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E Bergman

Publications and source records attributed to E Bergman.

29 records · Page 2Linked to original sources

Loss of primary sensory neurons in the very old rat: neuron number estimates using the disector method and confocal optical sectioning.

Loss of neurons has been considered to be a prime cause of nervous disturbances that occur with advancing age. However, the notion of a constitutive aging-related loss of neurons has been challenged recently in several studies that used up-to-date methods for counting neurons. In this study, we have applied stereological techniques with the objective of obtaining quantitative data on total neuron numbers and the distribution of neuron cross-sectional areas in the fifth cervical (C5) and fourth lumbar (L4) dorsal root ganglion (DRG) of 3- and 30-month-old Sprague-Dawley rats. Tissue data were recorded on a confocal laser-scanning microscope with the use of the optical-disector technique and random, systematic sampling. Aged rats of both sexes disclosed only a small decrease (approximately 12%) in the number of cervical and lumbar DRG neurons. Furthermore, there was no significant correlation between the degree of neuron loss and the extent of behavioral deficits among the aged individuals. The DRG neurons of aged rats had a smaller mean cross-sectional area (approximately 15%; P < 0.001) at both DRG levels. Further analysis of the male cohorts was carried out by using isolectin B4 and neurofilament subunit (phosphorylated 200 kDa; RT97) immunoreactivity (IR) as selective markers for unmyelinated and myelinated axons, respectively, and disclosed no significant change in the relative frequencies of immunoreactive neuron profiles in the old rats. However, RT97-IR DRG neurons of the aged rats had significantly smaller cross-sectional areas (approximately 9% in C5; approximately 16% in L4; P < 0.001) than the young adult rats, indicating a selective cell body atrophy among myelinated primary afferents during aging. The results indicate that loss of primary sensory neurons cannot exclusively explain the functional deficits in sensory perception among senescent individuals. It seems likely that other factors at the subcellular level and/or target interaction(s) contribute substantially to the sensory impairments observed with advancing age.

Animals↗

Alterations in mystacial pad innervation in the aged rat.

It is well established that sensory perception becomes impaired with advancing age and that, in parallel, dystrophy and degeneration of axons occur in sensory pathways. In this study, the impact of aging was examined in the mystacial pad, which receives a large variety of sensory nerve endings organized in a highly predictable pattern. Mystacial pad specimens from aged (30 months old) and young adult (2-3 months old) female Sprague-Dawley rats were processed, in parallel, for immunohistochemical analyses with antibodies against human neuronal cytoplasmic protein (protein gene product 9.5), transmitter enzymes, and several neuropeptides. Several changes in cutaneous innervation including both degenerative and regenerative processes were evident in the aged rat: (1) the Merkel endings and lanceolate endings that emanate from large-caliber afferents in the whisker follicles were reduced and showed signs of degeneration. Furthermore, a reduction of piloneural complexes at the intervibrissal hairs were evident, but only in aged rats that showed more severe behavioral sensorimotor disturbances. In contrast, Ruffini endings as well as mechanoreceptors emanating from medium-caliber axons, i.e., transverse lanceolate and reticular endings, appeared normal. (2) A reduction was evident among two sets of unmyelinated epidermal endings; however, the epidermal innervation affiliated with the intervibrissal hairs appeared normal in the aged rat. (3) A loss of sympathetic neuropeptide tyrosine (NPY) or tyrosine hydroxylase-immunoreactive (IR) and somatosensory Calcitonin gene-related peptide (CGRP)-IR perivascular axons was paralleled by an increase in presumed parasympathetic NPY/CGRP-IR axons. (4) Two "novel" networks of fine-caliber axons were observed in the outer and inner root sheaths of the whisker follicles in the aged rat. (5) NPY was present in a population of small-caliber, somatosensory CGRP-IR axons in the aged rat. This may represent a de novo synthesis, since, normally, NPY-like immunoreactivity is not observed in this set of axons. Our results suggest that the sensory impairments occurring with advancing age are part of a peripheral process instigated by changes in nerve-target interactions and/or incapacitation of the neuronal machinery to sustain the axonal integrity.

Aging↗

Interactory effect between marginal plaque and subgingival proximal restorations on periodontal pocket depth.

The purpose of the present study was to investigate the influence of plaque on periodontal pocket depth adjacent to proximal amalgam restorations after non-surgical periodontal treatment. From 120 randomly selected patients 200 proximal premolar- or molar sites with subgingival restorations (test sites) and 200 contralateral unrestored sites within the same patient (control sites) were included if plaque was present on test as well as on control sites. At baseline the periodontal mean pocket depth adjacent to subgingival restorations were found to be significantly deeper (0.25 mm) than for control sites. After treatment, 24% of the initially subgingivally located restorations were registered as supragingival restorations. The differences according to mean pocket depth between supragingival restorations and corresponding control sites after treatment were found to be statistically non-significant. At reexamination mean pocket depth adjacent to proximal restorations with plaque were significantly deeper than their contralateral unrestored sites (mean difference 0.34 mm), while a non-significant difference was calculated for subgingival restorations without plaque. Subgingival restorations with their apical borders still located subgingivally after periodontal treatment should be regarded as a risk factor in periodontitis progression. Consequently, placement of the restoration margin supragingivally is recommended, especially in periodontitis-prone patients with an insufficient plaque control.

Adult↗

Neuropeptides and neurotrophin receptor mRNAs in primary sensory neurons of aged rats.

Neuropeptides and neurotrophin receptors are regulated in primary sensory neurons in response to axonal injury, and axonal lesions are characteristic stigmata of aging primary sensory neurons. We have therefore examined the expression of neuropeptides and neurotrophin receptor mRNAs in 30-month-old (median survival age) Sprague-Dawley rats to see if similar adaptive mechanisms operate in senescence. The content of neuropeptides was examined with immunohistochemistry (IHC) and in situ hybridization (ISH), and the cellular mRNA expression of neurotrophin receptors was studied with ISH. All of the aged rats had symptoms of hind limb incapacity (posterior paralysis), but fore limbs did not seem affected. The size-distribution of neuronal profiles in cervical and lumbar dorsal root ganglia (DRGs) was similar in aged and young adult (2-3 months old) rats. In aged rats, the DRG neurons showed an increase in both immunolabelling and mRNA content of neuropeptide tyrosine (NPY), as well as an increased cellular expression of galanin mRNA. In the same animals, there were decreased cellular levels of calcitonin gene-related peptide (CGRP; IHC and ISH) and substance P (SP; IHC and ISH), while the difference in neuronal somatostatin (IHC and ISH) was small. The distribution of neuropeptide immunoreactivities in the dorsal horn of the corresponding spinal cord segments revealed a decreased labelling for CGRP-, SP-, and somatostatin-like immunoreactivities (LI) in the aged rats at both cervical and lumbar levels. NPY- and galanin-LI had a similar distribution in aged and young adult rats. NPY-immunoreactive fibers were also encountered in the dorsal column of aged but not young adult rats. ISH revealed that most of the primary sensory neurons express mRNA for the p75 low-affinity neurotrophin receptor (p75-LANR) and that there was no discernible difference between young adult and aged rats. The labelling intensity for mRNA encoding high-affinity tyrosine kinase receptors (TrkA, TrkB, and TrkC) was decreased in aged rat DRG neurons, while the percentage of neuronal profiles expressing mRNA for TrkA/B/C was similar in young adult and aged rats. The changed pattern of neuropeptide expression in primary sensory neurons of aged rats resembled that seen in young adult rats subjected to axonal injury of peripheral sensory nerves and may, thus, indicate aging-related lesions of sensory fibers. Since NPY is primarily present in large and galanin in small DRG neurons, the stronger effect on NPY as compared to galanin expression may indicate that aging preferentially affects neurons associated with mechanoreception (A alpha and A beta fibers) as compared to nociceptive units (A delta and C fibers). Furthermore, the observed changes in neuropeptide expression were most pronounced in lumbar DRGs, that harbors the sensory neurons supplying the affected hindlimbs of the rats.

Adaptation, Physiological↗

Blushing as a function of audience size.

Almost no experimental analysis of blushing has been done since Darwin's observations in 1872. Forty-eight college women watched a videotape intended to elicit blushing, and a videotape not intended to elicit blushing, but elicit physiological responses. A subject was alone, or with one or four persons present. Blushing, which was measured directly with a photoplethysmograph probe on the cheek, was greater during the blushing than nonblushing stimulation. Blushing increased as audience size increased from one to four, but not from zero to one. Audience size and kind of stimulation interacted statistically. Similar results were obtained with ear coloration, cheek temperature, and skin conductance responses, although confidence levels were lower. Cheek coloration and temperature were significantly correlated during nonblushing stimulation, and the zero and one audience conditions, but not during the four audience condition, when blushing was greatest. These results may be placed within the context of emotional effects of audience size generally, including stuttering and speech disturbance, disruption of learning, and self-reported tension.

Adult↗

Facial coloration and temperature responses in blushing.

Little work on the psychophysiology of blushing has been done since Darwin's 1872 observations. Facial vascular and temperature changes have been largely ignored in psychophysiology. We had 16 female and 16 male undergraduate volunteers watch a videotape intended to produce blushing (the individual's singing recorded the previous day), and a videotape not intended to produce blushing, but elicit physiological responses for comparison (a segment from Hitchcock's movie Psycho). Four people were present as a subject watched these video segments. Cheek and ear coloration, measured photoplethysmographically, cheek temperature, and finger skin conductance responses were significantly greater during stimulation intended to elicit blushing than during comparison stimulation. Gender interacted statistically with kind of stimulation only in cheek temperature. Only video segments of the subject's face that coincided with maximal cheek coloration during stimulation intended to produce blushing were judged reliably as blushing, and then more often in females than in males.

Adolescent↗