Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to comprehensively evaluate pathological involvement of the locus coeruleus (LC) and cortically projecting raphe nuclei in Alzheimer's disease (AD), we have recently completed a study (Zweig, et al., 1988) in which numbers of neurons containing neuromelanin within the LC and large nucleolus-containing neurons within the dorsal raphe nucleus (DR) and the central superior (raphe) nucleus (CSN) were determined in 25 cases of AD and 12 age-matched controls. Numbers of neurofibrillary tangles (NFTs) within these regions were also counted. Pathological results were compared with clinical data, including psychiatric evaluations, available for 21 of the AD cases. Neuronal loss in AD cases was most severe within LC at mid level (p less than .01) and within DR, caudally (p less than .05). Counts of NFTs within LC were also highest at mid level (p less than .05) in comparison with caudal level). Neuronal loss was not demonstrated within CSN, although NFTs were abundant within this nucleus. At individual levels, neuronal and NFT counts did not correlate. Relative severity of neuronal loss or NFTs was usually consistent from level to level within nuclei; internuclear correlations were weaker. Cases of AD complicated by depression had significantly fewer neurons at mid LC and rostral CSN levels than nondepressed cases (p less than .05). There was also a trend (nonsignificant) suggesting increased neuronal loss at all levels of LC and DR in depressed cases. Neuronal loss correlated negatively with age, particularly within LC. NFT counts correlated negatively with duration of illness, particularly within DR. As all but 3 individuals had severe dementia, NFT counts may reflect rate of progression of disease. Neuronal loss and NFTs frequently occur in the LC and cortically projecting raphe nuclei in AD (Curcio and Kemper, 1984, Hirano and Zimmermann, 1962, Ishii, 1966, Marcynuik et al., 1986, Yamamoto and Hirano, 1985, Bondareff and Mountjoy, 1986, Iverson et al., 1983, Mann et al., 1985, Tabaton et al., 1986). We have recently completed a comprehensive evaluation of pathological involvement of the LC, the DR, and the CSN in a series of aged controls and AD patients for whom detailed clinical information, including psychiatric evaluations, were available (Zweig et al., 1988). This report summarizes the findings of that study.
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PMID:Neuropathology of aminergic nuclei in Alzheimer's disease. 260 23

Neuronal responses of the rat somatosensory cortex grafted into damaged host barrel field to electrical stimulation of the host brain were investigated extracellularly in rats under light pentobarbital anaesthesia. The following structures of the host brain were stimulated: ventrobasal complex and posterior thalamic nuclei, ipsilateral area of vibrissae representation in the sensorimotor cortex and contralateral barrel field. Reactivity of the grafted neurones was lower, than in the intact barrel field, but the mean latencies of responses were not significantly different. Stimulation of the thalamic nuclei was more effective than that of the cortical areas both in grafted and intact barrel fields. Posttetanic depression after repetitive stimulation was often observed in the grafts, while posttetanic potentiation was more usual for the intact barrel field. The data show the sources of some functional afferent inputs to the grafts which may be responsible for neuronal reactions to somatosensory stimulation of the host animal.
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PMID:[Neuronal responses of the rate somatosensory cortex transplanted into the vibrissae representation field of the neocortex to the electrical stimulation of the recipient brain]. 324 21

Six cases of adult dementia with mesolimbic pathology are reported. The core clinical syndrome consists of parkinsonism, progressive dementia, and behavioral disturbances (generally depression). The histopathologic findings uniformly include a loss of pigmented neurons in the ventral tegmental area plus neurofibrillary tangles and/or cell loss in the entorhinal cortex and pyramidal cell layer of the hippocampus (perforant pathway). Neuronal depletion in the ventral tegmental area frequently is associated with similar cell loss in the adjacent substantia nigra and in the locus ceruleus. The development of neurofibrillary tangles in the perforant pathway occurs in the absence of senile plaques and is possibly related to diminished dopaminergic input.
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PMID:The association of ventral tegmental area histopathology with adult dementia. 335 99

Neuronal ceroidosis was observed in an 18-month-old male Blue Heeler dog which was euthanized after showing a progressive gait and behavior abnormality, depression, paresthesia, and vision deterioration. The brain was slightly atrophic. Histopathology revealed autofluorescent, periodic acid-Schiff, luxol fast blue, and oil red O-positive intracytoplasmic granules in the neurons of the brain and spinal cord. There was a moderate diffuse reduction in the number of cerebellar and cerebrocortical neurons. Ultrastructurally, these neuronal cytosomes were diverse with preponderance of membranous profiles and granular matrix.
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PMID:Neuronal ceroidosis (ceroid-lipofuscinosis) in a Blue Heeler dog. 396 93

1. An electrophysiological analysis has been made of the uptake of NAd in the sympathetic nerve terminals of the isolated vas deferens of the mouse. The amplitude of the excitatory junction potentials (e.j.p.s) recorded intracellularly in smooth muscle cells was taken as a measure of the NAd output per impulse from the terminals of sympathetic axons.2. Neuronal uptake blockers (desipramine and cocaine) greatly depressed the amplitude of all e.j.p.s after the first in a short train (< 100) at high frequencies (>/= 1 Hz).3. Blocking neuronal uptake did not affect the time course of decline in amplitude of the e.j.p. during long trains of stimulation over several minutes, apart from the immediate depression in the e.j.p. following the first few impulses.4. The time course of decline of the e.j.p. amplitude during continual stimulation, when both neuronal uptake and synthesis was blocked, was similar to that when only synthesis was blocked, apart from the immediate depression following the first few impulses.5. Phenoxybenzamine reversed the normal depression in e.j.p. amplitude observed at high frequencies (>/= 1 Hz) to facilitation. This facilitation lasted for several minutes of high frequency stimulation.6. A model has been proposed of the sympathetic nerve terminal, in which NAd is released by each nerve impulse in a train from a small pool in the nerve terminal, which is principally replenished by uptake of the NAd released by the immediately preceding impulses in the train. The pool is replenished to a less extent by transmitter located in two stores in the terminal which are in turn replenished by transmitter synthesis.
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PMID:An electrophysiological analysis of the uptake of noradrenaline at sympathetic nerve terminals. 472 36

Cellular effects of ethanol were investigated in the rat neostriatum with local perfusion and extracellular, single unit recording techniques. Neuronal activity was modulated specifically as a function of ethanol concentration over a wide test range. At extremely low doses (10(-9) and 10(-8) M), the neuronal responses to drug perfusion were exclusively excitatory. However, at the highest doses examined (10(-8) and 10(-4) M), the results were reversed. In the midrange, a number of apparently ineffective tests were obtained, along with bimodal (excitation followed by depression) responses. The unequivocal responsiveness to ethanol at very low concentrations raises the possibility of a physiological role for the endogenous substance.
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PMID:Ethanol effects on striatal neuron activity. 633 Dec 15

The depressant effects of iontophoretically applied dopamine and noradrenaline on glutamate-induced neuronal firing in the amygdaloid complex of cats were significantly reduced 1 and 2 h after induction of a local epileptiform afterdischarge of the kind used in kindling. Neuronal excitation by glutamate and depression by GABA were not significantly changed. This suggests that kindling is associated with a reduction of the inhibitory effects of endogenous catecholamines.
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PMID:Decreased sensitivity of neurons in the basolateral amygdala to dopamine and noradrenaline iontophoresis after a kindling stimulus. 669 Mar 20

Physiological investigations have indicated that the ventrolateral surface of the medulla oblongata is involved in the chemical drive to respiration. In this investigation, light and electron microscopic investigations of the 3 chemosensitive regions reveal the following. (1) Evaginations of the ventral surface abut the overlying pia mater thereby delimiting discrete compartments; invaginations of the surface delimit wide cisternae lined with basement membrane. Neuronal elements with numerous synapses, were found scattered among astrocytic processes of the marginal glia in intermediate and caudal chemosensitive areas Microvasculature are conspicuously absent from the marginal glia. Intramedullary vessels are surrounded by perivascular spaces and the endothelium shows zonulae occludentes at cell junctions. (2) Horseradish peroxidase (HRP) applied to the ventral surface diffused throughout the interstitial and perivascular compartments, into synaptic clefts and neuronal soma. Diffusion of HRP into blood vessels was blocked at zonulae occludentes. Following intravenous injection of HRP, no reaction product was found outside cerebral vasculature in chemosensitive areas. (3) In spontaneously breathing cats, 2% procaine applied to the caudal chemosensitive area resulted in respiratory depression which began with the second breath. It is proposed, that substances which stimulate or depress respiration, when applied to the ventral medullary surface, produce their effects on superficial neurons located in the intermediate and caudal chemosensitive areas after diffusion through interstitial spaces.
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PMID:Morphological observations on superficial medullary CO2--chemosensitive areas. 681 54

Cognitive disorders associated with HIV infection may be due to focal lesions (lymphoma, toxoplasmosis, progressive multifocal leukoencephalitis, etc.), metabolic encephalopathy (e.g. hepatic insufficiency) or psychiatric disorders (depression). In the absence of such causes a "cognitive and motor syndrome associated with HIV infection" has been defined on clinical criteria (Working group of the American Academy of Neurology, 1991). This syndrome is not consistently associated with any specific lesion. Neither the multifocal encephalitis of HIV or CMV infection nor the diffuse leukoencephalopathy associated with HIV are the only causes. The existence of a neocortical neuronal loss has been suggested by several retrospective studies, but our prospective study has not shown cortical or subcortical atrophy. Measurement of neuronal density in Brodmann's areas 4,9 and 40 has not revealed a significant loss either global, by layer, or by column. The only constant lesion was gliosis of the cortex and white matter. Neuronal loss, therefore, is not indispensable to the occurrence of cognitive disorders in AIDS. The mechanism of dementia might be: dysfunction of cortical neurons (dendritic abnormalities, virus/neurotransmitter competition); subcortical dysfunction, as suggested by the high density of microglial nodules in that region; white matter lesions which could be due to abnormalities in the blood-brain barrier. The expression of cell adhesion molecules (VCAM-1, VLA-4, ICAM-1 and LFA-1) by endothelial cerebral cells is not significantly different in AIDS patients, demented or not, and in patients with multiple sclerosis. In contrast, the expression of VCAM-1 by astrocytes is significantly increased in demented AIDS patients compared with non demented ones.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[HIV and dementia: neuropathology]. 747 30

The effect of repeated episodes of asphyxia on the fetal cardiovascular system and CNS was examined. The umbilical cord was occluded for 5 min, four times, at 30-min intervals in 11 chronically instrumented fetal sheep (118-126 d). Fetal electrocorticogram (ECoG), cortical impedance, ECG, heart rate, and blood pressure were continuously recorded for 3 d, after which neuronal loss was determined histologically. Each occlusion resulted in fetal hypoxemia and bradycardia accompanied by increased T/QRS ratio. Progressively severe hypotension and lactic acidosis developed during successive occlusions. The ECoG was depressed and cortical impedance increased with each occlusion. During the final occlusion, blood pressure fell to 3.5 +/- 1 kPa and heart rate to 93 +/- 9 bpm, T/QRS ratio increased to 0.44 +/- 0.3, and lactate rose to 7.2 +/- 1.2 mM/L. Three animals died from cardiac fibrillation during recirculation after the third or fourth occlusion. After the asphyxial episodes, blood pressure and heart rate returned to normal, and the T wave was inverted for 310 +/- 155 min. Lactate returned to baseline within 24 h. The ECoG remained depressed for 90 +/- 35 min, and intermittent seizures developed at 3.3 +/- 1.4 h after the last occlusion. Neuronal loss was primarily found in the striatum. The extent of neuronal loss correlated with the degree of hypotension, increase in T/QRS ratio, duration of postasphyxial ECoG depression, and number of seizures. These results indicate that transient asphyxial episodes compromise the ability of the heart to tolerate additional insults and further suggest that neuronal loss is a consequence of cardiovascular compromise secondary to asphyxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Repeated episodes of umbilical cord occlusion in fetal sheep lead to preferential damage to the striatum and sensitize the heart to further insults. 765 53


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