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Biomedical subjects

F E Bloom

Publications and source records attributed to F E Bloom.

At least 343 records · Page 19Linked to original sources
PubMed1979

Immunocytochemical localization, in synapses, of protein I, an endogenous substrate for protein kinases in mammalian brain.

Protein I is a principal endogenous substrate for cyclic AMP- and Ca2+-dependent protein kinases of mammalian brain. Antibodies raised against purified protein I have been used to localize this protein in the rat central nervous system. At the light microscope level, immunoreactivity was detected in punctate deposits in selected zones of synaptic termination. These deposits varied in density among brain regions. At the electron microscope level, immunoreactivity was observed at some but not all synaptic regions and was restricted to the perimeter of synaptic vesicles and to submembranous material in the postsynaptic neuron.

Animals↗
PubMed1979

Opioid peptides and alpha-melanocyte-stimulating hormone in genetically obese (ob/ob) mice during development.

Compared to littermate controls (C57BL/6J ob/?), body weights of genetically obese (ob/ob) mice are significantly higher at 1-6 months of age; the greatest percentage weight gain of the ob/ob group occurs during the first 3 months of life. Levels of pituitary immunoreactive beta-endorphin and immunoreactive alpha-melanocyte-stimulating hormone are also significantly elevated in ob/ob animals compared to controls. However, these pharmacological differences only emerge at 4-6 months of age--3 months after the appearance of obesity. High levels of immunoreactive endorphin in the pituitary are, therefore, more likely to be a consequence than a cause of obesity. Furthermore, numerous other neurologic abnormalities, which may or may not play a role in the obesity syndrome, are evident in ob/ob mice. Compared to controls, ob/ob total brain, hypothalamus, and pituitary weights are 11%, 16%, and 23% less, respectively. Levels of immunoreactive Leu5-enkephalin in pars nervous are also 200% higher in ob/ob mice; this increase is apparent at 1-6 months of age and is highly correlated with changes in body weight.

Aging↗
PubMed1979

Cyclic nucleotides in central synaptic function.

A wide array of interdisciplinary experiments have served to strengthen the general premise that some central synaptic effects of neurotransmitters may be mediated by cyclic nucleotides. Specific instances of such second messenger mediation are most strongly supported for certain noradrenergic connections of the locus coeruleus (LC) and for dopaminergic connections within the caudate nucleus. In these sites catecholamines selectively activate intraneuronal cyclic AMP synthesis, and exogenously applied cyclic AMP closely mimics the biophysical actions of the catecholamine on target neurons. In cerebellar cortex, iontophoresis of norepinephrine, stimulation of LC, or iontophoresis of cyclic AMP lead to hyperpolarization and increased membrane resistance. Although overtly inhibitory when examined in isolation, the effects of the LC system coupled to adenylate cyclase can initiate a holistic set of target cell responses which can enhance or "enable" the actions of other synaptic inputs to the target cells. Electrophysiologic and immunocytochemical evidence suggests that this heterosynaptic interaction may arise from phosphorylation of the synaptic membrane substrate of cyclic AMP-dependent protein kinase, or Protein 1.

Acetylcholine↗
PubMed1978

Changes in posterior hypothalamic self-stimulation following experimental cerebral infarction in the rat.

Bioplar stimulating electrodes were placed bilaterally in the posterior hypothalamus of rats following which the animals were shaped for intracranial self-stimulation (ICSS). When ICSS rates were stable for 1 wk, the right middle cerebral artery was ligated. During the 25-day postinfarction period, the rate of ICSS at specified current values was compared with preoperative rates. At 2 days after operation, there was a 33% decrease in the maximum frequency of ipsilateral ICSS. However, by 8 days after experimental stroke, there was a 16% increase in the maximal rate of ICSS above the preoperative value, and the rate returned to control levels by 20 days after surgery. The minimum current necessary to elicit the maximal rate of response also changed in a biphasic manner, i.e., the minimum required current was greater than preoperative control levels until 8 days after operation but then dropped below control level until 20 days postoperatively. There were no changes in the current or rate of response in the contralateral electrode. These results are discussed in relation to what may be the underlying neurophysiological changes causing these biphasic alterations in ICSS.

Animals↗
PubMed1978

beta-Endorphin induces nonconvulsive limbic seizures.

The endogenous opioid peptide, beta-endorphin, induces nonconvulsive limbic epileptiform activity when administered intraventricularly to rats. Epileptiform activity is elicited by beta-endorphin in doses that are devoid of analgesic or behavioral signs. Equimolar intraventricular doses of morphine or of the enkephalin analog [DAIa2,Met5]enkephalin-NH2 fail to elicit this limbic epileptiform activity. These observations, together with the recent immunohistochemical localization of beta-endorphin to midline limbic structures, suggest that beta-endorphin may have an important role in the regulation of limbic excitability.

Animals↗
PubMed1978

In vitro release of [5-methionine]enkephalin and [5-leucine]-enkephalin from the rat globus pallidus.

Endogenous [5-methionine]enkephalin (Metenkephalin) and [5-leucine]enkephalin (Leu-enkephalin) are released from perfused slices of rat globus pallidus by increased K(+) in a Ca(2+)-dependent manner. Tissue perfused for 40 min contained only 26% of the Met-enkephalin and 44% of the Leu-enkephalin found in the freshly dissected tissue. After perfusion, the mean (+/-SEM) ratio (wt/wt) of Met-enkephalin to Leu-enkephalin was 3.4 +/- 0.2 compared with 5.8 +/- 0.2 in the fresh tissue. The degradation of trace amounts of synthetic [(3)H]enkephalins in the perfusing medium during stimulated release seems to reflect the accelerated degradation of enkephalin released from the tissue: 63% of the Met-enkephalin and 23% of the Leu-enkephalin were degraded in a medium containing bacitracin (30 mug/ml). The mean ratio (wt/wt) of the Met-enkephalin to the Leu-enkephalin recovered after release by exposure of slices to 50 mM K(+) was 2.7 +/- 0.3. When perfusates were corrected for degradation, this ratio increased to about 5.5 which is higher than that found in the perfused tissue. The differences in release, tissue loss, and catabolism of the two enkephalins may be reflecting differences in the metabolic systems operating on the pentapeptides, but this interpretation will have to be validated by in vivo release experiments. In any event these observations strongly suggest that both enkephalins can be considered candidate neurotransmitters in the rat globus pallidus.

Animals↗
PubMed1977

A fluorescent histochemical study of changes in noradrenergic neurons following experimental cerebral infarction in the rat.

Following surgical ligation of the middle cerebral artery in the rat, central catecholamine containing neurons were studied using the glyoxylic acid histochemical technique. By 5 days after the ischemic lesion, the density of fluorescent varicosities decreased in both uninjured cerebral cortex and the cerebellar cortex and the intensity of fluorescence of somata in the ipsilateral and contralateral locus coeruleus decreased as compared with controls. At 20 days afer lesioning, catecholamine containing neurons looked normal under fluorescence microscopic examination, except fine varicose fluorescent axons were present for the first time among the cellular debris of the lesion and appeared to have sprouted into the lesion site. However, by 40 days after surgery, there was a marked increase in the density of fluorescent varicosities in the uninjured ipsilateral cerebral cortex, in the contralateral cerebral cortex, and in the cerebellum. These observations confirm the view that an ischemic cortical lesion can lead to profound changes in cetecholamine containing neurons in distant areas of the brain which are uninjured by the local infarction.

Animals↗