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Biomedical subjects

E Melamed

Publications and source records attributed to E Melamed.

At least 235 records · Page 13Linked to original sources
PubMed1980

Circling behavior in rats with partial, unilateral nigro-striatal lesions: effect of amphetamine, apomorphine, and DOPA.

Partial, unilateral lesions of the nigro-striatal tract were produced in rats by injecting various quantities of 6-hydroxydopamine into the substantia nigra. The extent of each animal's lesion was estimated by comparing tyrosine hydroxylase activities in its lesioned and control striata. L-DOPA and apomorphine induced contralateral (i.e., away from the lesion) circling behavior only in rats in which more than 90% of the nigro-striatal system had been destroyed. In contrast, d-amphetamine caused turning in the ipsilateral direction when as few as 50% of the nigro-striatal neurons had been destroyed.

Amphetamine↗
PubMed1980

The synthesis of prostaglandins by bovine cerebral microvessels.

Bovine cerebral microvessels (arterioles and capillaries) synthesize prostacyclin (PGI2, measured as 6-keto PGF1 alpha), PGF2 alpha, PGE2 and thromboxane A2 (measured as TXB2) when incubated in glucose-bicarbonate buffer for 30 minutes. Rapid freezing and thawing decreased the subsequent synthesis of 6-keto PGF1 alpha by cerebral microvessels and raised the basal levels of this metabolite within the incubation medium. At low concentrations, the addition of arachidonic acid (0.16 microM) did not stimulate prostacyclin or prostaglandin production; at higher concentrations (16 microM), the synthesis of PGI2 and PGF2 alpha was inhibited. Activation of lipase by the peptide melittin stimulated the synthesis of all arachidonic acid metabolites to the same extent. Thus cerebral microvessels deacylate cellular lipids and metabolize endogenous arachidonic acid to form prostaglandins, prostacyclin and related compounds as previously demonstrated in larger blood vessels. The synthesis and release of these molecules may be important for modulating the tone and reactivity of small blood vessels within the brain.

Animals↗
PubMed1980

Tyrosine administration increases striatal dopamine release in rats with partial nigrostriatal lesions.

Partial, unilateral nigrostriatal lesions of varying severity were produced in rats by injecting graded doses of 6-hydroxydopamine into the substantia nigra. Formation of the dopamine metabolites dihydroxyphenylacetic acid and homovanillic acid in each surviving nigrostriatal neuron (estimated by the ratios of dihydroxyphenylacetic acid to dopamine and homovanillic acid to dopamine in the striatum) increased significantly when dopamine concentrations in striata containing lesions had been reduced to 25% or less of control values, but remained unchanged in rats with less severe lesions. These findings suggest that, in rats with severe damage of nigrostriatal dopaminergic neurons, surviving neurons increase their firing rates and accelerate dopamine synthesis and release. In rats that had lesions and enhanced striatal dopamine release, but not in rats with lesser lesions (i.e., which reduced ipsilateral dopamine concentrations by less than 75%), administration of tyrosine (250 mg/kg) caused further significant increases in formation of dihydroxyphenylacetic acid and homovanillic acid. These findings provide further evidence that tyrosine availability can enhance dopamine synthesis in and release from nigrostriatal neurons if the firing rates of these neurons are accelerated.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1980

Precursor control of neurotransmitter synthesis.

Studies performed during the past decade have shown that the rates at which certain neurons produce and release their neurotransmitters can be affected by precursor availability, and thus by the changes in plasma composition that occur after ingestion of the precursors in purified form or as constituents of foods. Thus, tryptophan administration or a plasma ratio of tryptophan to other large neutral amino acids, thereby raising brain tryptophan levels, increasing the substrate saturation of tryptophan hydroxylase, and accelerating the synthesis and release of serotonin. Tyrosine administration or a high-protein meal similarly elevates brain tyrosine and can accelerate catecholamine synthesis in the CNS and sympathoadrenal cells, while the consumption of lecithin or choline increases brain choline levels and neuronal acetylcholine synthesis. The physiologic and biochemical mechanisms that must exist in order for nutrient consumption to affect neurotransmitte synthesis have been characterized and include: 1) the lack of significant feedback control of plasma levels of the precursor; 2) the lack of a real "bloodbrain barrier" for the precursor, i.e. the ability of the plasma level of the precursor to control its influx into, or efflux from, the CNS; 3) the existence of a low-affinity (and thus unsaturated) transport system mediating the flux of the precursor between blood and brain; 4) low-affinity kinetics for the enzyme that initiates the conversion of the precursor to the transmitter; and, 5) the lack of end-product inhibition of the enzyme, in vivo, by its ultimate product, the neurotransmitter. The extent to which neurotransmitter synthesis in any particular aminergic neuron happens to be affected by changes in the availability of its precursor probably varies directly with the neuron's firing frequency. This relationship allows precursor administration to produce selective physiologic effects by enhancing neurotransmitter release from some but not all of the neurons potentially capable of utilizing the precursor for this purpose. It also allows the investigator to predict when administering the precursor might be useful for amplifying a physiologic process, or for treating a pathologic state. (for example, tyrosine administration raises blood pressure in hypotensive rats, lowers it in hypertensive animals, and has little effect on blood pressure in normotensive animals; the elevation in blood pressure probably reflects enhanced catecholamine release from sympathoadrenal cells, while the reduction in hypertensive animals probably results from increased catecholamine release within the brain-stem.) Such predictions are now being tested clinically in many institution. Available evidence suggests that lecithin or cholie administration can diminish the frequency of abnormal movements in patients with tardive dyskinesia...

Behavior↗
PubMed1979

Neurotransmitters and the fifth cranial nerve: is there a relation to the headache phase of migraine?

The headache phase of migraine may develop as the result of an abnormal interaction (and perhaps an abnormal release) of vasoactive neurotransmitters from terminals of the trigeminal nerve with large intracranial and extracranial blood-vessels. These blood-vessels, which dilate during the headache phase of migraine, are thought to receive axonal projections from all three divisions of the trigeminal nerve. Substance P, a potent vasodilating peptide, seems to be released from trigeminal nerve endings in response to nervous stimulation and is involved in the transmission of painful stimuli within the periphery. The vasoactive molecule serotonin, implicated in the pathogenesis of migraine, coexists with substance P in some terminals of the central nervous system and is present within the trigeminal ganglia. Within this nerve serotonin may modulate the function of primary sensory neurons. The abnormal release of substance P or as yet unidentified peptides or other transmitters from the fifth cranial nerve may explain both the hemicranial pain and the vasodilation which are characteristic of the headache of migraine.

Cerebrovascular Circulation↗
PubMed1979

Early-morning dystonia. A late side effect of long-term levodopa therapy in Parkinson's disease.

Four women with Parkinson's disease undergoing prolonged levodopa therapy had daily episodes of dystonic posturing, affecting one lower extremity, several years after initiation of treatment. The dystonia occurred only in the early morning, on awakening and before the first dose of levodopa, when the patients were in the akinetic-rigid state with no dyskinesias. It further interfered with gait, slowly subsided within one to two hours, and did not recur until next morning. This abnormal involuntary posture was unaffected by manipulations of daily levodopa dosage and schedule, completely disappeared after withdrawal of drug therapy, and recurred following its readministration. Additional adverse reactions including dyskinesias, "on-off" phenomena, and declining efficacy of levodopa were present in all patients. Early-morning dystonia may represent another late side effect secondary to long-term levodopa administration in parkinsonism.

Adult↗
PubMed1979

Regional cerebral blood flow in patients with Parkinson's disease.

Regional cerebral blood flow (rCBF) was measured by the xenon 133 inhalation method in 60 patients with Parkinson's disease and compared with flow data obtained in 51 age-matched normal control subjects. Mean brain rCBF was significantly reduced in patients with parkinsonism (9.5%, P less than .001). The most marked and significant rCBF decreases were observed in the older patients (18.8%, P less than .001). There was no correlation between degree of rCBF reduction and duration of parkinsonism. Decreases in hemispheric mean rCBF values were similar in both hemispheres even in patients with unilateral signs. The present study provides additional evidence for involvement of the cerebral cortex in Parkinson's disease. The rCBF decline may be associated in part with high prevalence of mental impairment and cortical atrophy and with diminished cerebral metabolic rate due to brain dopamine deficiency in patients with parkinsonism.

Adult↗
PubMed1979

Cortical activation pattern during saccadic eye movements in humans: localization by focal cerebral blood flow increases.

Regional cerebral blood flow (rCBF) was measured in human subjects during saccadic eye movements by a 254-channel dynamic gamma camera. Focal rCBF increases were repeatedly observed in an area within the middle precentral and premotor regions which corresponds to the frontal eye field in humans. Our findings suggest that this region is localized between the "face" and "hand" areas in the precentral gyrus and extends anteriorly out of the primary motor strip into the adjacent premotor zone. In addition, saccades were associated with focal blood flow increases in regions corresponding to the frontal supplementary motor area and to the posterior temporooccipital visual association cortex. Similar changes in patterns of rCBF occurred during contralateral and ipsilateral horizontal saccades and also during vertical saccades, and did not differ between the right and left hemispheres. Focal rCBF increases were observed in the frontal eye field during several additional test procedures including ocular fixation and visual perception of a nonmoving target, auditory stimulation with closed eyes, and reading. It is presumed that these focal flow increases reflect increased localized neuronal activity and metabolic rate and therefore permit visualization of the cortical activation pattern associated with saccadic eye movements in humans.

Cerebral Cortex↗
PubMed1979

Hyperparathyroidism presenting with unusual neurological features.

A case of hyperparathyroidism, who presented with unusual complex neurological symptomatology is reported. Mental confusion, asterixis and elevated cerebrospinal fluid protein with marked pleocytosis dominated the neurological picture. All these findings subsided upon correction of hypercalcemia, suggesting direct relationship between cerebrospinal fluid abnormalities, asterixis and this metabolic disturbance.

Adenoma↗
PubMed1978

Direct mapping of beta-adrenergic receptors in the rat central nervous system by a novel fluorescent beta-blocker.

DL-N-(2-Hydroxy-3-napthyloxypropyl)-N'-dansylethylenediamine, dansyl analogue of propranolol (DAPN) is a novel fluorescent beta-adrenergic antagonist with high affinity to beta-receptors. The distribution pattern of DAPN fluorescence was studied in the rat central nervous system subsequent to its intravenous administration to living rats. DAPN distinctly labels specific regions and cells in the central nervous system (CNS). Highly dense DAPN fluorescence was observed in the pyramidal cell layer of the hippocampus, the granule cell layer of the dentate gyrus, the basal layers of the piriform cortex and the neocortex, the cerebellar Purkinje cell layer, and the spinal a-motoneurons. Pretreatment of control rats with DL-and L-propranolol markedly decreased the intensity and density of DAPN fluorescence in the tissue sections, whereas prior administration of D-propranolol had almost no effect. Pretreatment with large doses of reserpine did not alter the pattern of DAPN fluorescence. These findings were identical to those observed with another fluorescent beta-blocker, 9-aminoacridino-propranolol (9-AAP). Our data suggest that fluorescent beta-adrenergic antagonists may be used in vivo for the direct probing of the beta-receptors within the mammalian CNS.

Animals↗
PubMed1978

Bihemispheric decreases of regional cerebral blood flow in dementia: correlation with age-matched normal controls.

Regional cerebral blood flow (rCBF) was measured by the xenon 133 inhalation method in 20 patients with senile and presenile dementia, and values were compared with flow data obtained in a series of 44 age-matched normal controls. The rCBF was reduced in patients with both presenile and senile dementia, and the degree of decrease exceeded the age-related rCBF decline in normal subjects. Similar rCBF reductions were observed in the left and right cerebral hemispheres and in general were homogeneously distributed in the various areas. The rCBF reductions in normal aging and in dementia may be associated with similar underlying cerebral morphological changes. Our findings suggest that the greater rCBF decreases in dementia compared with the values in age-matched controls may quantitatively reflect more severe pathological alterations in the brains of patients with intellectual deterioration.

Adult↗