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Biomedical subjects

J B Martin

Publications and source records attributed to J B Martin.

At least 145 records · Page 8Linked to original sources
PubMed1987

Neuropeptide Y, somatostatin, and reduced nicotinamide adenine dinucleotide phosphate diaphorase in the human striatum: a combined immunocytochemical and enzyme histochemical study.

Neuropeptide Y and somatostatin immunoreactive neurons and processes were examined in human striatum using both immunofluorescence and avidin biotin immunoperoxidase methods. Reduced nicotinamide adenine dinucleotide phosphate diaphorase activity was histochemically determined by the reduction of nitro blue tetrazolium. Immunofluorescence using a monoclonal anti-somatostatin antibody and a polyclonal anti-neuropeptide Y antibody, followed by diaphorase histochemistry, showed that these three neurochemical markers are co-localized in a single population of medium-sized aspiny intrinsic neurons. Cells were evenly distributed in clusters throughout the striatum, but fiber density was higher in the nucleus accumbens and ventromedial regions of the caudate and putamen. Double-stained reduced nicotinamide adenine dinucleotide phosphate diaphorase-acetylcholinesterase sections demonstrated that these neurons are located in zones of high acetylcholinesterase activity, often at the interface of these zones with regions of low enzyme activity. These biochemically distinctive neurons are uniquely situated to modulate activity between striatal compartments. Our findings provide new information about the modular organization of the striatum and extend these observations in human brain.

Aged↗
PubMed1987

Amino acid neurotransmitter abnormalities in Huntington's disease and the quinolinic acid animal model of Huntington's disease.

Concentrations of gamma-aminobutyric acid (GABA), glutamate, aspartate, and taurine were measured in postmortem tissue from the brains of patients with Huntington's disease (HD) and in the quinolinic acid (QA) lesioned rat striatum. The aim of the study was to assess further the ability of the QA model of HD to reproduce the neurochemical features of the disease. Nine cortical and 9 subcortical regions were examined from 17 pathologically graded cases of HD and 10 controls. Significant reductions in both GABA and glutamate were found in HD striatum. The reductions were greater in the more severely affected grades of HD, and there was a gradient of amino acid loss across the striatal nuclei (caudate greater than putamen greater than nucleus accumbens) which was consistent with the known pattern of pathological involvement. Taurine and aspartate concentrations showed no significant change. GABA reductions were found in both segments of the globus pallidus (external greater than internal) and both parts of the substantia nigra (reticulata greater than compacta). In advanced cases of HD, there were significant reductions in glutamate in Brodmann cortical areas 3-1-2, 6, 9, and 17, but GABA, aspartate, and taurine were unaltered in the cortex. The QA lesions reproduced the striatal deficits of both GABA and glutamate but, in contrast to HD, there was a decrease in taurine, possibly due to species differences. Chronic QA lesions resulted in a secondary dying back of corticostriatal glutamatergic terminals, but did not produce a change in cortical glutamate concentration. This suggests that reductions in cortical glutamate in HD may reflect a primary loss of glutamatergic neurons. Our findings extend previous observations on amino acid neurotransmitters in HD and, with the exception of taurine, confirm the general applicability of the QA model.

Amino Acids↗
PubMed1987

Morphologic and histochemical characteristics of a spared subset of striatal neurons in Huntington's disease.

We have previously found that a biochemically distinct subset of neurons, containing nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), is selectively resistant to the degenerative process that affects the striatum in Huntington's disease (HD). We report the morphologic and histochemical characteristics of these striatal neurons and their distribution with respect to the histochemical compartments as defined by acetylcholinesterase (AChE) activity. Sections of striatum were stained histochemically for NADPH-d and AChE and immunocytochemically for somatostatin and neuropeptide Y-like immunoreactivity. The diaphorase end-product was contained within medium-sized neurons which corresponded morphologically to a category of aspiny interneurons. Combined techniques showed that NADPH-d, somatostatin, and neuropeptide Y coexisted within the same neurons in controls and patients with HD. The density of these neurons was greater in the ventral putamen and the nucleus accumbens than in the remainder of the striatum. The distinctive AChE pattern of high and low enzyme activity was altered in HD. The AChE-rich matrix zone was markedly reduced in size, while the total area of zones of low enzyme activity was not different from that found in control striatum. The relation between these AChE chemical compartments and the distribution of preserved diaphorase neurons remained intact; NADPH-d neurons were predominantly observed in the matrix zone.

Acetylcholinesterase↗
PubMed1987

Oxytocin in Alzheimer's disease: postmortem brain levels.

Oxytocin (OXY) injected into the hippocampus is reported to interfere with the formation of memory in experimental animals. Memory impairment is one of the distinguishing features of Alzheimer's disease. We have studied OXY immunoreactivity in postmortem brain tissue from 12 cases of histologically confirmed Alzheimer's disease and 13 controls. OXY concentration was increased 33% in the hippocampus and temporal cortex of Alzheimer brains (p less than 0.05), but normal in all other regions examined. Elevated hippocampal OXY levels may contribute to the memory disturbance associated with Alzheimer's disease.

Adult↗
PubMed1987

The autosomal dominant form of "pure" familial spastic paraplegia: clinical findings and linkage analysis of a large pedigree.

We studied 33 affected members in a family with autosomal dominant "pure" familial spastic paraplegia (FSP). Symptoms began in the fourth or fifth decade, expression varied, and progression was slow. We excluded close linkage to the HLA locus (distal end of short arm of chromosome 6); C8 alpha-gamma locus (proximal end of short arm of chromosome 1); PGM1 (middle region of short arm of chromosome 1); and P blood group (location unknown). Although there was no statistically significant linkage between FSP and any of the other markers, lod scores were positive with loci for GC (vitamin D binding globulin) located on chromosome 4 (4q11-q13) and Rh located on chromosome 1 (1p34-p36).

Adolescent↗
PubMed1987

Health promotion and disease prevention beliefs and behaviors of dietetic practitioners.

Fifty-three percent of a random sample of 500 members of the Texas Dietetic Association responded to a survey designed to determine their personal health behavior, beliefs, and patient counseling practices related to health promotion and disease prevention. This article reports the responses of the 180 practitioners involved in direct patient care in order to depict the health promotion/disease prevention beliefs and behaviors of that particular group. Health habits (e.g., smoking, physical activity, and dietary patterns) of dietetic practitioners were better than those of the general female population. Personal health habits related to not smoking and to getting regular exercise were significantly associated with belief in the importance of that behavior for others. Although most of the dietetic practitioners indicated that the identified health behaviors were important to the health of the average person, only a few practitioners gave them routine attention in their practice. Respondents generally expressed a lack of confidence in their ability to educate clients about specified health behaviors, with the exception of weight control, high-fat diets, elevated blood pressure, and exercise patterns. The practitioners' confidence in their counseling skills was significantly correlated with intensity of counseling (p less than or equal to .001) and the likelihood of client compliance, except in the area of weight control. The majority of the dietitians strongly agreed that health promotion will be more important in the future.

Attitude of Health Personnel↗
PubMed1986

Topography of enkephalin, substance P and acetylcholinesterase staining in Huntington's disease striatum.

The distribution of Met-enkephalin (Enk) and substance P (SP) was examined in the striatum of Huntington's disease (HD) patients using immunoperoxidase techniques. Both Enk- and SP-like immunoreactivities (ir) were strikingly diminished in the dorsal caudate nucleus and putamen, while patchy staining persisted in the ventral putamen and nucleus accumbens. This was in sharp contrast to the patch-matrix pattern of acetylcholinesterase (AChE) staining which persisted throughout the entire striatum in HD. The regional loss of Enk- and SP-ir parallels the pattern of neuronal depletion in HD. The disparity between AChE staining and Enk- and SP-ir in HD suggests that AChE-positive neurons or fibers are resistant to the destructive process in areas where intrinsic neuronal populations are depleted.

Acetylcholinesterase↗
PubMed1986

Somatostatin immunoreactivity is reduced in Parkinson's disease dementia with Alzheimer's changes.

Somatostatin-like immunoreactivity (SLI) was measured in postmortem brain tissue from 15 control patients, 7 non-demented parkinsonian patients and 7 demented parkinsonian patients who had Alzheimer-type cortical pathology. The non-demented parkinsonian patients had normal concentrations of SLI in the cerebral cortex, hippocampus, amygdala, putamen, caudate or globus pallidus. Demented parkinsonian patients with Alzheimer-type cortical pathology had significantly reduced (approximately 40%) levels of SLI in both the frontal (Brodmann area 6) and temporal (Brodmann area 21) cortex. These findings suggest that parkinsonian dementia with Alzheimer-type pathology like Alzheimer's disease itself, is associated with reduced concentrations of cortical somatostatin.

Adult↗
PubMed1986

The effect of neuropeptide Y on striatal catecholamines.

Neuropeptide Y and peptide YY were injected into rat striatum and their effects on dopamine, serotonin and their metabolites were examined at 1 h. Neuropeptide Y induced a dose-dependent increase in dopamine turnover in the ipsilateral striatum with no effect on serotonin turnover. When neuropeptide Y was coinjected with somatostatin there was an additive effect in increasing dopamine turnover. There was no alteration in striatal concentrations of gamma-aminobutyric acid, glutamate, or aspartate with either neuropeptide Y or somatostatin injections. These results suggest that neuropeptide Y may play a role with somatostatin in regulating striatal dopaminergic transmission.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

A comparison of regional somatostatin and neuropeptide Y distribution in rat striatum and brain.

Somatostatin-like immunoreactivity (SLI) and neuropeptide Y-like immunoreactivity (NPYLI) were detected using specific radioimmunoassays in extracts from rat brain. Since we have previously found a topographic distribution of SLI in rat striatum the distribution of NPYLI was examined in the same regions. NPYLI showed an identical distribution to SLI in rat striatum and levels were significantly correlated (r = 0.93, P less than 0.01). Concentrations of both neuropeptides were consistently highest in ventromedial striatum and nucleus accumbens while they were lowest in dorsolateral striatum. These findings provide further evidence of neurochemical heterogeneity in the striatum. Concentrations of NPYLI and SLI were also significantly correlated in cerebral cortex (r = 0.99, P less than 0.01). Concentrations of NPYLI were generally higher than SLI and showed a similar predilection for limbic system nuclei. The present findings support the concept that somatostatin and neuropeptide Y may be co-localized in both striatal and cortical neurons.

Animals↗
PubMed1986

Reduced concentrations of arginine vasopressin and MHPG in lumbar CSF of patients with Korsakoff's psychosis.

The concentrations of arginine vasopressin (AVP), somatostatin (SS), and the primary brain metabolites of norepinephrine (MHPG), serotonin (5-HIAA), and dopamine (HVA) were measured in samples of lumbar CSF obtained from ten amnesics with Korsakoff's psychosis, four patients with a history of Korsakoff's psychosis who had recovered from the amnesic symptoms of this disease, and control subjects. Significant deficits were observed in the amnesic group for AVP and MHPG, but not for the other substances measured. Subjects who had recovered from the amnesic symptoms of Korsakoff's psychosis had increased concentrations of AVP and MHPG, but not of SS or the other monoamine metabolites.

Adult↗
PubMed1986

Somatostatin-28(1-12)-like immunoreactivity is reduced in Alzheimer's disease cerebral cortex.

A deficiency in somatostatin is the most consistently described neurochemical alteration in Alzheimer's disease (AD) attributable to intrinsic cortical neurons. Somatostatin-28 (SOM-28), an N-terminal-extended form of somatostatin, can be cleaved to form somatostatin-28(1-12)(SOM-28(1-12) ) and somatostatin-14 (SOM-14). We have measured concentrations of SOM-28(1-12)-like immunoreactivity in 8 cortical regions from 12 patients with AD and 13 controls. Significant reductions (P less than 0.001) were found in all cortical regions examined with the largest decrease in temporal lobe. Reductions were significantly correlated with decreases in somatostatin-14-like immunoreactivity in the same regions. The similar reductions of two prosomatostatin-derived peptides in AD cerebral cortex supports the contention that decreased somatostatin immunoreactivity in AD is caused by a degeneration of somatostatin cortical neurons and terminals.

Aged↗
PubMed1986

An examination of neuropeptide Y postmortem stability in an animal model simulating human autopsy conditions.

A rabbit antiserum to neuropeptide Y (NPY) was used to develop a radioimmunoassay for measuring NPY in brain tissue. By high-performance liquid chromatography, two peaks of immunoreactivity were detected in human postmortem cortex. A minor peak was seen at the void volume, while the majority of immunoreactivity comigrated with synthetic NPY standards. Using the Spokes-Koch rat model simulating human autopsy conditions, it was shown that cortical, hippocampal and striatal concentrations of NPY-like immunoreactivity are stable for up to 24 h.

Animals↗