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Biomedical subjects

W J Freed

Publications and source records attributed to W J Freed.

At least 163 records · Page 9Linked to original sources
PubMed1979

Calcitonin: inhibitory effect on eating in rats.

Subcutaneous and intracerebral injections of calcitonin inhibited feeding in rats. The anorectic activity of calcitonin was destroyed by exposing the hormone to heat, trypsin, or hydrogen peroxide. Calcitonin did not produce a conditioned taste aversion to saccharin, and maximum inhibition of feeding occurred 4.5 to 8.3 hours after subcutaneous administration. It is concluded that calcitonin inhibits feeding by acting directly on the central nervous system.

Animals↗
PubMed1979

Brain grafts reduce motor abnormalities produced by destruction of nigrostriatal dopamine system.

In order to determine if brain tissue grafts can provide functional input to recipient central nervous system tissue, fetal rat dopamine-containg neurons were implanted adjacent to the caudate nucleus of adult recipients whose endogenous dopaminergic input had been destroyed. The grafts showed good survival and axonal outgrowth. Motor abnormalities, which had been induced by the destruction of the endogenous dopaminergic input to the caudate, were significantly reduced after grafting of the fetal brain tissue. These data suggest that such implants may be potentially useful in reversing deficits after circumscribed destruction of brain tissue.

Animals↗
PubMed1979

Anticonvulsant properties of betaine.

It has been shown previously that convulsions induced by homocysteine are blocked by betaine. In the present study, betaine was found to block the induction of convulsions by electroconvulsive shock and by pentylenetetrazol at least at effectively as it blocked convulsions induced by homocysteine. Thus, betaine has a general anticonvulsant action, the reason for which is unknown.

Animals↗
PubMed1978

Glutamic acid and ethanol dependence.

Glutamate diethyl ester, a specific glutamate antagonist, attenuated the seizures and decreases in behavioral activity that were observed in mice during withdrawal. Prior to withdrawal, ethanol-dependent animals were supersensitive to kainic acid, a potent glutamate agonist, but they were not supersensitive to the convulsant drug pentylenetetrazol. These findings suggest that supersensitivity to glutamate develops during ethanol dependence, and that this phenomenon contributes to the signs of ethanol withdrawl.

Alcoholism↗
PubMed1977

Water-intake volume regulation in the rat: schedule-induced drinking compared with water-deprivation-induced drinking.

Hungry rats drink extremely large amounts of water when they are intermittently fed small amount of food (schedule-induced polydipsia). Are such animals motivated to drink for long durations, to ingest large amounts of fluid, or to do both? When drinking-tube apertures were decreased to slow the rate of water ingestion, each of eight rats spent more time drinking (M = 11.5 min) than when larger apertures were used (M = 7.8 min). The mean volumes ingested were not different. These equal volumes were generated by adjustment of each drink duration in accordance with ingestion rate even during the first few drinks of the sessioons, even when the drinking tubes were frequently switched (every 1-3 min) during the sessions. During drinking induced by water deprivation when food was concurrently available, restriction of the driking-tube apertures reduced intake volumes by 18%-19%. However, when food was not concurrently available during water-deprivation-induced driking, regulation of intake volumes was comparable with that found during schedule-induced polydipsia. These data pose difficulties for theories that ascribe a crucial role to the motor aspects of schedule-induced drinking.

Animals↗
PubMed1976

Effects of intraventricular glutamic acid on the acquisition, performance, and extinction of an operant response, and on general activity.

This study was designed to investigate the effects of intracerebral injections of glutamic acid on acquisition and extinction of a bar-press response, performance of that response, and behavior activity. Nineteen food-deprived rats bearing chronic ventricular cannulae were tested in operant conditioning chambers or in an open field. Just prior to each testing session each animal was injected intraventricularly with 10 mul of either normal or acidified saline solution (control groups), or 10 mul of 100 mMol glutamic acid solution. Acquisition of the bar-pressing response by the glutamic acid group was significantly retarded as compared to the control groups, and the responding of the glutamic acid group was suppressed during the beginning of the first few sessions of testing on a fixed-interval schedule and during extinction. Other behavioral measures, such as operant level, performance of the response on a continuous schedule, performance on fixed-interval and extinction schedules except during the start of the first few sessions, and behavioral activity, were either unaffected or only slightly affected. It is concluded that interference with the normal neurophysiological activity of glutamic acid in the central nervous system interferes with learning and suppresses behavioral output in certain situations.

Animals↗
PubMed1976

Effects of intracisternal GABA or glutamic acid upon behavioral activity in the rat.

It has been postulated that GABA acts as an inhibitor of command neurons, the activity of which initiates behavior. A prediction of this hypothesis is that elevations in functional GABA levels in the brain will cause decreases in behavioral output. Accordingly, in this study rats were injected intracisternally with either saline or one micromole of GABA or its excitatory precursor, glutamic acid, and behavioral activity in a novel environment was recorded as it habituated over the course of the subsequent 4 hours. The activity of the animals that were injected with GABA was greatly decreased, while the activity of the animals that were injected with glutamic acid was apparently unaffected, as compared to animals given saline. These data provide support for the hypothesis that GABA functions as an inhibitory neurotransmitter for behavior-activating command neurons.

Aminobutyrates↗
PubMedDate not supplied

In vitro properties of a newly established medulloblastoma cell line, MCD-1.

Medulloblastomas are poorly differentiated brain tumors believed to arise from primitive pleuripotential stem cells, and tend to express mixed neuronal and glial properties. In the present study, we examined immunohistochemical and neurotransmitter phenotypic properties in a newly established medulloblastoma cell line, MCD-1. MCD-1 cells were immortal, not contact-inhibited, but did not grow in soft agar. Immunohistochemical studies showed positive staining for neurofilament protein (NF), neuron-specific enolase (NSE), synaptophysin, MAP 2, tau, NCAM 180, vimentin, and S-100 protein. The cells expressed specific uptake of glutamate, serotonin, and choline, but not GABA or dopamine. A significant increase in process extension was seen in response to agents that enhance intracellular cyclic AMP, especially 3-isobutyl-1-methylxanthine (IBMX). Process formation induced by IBMX was associated with a decrease in cell proliferation as evidenced by a reduction in numbers of cells incorporating 5-bromo-2-deoxyuridine (BrdU). No increase in process extension was observed following exposure to NGF or retinoic acid. MCD-1 cells were shown to produce transforming growth factor beta (TGF beta), and were immunopositive for mutant p53. Transfection assays with the PG13-Luc reporter plasmid, which contains a p53-responsive enhancer element and a luciferase reporter gene, suggested MCD-1 cells are deficient in wild-type p53 and do not activate p53 on treatment with the anticancer agent adriamycin. The MCD-1 cell line is suggested to represent an abnormally differentiated cell type, which has some properties consistent with a multipotent neuronal phenotype while retaining some properties of immature cells of a glial lineage. The MCD-1 cell line can be used to provide a model of a medulloblastoma cell line that is resistant to growth-controlling and anticancer agents.

1-Methyl-3-isobutylxanthine↗
PubMedDate not supplied

The role of nerve-growth factor (NGF) in the central nervous system.

NGF is a protein that stimulates growth and differentiation of sympathetic and sensory components of the peripheral nervous system. The purpose of this review is to examine the evidence that NGF has similar activity in the central nervous system. First, the primary mode of interaction of NGF with the nerve cell will be discussed, and the possibility that such an interaction takes place in the brain will be examined. Recent studies have demonstrated that NGF promotes regenerative sprouting of damaged catecholamine-containing neurons in the brain. The next part of the paper reviews this literature, and other findings that indicate or contraindicate a role of NGF in brain maturation of maintenance. The final part of this paper suggests specific avenues for future research in this area, and presents conclusions regarding the literatureon brain activity of NGF to date.

Animals↗