABA, 5-HT, Leu-enkephalin, and somatostatin. A dose of 50 nmol ECMA caused a prolonged 70% depletion of CAT activity and a 40% depletion of AChE activity. The other biochemical parameters were unchanged. This result corresponds to the morphological finding that 2 populations of cholinergic cells were destroyed and that the AChE activity associated with their terminal arbors was lost. A third population of cholinergic cells, located towards the middle of the inner nuclear layer, was resistant to the toxic effects of ECMA. The other cell types, except for somatostatin-immunoreactive cells and photoreceptors, which showed transient effects, were unaffected. ECMA therefore appears to be a highly specific toxin for cholinergic cells in the retina.

Acetylcholine↗
PubMed1986

Putative cholinergic interneurons in the optic tectum of goldfish.

We have demonstrated that a significant fraction of cells in layer 1 of goldfish optic tectum are immunoreactive for choline acetyltransferase. These cells constitute 4-7% of type XIV cells, which are thought to be intrinsic neurons and represent 95% of all tectal cells. The number of immunoreactive type XIV cells is unchanged following short-term enucleation. The possible integrative role of these putative cholinergic neurons is discussed in relation to sensory functions of the optic tectum.

Animals↗
PubMed1986

Hemodynamic responses of the acutely stressed neonatal right ventricle: a maturational study in lambs.

Right ventricular Starling responses to acute volume infusion in newborn lambs were compared to those in older groups of lambs. When peak stroke volume/kg was reached during infusion, right ventricular end-diastolic pressures for the newborn group were significantly lower (p less than 0.001) than those obtained for older groups, in spite of significantly higher resting and peak stroke volumes in the two younger groups. Newborn lambs developed tricuspid regurgitation and right-to-left foraminal shunting, demonstrated by echocardiography, at a mean end-diastolic pressure of 7.5 mm Hg. No right-to-left shunting was noted in older lambs. This study demonstrated a blunted Starling response in the newborn lamb's right ventricle. The response to volume loading improved with maturation, but was still less than that reported for the left ventricle. Clinical implications regarding right ventricular immaturity and inadequate response to altered hemodynamic situations are raised.

Aging↗
PubMed1986

The gut supports neurogenic differentiation of periocular mesenchyme, a chondrogenic neural crest-derived cell population.

Periocular mesenchyme (PM) is a mesencephalic neural crest derived cell population which as a result of an interaction with the retinal pigment epithelium forms the scleral cartilage of the avian eye. Enteric neurons are derived from vagal crest cells which invade the gut. To study factors which regulate neuronal differentiation, we investigated whether the gut could direct neurogenesis in PM, a cell population that does not produce neurons in vivo. We report here that PM cultured in the presence of aneural chick hindgut on the chorioallantoic membrane (CAM), invaded the gut and formed large numbers of neurons. These were localized in enteric ganglia and contained neurofilament immunoreactivity, vasoactive intestinal peptide immunoreactivity, and somatostatin immunoreactivity. In the control PM cultured alone on the CAM, a small number of cells contained neurofilament immunoreactivity but lacked the appearance of mature neurons.

Animals↗
PubMed1986

Monoclonal antibodies and polyvalent antiserum to chicken choline acetyltransferase.

Monoclonal antibodies (mAbs) to chick choline acetyltransferase (ChAT) were obtained from mouse-hybridoma cultures after immunization with partially purified enzyme isolated from optic lobes. Antibodies that bound active enzyme were detected in 11 hybridoma cultures. The mAbs showed cross-reactivity to ChAT from quail and beef but not to ChAT from several other species. An affinity column prepared with one of the mAbs was used to purify ChAT to apparent homogeneity. Polyclonal antiserum to mAb affinity-purified ChAT was produced in a rabbit. This antiserum inhibited chick ChAT activity and quantitatively precipitated ChAT activity from solution. On immunoblots, the antiserum stained ChAT and two other proteins. After preadsorption of the antiserum with effluent from the mAb affinity column, the antiserum became monospecific for ChAT. This antiserum was useful for immunocytochemical localization of ChAT, it selectively stained neuronal cell bodies in chick spinal cord and rat brain at locations known to contain cholinergic neurons.

Animals↗
PubMed1985

Cholinergic and acetylcholinesterase-containing neurons of the chicken retina.

In the chicken retina, choline acetyltransferase-like immunoreactivity (ChAT-LI) defines three populations of cholinergic amacrine cells and two terminal bands in the inner plexiform layer (IPL). Acetylcholinesterase (AChE) histochemistry defines two prominent bands within the IPL which corresponded to those containing ChAT. Other AChE-positive bands in the IPL are not associated with cholinergic transmission sites. Cholinergic cell bodies contain AChE, but the most intensely AChE-positive cells do not appear to be cholinergic. AChE histochemistry may be used to define the major cholinergic synaptic sites in the IPL, and may be a useful marker of IPL lamination.

Acetylcholinesterase↗
PubMed1985

Cardiac decompensation following verapamil therapy in infants with supraventricular tachycardia.

Three infants with supraventricular tachycardia and congestive cardiac failure were given verapamil intravenously. In two of the infants, the rhythm was converted to sinus, but the third infant required direct current cardioversion. However, each infant demonstrated hemodynamic decompensation shortly after verapamil administration and required cardiopulmonary resuscitation. All three patients were stabilized and their tachycardia was controlled with digoxin. All three were doing well at the time of follow-up evaluation, and there was no evidence of structural heart disease. The risk of cardiac decompensation in infants with supraventricular tachycardia and congestive cardiac failure should be kept in mind prior to administration of verapamil. Alternative methods for conversion of supraventricular tachycardia should be considered.

Electric Countershock↗
PubMed1983

Dual accessory nodoventricular pathways: role in paroxysmal wide QRS reciprocating tachycardia.

Clinical electrophysiological study in an otherwise healthy 21-year-old male with paroxysmal wide QRS tachycardia (cycle length 300 ms, heart rate 200/min) suggested the presence of two nodoventricular (NV) bypass connections. The first NV connection pre-excited the base of the interventricular septum (NVs), as evidenced by a short HV interval during sinus rhythm (15-20 ms), with local ventricular activation occurring earlier at the septal base than at either the right ventricular apex or the base of the left ventricle. The second NV connection appeared to connect the AV junction with the right ventricle (NVRV). Intracardiac recordings from a portion of the right-bundle branch of the interventricular conduction system demonstrated right ventricular pre-excitation by NVRV during both atrial pacing and reciprocating tachycardia. The latter finding supported participation of NVRV in the tachycardia. Further, following exclusion of atrial participation in the arrhythmia, premature depolarization of the right ventricle and interventricular septum appeared to advance the tachycardia without altering the timing of His bundle depolarization, implicating NVS in the retrograde limb of a re-entry circuit. Consequently, this study demonstrated the presence of two NV connections and provided further support to the concept that NV accessory bypass connections may comprise portions of a re-entry pathway during reciprocating tachycardia in man.

Adult↗
PubMed1983

Postoperative hemodynamic and electrophysiological evaluation of the Senning procedure.

To determine efficacy of the Senning procedure for correction of transposition of the great arteries we performed detailed hemodynamic and electrophysiological studies in 6 consecutive children operated upon at 5-18 months of age. Cardiac catheterizations were performed 10-19 months following surgery. All patients were asymptomatic on no medication. Hemodynamic studies demonstrated no evidence of pulmonary venous obstruction, pulmonary hypertension, or left ventricular outflow tract obstruction. 1 patient had mild upper baffle limb obstruction. Angiography demonstrated tricuspid insufficiency in 2 patients and a small atrial level shunt in 1. Ambulatory electrocardiographic monitoring in 5 of 6 patients revealed multiple premature ventricular contractions in 1. Invasive electrophysiological studies for sinus node function were normal. Corrected sinus node recovery time was 36-348 ms while total sinoatrial conduction time, determined in 4 patients, ranged between 83 and 128 ms. At our institution the Senning procedure has a low incidence of residual hemodynamic or electrophysiological abnormalities. Detailed postoperative evaluation is necessary to determine extent of residual problems.

Electrocardiography↗
PubMed1983

Surfactants selectively ablate enteric neurons of the rat jejunum.

Surfactants, a group of nonspecific membrane perturbating substances, can cause nerve damage. Various concentrations of the cationic surfactants benzalkonium chloride (BAC) and benzethonium chloride, the anionic surfactants sodium ricinoleate, dioctyl sodium sulfosuccinate and sodium lauryl sulfate and the nonionic surfactant Triton X-100 were applied to the serosal surface of the rat jejunum every 5 min for 0.5 hr and then rinsed off with saline. Thirty days after surfactant application, the treated and an untreated segment of jejunum were removed and examined histologically. All surfactants which were tested significantly reduced the number of ganglion cells in the myenteric plexus. In addition, sodium ricinoleate significantly reduced the number of ganglion cells in the submucosal plexus. Higher concentrations of the cationic agents BAC and benzethonium chloride caused a generalized tissue damage including disruption of the smooth muscle, lymphocytic infiltration, intestinal perforation and death. Using BAC as a prototype surfactant, peptidergic neuron distribution and gut electrical activity were examined. BAC treatment markedly reduced the immunoreactivity of somatostatin, substance P, met-enkephalin and vasoactive intestinal peptide in the myenteric plexus. In addition, the electric properties of the smooth muscle were altered. BAC treatment resulted in an erratic, markedly distorted basic electric rhythm and an alteration in spike potential generation. These studies demonstrate that surfactants in appropriate concentrations selectively ablate the myenteric neurons and alter peptidergic neuron distribution and gut electrical parameters in the rat jejunum.

Animals↗
PubMed1983

The development of peptidergic neurons in the foregut of the chick.

We have used antisera specifically directed against Met-enkephalin (met-ENK), somatostatin (SOM), substance P (SP), and vasoactive intestinal peptide (VIP), to study the development of neurons containing these peptides in the foregut of the chick. All four peptides were detected early in ontogeny, at 4 to 9 days of incubation (d.i.), and were localized primarily to cell bodies in the primitive myenteric plexus. There were differences in the times at which they were first detected and in the sequence of their appearance in the proventriculus, gizzard, and duodenum. The differentiation of these peptidergic neurons in the duodenum was examined in some detail. Cell bodies containing these peptides were first detected in the primitive myenteric plexus at 5 to 7 d.i. and increased in number from 7 to 11 d.i. Processes containing varicosities became prominent between 11 and 13 d.i. VIP was the first of the peptides to appear in the submucosal plexus and was found in more proximal regions of the duodenum at 5 d.i. Shortly thereafter, SOM- and SP-containing cell bodies were seen; met-ENK-containing cell bodies were never detected in the submucosal plexus. At 13 d.i., the circular smooth muscle contained a number of VIP-immunoreactive and a smaller number of SOM-immunoreactive processes. met-ENK- and SP-immunoreactive processes appeared in the circular smooth muscle between 17 and 21 d.i.; VIP- and SP-immunoreactive processes appeared in the mucosal plexus at 17 to 21 d.i. Our results suggest that neuropeptides appear very early in the ontogeny of enteric neurons, at the same time or even before cholinergic and serotonergic neurons express their phenotypes. These findings argue against a sequential developmental order in which peptidergic neurons appear after those containing acetylcholine and serotonin.

Animals↗
PubMed1982

Modification of the Smeloff mitral prosthesis.

The simplicity of the ball valve with its random seating capabilities coupled with its durability, reliability, and predictability has made it the attractive choice of many surgeons. A low incidence of embolic phenomena with the Smeloff full-orifice, double-caged, bare-strutted ball valve has made us reluctant to alter the design over 17 years. Recent evaluation of the reasons for reoperation on the Smeloff mitral valve implantation in 376 cases revealed 16 cases in which development of fibrous subvalvular pannus with signs and symptoms of mitral stenosis occurred. The mean occurrence time was 7.5 years for adults and 4.6 years for children under age 8 years. No such problem has been encountered with the valve in the aortic position. Many of these patients are maintained on aspirin and Persantine alone. Valve design was explored as a possible cause of mitral subvalvular stenosis. Alterations of the design were examined in the engineering laboratory and in dog implantations by catheterization, electrophysiologic evaluation, and echocardiography. The results were encouraging.

Adult↗