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Biomedical subjects

S A Berman

Publications and source records attributed to S A Berman.

At least 37 records · Page 2Linked to original sources
PubMed1993

The effect of nicotine on recurrent inhibition in the spinal cord.

Recurrent inhibition via Renshaw cells provides a mechanism by which spinal and supraspinal centers exert control over movement. The conditioned H-reflex technique of Pierrot-Deseilligny and Bussel permits noninvasive assessment of recurrent inhibitory pathways. We employed this technique to investigate changes in Renshaw cell activity due to nicotine (a potent CNS cholinergic agonist that excites Renshaw cells in animals) contained in inhaled tobacco smoke. In 10 normal subjects, cigarette smoking caused a large, rapid drop in the conditioned H-response amplitude, implying increased activation of Renshaw cells. The time course of the change in conditioned H-response amplitude closely approximated the known pharmacokinetics of inhaled nicotine. Nicotine administered via chewing gum had a much slower and less dramatic effect, probably due to the slower rise in blood levels with this mode of administration. Increased activity in Renshaw cells may contribute to spasticity in spinal cord-injured patients, raising the possibility that cigarette smoking could cause further increases in tone in such patients.

Administration, Cutaneous↗
PubMed1992

Pathological left-handedness and preserved function associated with a slowly evolving brain tumor.

The authors report the serial neuropsychological evaluations of a patient with acquired left-handedness who had a massive brain tumor that infiltrated the entire temporal and posterior parietal lobes of the left hemisphere. Although the patient had pre-operative impairment of non-verbal memory, follow-up assessment 31 and 66 months after the tumor was resected revealed cognitive functions to be in the high-average to superior range. This case demonstrates the sparing of neuropsychological functions that can be seen with a slowly evolving lesion. The authors suggest that such functional sparing may be due to transfer of function rather than to the residual function of tumor-infiltrated neuronal tissue. Possible mediators of functional preservation include slow lesion growth, the patient's youth at disease onset and the large size of the lesion.

Adult↗
PubMed1992

Recurrent inhibition is increased in patients with spinal cord injury.

Mechanisms underlying the development of spasticity after spinal cord injury are not understood. One spinal interneuron likely to be affected is the Renshaw cell, which acts to produce recurrent inhibition in motor neurons as well as inhibiting Ia interneurons. Descending pathways exert both excitatory and inhibitory control over Renshaw cell activity. We studied Renshaw cell activity in normal subjects and in patients with varying levels of spasticity after spinal cord injury using the conditioned H-reflex technique of Pierrot-Deseilligny and Bussel. A submaximal stimulus to the tibial nerve is presented prior to a supramaximal stimulus so that action potential collision permits an H reflex (H') to be elicited in response to the supramaximal stimulus. The amplitude of this H' reflex is affected by activity in recurrent inhibitory pathways. Patients with both complete and partial spinal cord lesions were studied; date of injury ranged from 1 month to 216 months prior to evaluation. In the 18 patients in whom H reflexes could be recorded, H' reflexes were absent in 13, in contrast to their uniform presence in normal subjects. We conclude that recurrent inhibition via Renshaw cell activity is increased in spinal cord injury, and that measures of recurrent inhibition may correlate well with some clinical measures of spasticity.

Adult↗
PubMed1992

Case report: acquired antisocial personality disorder associated with unilateral left orbital frontal lobe damage.

We report on our analysis of a patient who developed personality changes which strongly resembled an antisocial personality disorder after surgical resection of a pituitary tumor. Despite behavioral changes that were obvious to friends, family and health care professionals, formal neuropsychological and personality testing revealed no specific cognitive deficits or psychopathology. We hypothesize that damage to a circumscribed region of the left orbitofrontal cortex, illustrated by magnetic resonance imaging, underlies these personality alterations. In contrast to previous reports, which ascribe such personality changes to bilateral frontal lobe injury, we suggest that unilateral frontal lobe damage alone may have resulted in the development of this syndrome.

Adenoma↗
PubMed1991

Calcium and ionophore A23187 stimulates deposition of extracellular matrix and acetylcholinesterase release in cultured myotubes.

Calcium (Ca2+) and calcium-transporting ionophores stimulate protein secretion in many cellular systems. We demonstrate here than increases in intracellular calcium concentration induce a time- and concentration-dependent deposition of extracellular matrix and an increase in acetylcholinesterase secretion. Scanning and transmission electron-microscopy revealed that treatment with the calcium ionophore A23187, or high extracellular Ca2+ levels (5 mM to 15 mM) produce significant deposits of extracellular matrix around the myotubes, as well as a marked increase in the acetylcholinesterase reaction-product. Blocking muscle contraction was not necessary for the induction of AChE secretory activity. Sucrose density-gradients of media conditioned by muscle cells revealed 3 separate acetylcholinesterase molecular forms. However, incubation with A23187 increased only the 4.5 S and the 7.2 S molecular forms, whereas the 12.0 S form showed no significant differences from controls. Polyacrylamide gel electrophoresis, and autoradiography using [3H]diisopropyl fluorophosphate revealed a broad band at 65,000 daltons. This band was broader than for controls when medium was obtained from A23187-treated cells. Our results show that increasing intracellular Ca2+ concentration induces marked deposition of extracellular matrix and increased acetylcholinesterase secretion, with an apparent selectivity for the monomeric and dimeric acetylcholinesterase molecular forms.

Acetylcholinesterase↗
PubMed1990

Localization of an acetylcholine receptor intron to the nuclear membrane.

The first intron of the RNA for the acetylcholine receptor (AChR) alpha subunit shows a ringlike distribution around nuclei in multinucleated myotubes by in situ hybridization. This pattern is not observed for an actin intron or U1 RNA. Quantitation of the intron sequences reveals large variations in the amount of both the AChR and actin introns between nuclei within the same myotube, although all nuclei express equivalent amounts of U1 RNA. This differential RNA expression indicates that nuclei can individually control expression of messenger RNAs. The restricted distribution of the AChR intron RNA suggests a previously unknown step in RNA processing.

Actins↗
PubMed1990

Factors released by ciliary neurons and spinal cord explants induce acetylcholine receptor mRNA expression in cultured muscle cells.

The nuclei of cultured noninnervated muscle cells are heterogeneous with respect to production of mRNA for the nicotinic acetylcholine receptor (AChR). Some nuclei actively express AChR mRNA while others have a low level of activity or are inactive. To determine if innervation, or a factor released by neurons, influences nuclear expression of AChR mRNA, we examined mRNA at a single cell level via in situ hybridization and autoradiography with an alpha-subunit AChR genomic probe. Four days after plating, we co-cultured chicken primary muscle cells with spinal cord explants, ciliary neurons, or dorsal root ganglia (DRG) cells. In situ hybridization of the spinal-cord and muscle-cell co-cultures with the AChR alpha-subunit probe revealed a high density of silver grains on muscle cells, which were within two explant diameters of the spinal cord explant, and a graded decrease in silver grain density as the distance from the explant increased, as well as the appearance of a strikingly nonhomogenous distribution of active and inactive muscle cell nuclei. When ciliary neurons were uniformly distributed over the muscle cells, a high level of AChR mRNA was induced, but no gradients appeared. Neither an increased mRNA level nor a gradient was observed when DRG cells were co-cultured with muscle cells. When ciliary neurons are cultured within Costar permeable inserts, which prevent any contact between the neurons and the underlying muscle cells, AChR messenger RNA is still induced, showing that diffusible factors are responsible. Our results indicate that molecules released by cholinergic neurons regulate the expression of AChR mRNA in the myotubes and raise the possibility that AChR expression depends on both neuronal signals and on intracellular information from the muscle cell.

Animals↗
PubMed1990

Simultaneous visualization of neuronal protein and receptor mRNA.

We describe a combined immunocytochemistry/in situ hybridization technique which allows for the simultaneous localization of protein and mRNA in a single cell. We have carried out these studies either on non-innervated skeletal myotubes or on myotubes which we have innervated with spinal cord explants or ciliary neurons. Our methods allowed us to detect acetylcholine receptor gene mRNA sequences which are expressed in low abundance within the cells and to determine the intracellular and intranuclear domains where these sequences are concentrated, as well as to identify neurons and their processes. The isotopic detection of RNA in combination with fluorescence microscopy produces high-resolution double-label images, with little background and good preservation of morphology, providing a powerful tool for detection of gene expression and protein content at the single-cell level.

Animals↗
PubMed1989

Differential expression of acetylcholine receptor mRNA in nuclei of cultured muscle cells.

Muscle cells in vitro and in vivo are multinucleated and express acetylcholine receptors (AcChoRs). On innervated cells, the AcChoRs form clusters which lie under the nerve terminals. However, noninnervated cells in culture also express clusters of AcChoR. Both in vivo and in vitro the AcChoR clusters appear to be associated with clusters of nuclei. We have used in situ hybridization to determine whether all the nuclei in cultured chicken embryo myotubes are equally active in expressing the AcChoR alpha subunit message. Cells were hybridized with 35S-labeled probes that contained either both an exon and an intron region or only exon sequences. Control cultures were hybridized with a labeled actin DNA probe or poly(U). The hybrids were detected by emulsion autoradiography; simultaneously, the nuclei were visualized with bisbenzamide. Cells hybridized with the intron/exon probe showed a striking preferential silver grain localization in and around some of the myotube nuclei, whereas those hybridized with the exon probe gave a rather homogeneous grain distribution in the cytoplasm. These results show that myotube nuclei possess differential activation capacities for the expression of AcChoR alpha subunit mRNA and that this difference is due to differential rates of transcription.

Animals↗
PubMed1989

Increased N-myc mRNA expression associated with dibutyryl cyclic AMP induced neuroblastoma differentiation.

The N-myc cellular oncogene is frequently amplified and expressed at a high level in neuroectodermal tumor cells such as neuroblastoma and retinoblastoma. We examined N-myc expression in NCB-20 hybrid (N18TG2 neuroblastoma x embryonic Chinese Hamster brain) cells. After five days of culture, cells treated with 1 mM db cAMP show extensive neurite outgrowth and secrete acetylcholinesterase into the media at a level three times higher than untreated control. In situ hybridizations, dot blots, and Northern analyses reveal four- to eight-fold higher levels of N-myc mRNA in the treated, differentiated cells than in the untreated, undifferentiated controls. Our results show that the highly differentiated state is not incompatible with a high level of N-myc mRNA.

Acetylcholinesterase↗
PubMed1988

Phorbol esters inhibit the synthesis of acetylcholine receptors in cultured muscle cells.

The acetylcholine receptor (AChR) synthesis, insertion and degradation rates are regulated by numerous intracellular and extracellular agents. Recent studies have shown that Ca2+ and Ca2+ ionophores have a profound regulatory effect on the appearance of AChR clusters and AChR synthesis. These regulatory effects may be mediated through the activation of calcium and phospholipid-dependent protein kinases by agents such as phorbol esters. In this study, we have utilized 4-beta-phorbol-12-myristate-13-acetate (PMA) in order to determine whether the activation of protein kinase C exerts a regulatory effect on the expression of AChRs in cultured chick myotubes. Our results show that 4-beta-phorbol-12-myristate-13-acetate decreased intracellular AChRs and suppressed AChR synthesis without affecting the turnover rate. Control and PMA treated cells labeled with [35S] methionine and immunoprecipitated with a monoclonal antibody to the alpha subunit of AChRs (mAb35) revealed a significant decrease in radioactivity precipitated after exposure to PMA. Polyacrylamide gel electrophoresis revealed no major changes in protein patterns, or in newly synthesized proteins as determined by [35S] methionine incorporation and autoradiography. Other enzymes important in muscle metabolism were not affected by PMA treatment. Our results indicate that activation of protein kinase C results in the suppression of AChRs synthesis and dispersal of AChR clusters.

Animals↗
PubMed1987

Coated and smooth vesicles participate in acetylcholine receptor transport.

The removal of the acetylcholine receptors (AChRs) from the surface of muscle cells serves as an important mechanism in the regulation of the AChR turnover rate. Our previous studies have shown that cultured myotubes contain coated pits and vesicles bearing alpha-bungarotoxin (alpha BTX)-binding sites (Bursztajn 1984; Bursztajn and Fischbach 1984). In this study we have used alpha BTX conjugated to horseradish peroxidase (HRP) and quantitative electron microscopy to determine the intracellular pathway(s) of acetylcholine receptors during the internalization process. To accomplish this, cultured rat myotubes were incubated with alpha BTX-HRP at 4 degrees C after which cells were washed and incubated at 37 degrees C for 0 min to 2 h. After warming the cells, coated pits, coated vesicles and smooth membraned vesicles containing the peroxidase reaction product were present. A threefold increase in coated vesicles containing the reaction product was observed 1 min after warming the cells. The number of smooth-membraned vesicles remained constant at this time point. However, 5 to 15 min after warming the cells, a fivefold increase in the number of smooth membraned vesicles was observed. After 1 h at 37 degrees C the reaction product was present in the lysosomal like bodies, but was not observed in the Golgi complex or the small coated vesicles associated with the Golgi complex. Our observations indicate that there is a size segregation between those coated vesicles containing alpha BTX-HRP reaction product and those in which reaction product is absent. Our studies also suggest that within minutes of AChR internalization coated vesicles lose their coat and become smooth-membraned vesicles.

Animals↗
PubMed1985

Insertion and internalization of acetylcholine receptors at clustered and diffuse domains on cultured myotubes.

Two populations of acetylcholine receptors (AChRs) are present in cultured myotubes. One forms large aggregates or clusters and the other has a much lower density of AChRs, which are diffusely distributed. Both clustered and diffuse AChRs are inserted and removed (internalized) from the sarcolemma. To determine the insertion and removal rates of AChRs in these two plasma membrane domains, we used a double label technique to distinguish and quantitate newly inserted and "old" AChRs. Application of our method revealed that the rate of AChR internalization is the same at the clustered and diffuse regions of the plasma membrane, whereas the rate of insertion is threefold greater at the clusters than elsewhere in the plasma membrane. Thus, the increase in AChR number at the clusters is not due to an increase in their half-life, but to an increase in their rate of insertion.

Animals↗
PubMed1984

Correlation of CT cerebral vascular territories with function: 3. Middle cerebral artery.

Schematic displays are presented of the cerebral territories supplied by branches of the middle cerebral artery as they would appear on axial and coronal computed tomographic (CT) scan sections. Companion diagrams of regional cortical function and a discussion of the fiber tracts are provided to simplify correlation of clinical deficits with coronal and axial CT abnormalities.

Brain↗
PubMed1981

Correlation of CT cerebral vascular territories with function: II. Posterior cerebral artery.

This paper presents schematic displays of the cerebral territories supplied by branches of the posterior artery as they would appear on axial and coronal computed tomographic (CT) scan sections. Companion diagrams of regional cortical function and a discussion of the fiber tracts are provided to simplify correlation of clinical deficits with coronal and axial CT abnormalities. Illustrations of the vascular supply and functional relay points (nuclei) of the thalamus are provided.

Brain↗
PubMed1980

Correlation of CT cerebral vascular territories with function: I. Anterior cerebral artery.

Schematic displays of the cerebral territories supplied by branches of the anterior cerebral artery as they would appear on axial and coronal CT scan sections are presented. Companion diagrams of regional cerebral function are also provided to simplify correlation of clinical deficits with coronal and axial CT abnormalities. Selected examples illustrate that these facilitate more detailed and precise CT interpretation in clinical practice.

Brain Mapping↗