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Biomedical subjects

F E Bloom

Publications and source records attributed to F E Bloom.

At least 325 records · Page 18Linked to original sources
PubMed1980

Locomotor activation induced by infusion of endorphins into the ventral tegmental area: evidence for opiate-dopamine interactions.

beta-Endorphin in nanomole quantities produced a stimulation of locomotor activity when infused into the region of the dopamine cell bodies of the ventral tegmental area (VTA) in rats. alpha-, gamma-, and des-Tyr-gamma-endorphin produced similar effects, but the D-alanine analogues of alpha and gamma-endorphin produced a larger and longer-lasting activation, presumably reflecting their resistance to degradation. This locomotor activation was reversible by pretreatment with naloxone and by destruction of the terminal projections of the mesocorticolimbic dopamine system originating in the VTA. These results demonstrate that locally infused endorphin can interact with the opioid receptors in the VTA, and they suggest a means by which endorphins activate limbic excitability.

Animals↗
PubMed1980

Impulse activity of locus coeruleus neurons in awake rats and monkeys is a function of sensory stimulation and arousal.

By means of extracellular recordings, individual norepinephrine-containing neurons in the locus coeruleus of unanesthetized behaviorally responsive rats and squirrel monkeys were found to respond to specific sensory and behavioral conditions. In rats, distinct clusters of action potentials followed the presentation of various nonnoxious auditory, visual, or somatosensory stimuli at latencies of 15-60 msec. Increased discharge rates were also seen during periods of spontaneous electroencephalogram arousal in both species. In monkeys, these cells responded most vigorously to complex arousing stimuli such as a preferred food. Because the noradrenergic innervation of most forebrain regions arises from the locus coeruleus, these results allow prediction of situations under which this massive projection system would be active and suggest a physiological role for this chemically identified network in specific behavioral processes.

Action Potentials↗
PubMed1980

Morphine and opioid peptides reduce paraventricular neuronal activity: studies on the rat hypothalamic slice preparation.

Extracellular discharges of neurons in the paraventricular nucleus (PVN) were recorded from slices of rat hypothalamus in vitro. PVN neurons (n = 14) were identified by the criteria of (i) phasic activity patterns and (ii) antidromic invasion from the neurohypophysial tract. Neurons not displaying either of these features were considered unidentified with respect to physiological function (n = 85). The majority of unidentified neurons responded to bath application of morphine (1 microM), [D-Ala2,Met5]enkephalin (1 microM) or beta-endorphin (0.01-1 microM) with a prompt, reversible, dose-related reduction in spike discharge frequency. Naloxone (1 microM) antagonized the opioid-induced depressions in some, but not all, cases. At the concentrations tested, no tachyphylaxis to the effects of the opioids was observed. The opioid effects on putative neurohypophysial neurons were less pronounced; while 2 were depressed, the remaining 12 displayed no change in frequency or pattern of discharge to micromolar concentrations of morphine, [D-Ala2,Met5]enkephalin, or beta-endorphin. Our results indicate that opioids depress neuronal activity in the rat PVN via an interaction with a specific opiate receptor but that this effect is more pronounced on unidentified neurons than on putative neurohypophysial neurons in the slice.

Animals↗
PubMed1979

Perinatal development of the endorphin- and enkephalin-containing systems in the rat brain.

Radioimmunoassay and microdissection procedures were used to study the perinatal development of the endorphin- and enkephalin-containing systems in the rat brain. In contrast to values reported on adult rat, endorphin levels are much higher than enkephalin levels on embryonic day 16. The highest endorphin values are found in the diencephalon, midline telencephalon and medulla-midbrain regions. Perinatally, enkephalin content increases at a faster rate than endorphin in all brain regions, producing a marked drop of the endorphin/enkephalin ratios. Between postnatal days 6 and 25, both endorphin and enkephalin levels increase, approaching their adult distribution pattern. No correlation was found between regional distributions or rates of increase of endorphin and enkephalin in any of these developmental stages, suggesting that the two peptide systems develop independently from each other.

Age Factors↗
PubMed1979

Opioid peptides may excite hippocampal pyramidal neurons by inhibiting adjacent inhibitory interneurons.

The atypical excitation by opiates and opioid peptides of hippocampal pyramidal cells can be antagonized by iontophoresis of naloxone, the gamma-aminobutyric acid antagonists bicuculline, or magnesium ion. The recurrent inhibition of these cells evoked by transcallosal stimulation of the contralateral hippocampus is blocked by enkephalin but only shortened by acetylcholine. The results suggest that the opioids excite pyramidal neurons indirectly by inhibition of neighboring inhibitory interneurons (probably containing gamma-aminobutyric acid). This mechanism may be pertinent to the electrographic signs of addictive drugs.

Animals↗
PubMed1979

Stimulation of human periaqueductal gray for pain relief increases immunoreactive beta-endorphin in ventricular fluid.

Immunoreactive beta-endorphin was measured in the ventricular fluid of six patients with chronic pain. Stimulation of the periaqueductal gray matter in three patients with pain of peripheral origin resulted in significant increases (50 to 300 percent) in the concentration of ventricular immunoreactive beta-endorphin. In three other patients suffering deafferentation dysesthesia, stimulation of the posterior limb of the internal capsule did not alter the concentration of this peptide. These results provide evidence of the release of human immunoreactive beta-endorphin in vivo and suggest that naloxone-reversible pain relief achieved by stimulation of the periaqueductal gray matter may be in part mediated by the activation of beta-endorphin-rich diencephalic areas.

Aged↗
PubMed1979

Widespread distribution of protein I in the central and peripheral nervous systems.

Protein I, a naturally occurring substrate for cyclic AMP-dependent and calcium-dependent protein kinases, previously has been found only in mammalian brain, where it has been demonstrated to be located in neurons. Various tissues and organs outside the brain have now been examined for the possible occurrence of protein I, by using both an immunohistochemical approach and a chemical procedure involving radioimmunolabeling of polyacrylamide gels. Protein I has been found in the inner plexiform layer of the retina, in the posterior pituitary, and in the autonomic nervous system. In tissue composed predominantly of cells other than nerve cells, immunoreactivity was present only where innervation was present. Protein I appeared to be localized in some, but not all, nerve terminals and synapses.

Animals↗