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Biomedical subjects

F Bloom

Publications and source records attributed to F Bloom.

At least 37 records · Page 2Linked to original sources
PubMed1979

Iontophoresis of Li+ antagonizes noradrenergic synaptic inhibition of rat cerebellar Purkinje cells.

Li salts provide effective therapy for manic-depressive psychosis, but the site and mechanism of this effect are not known. We have tested the ability of Li, applied by microiontophoresis, to modify the responsiveness of rat cerebellar Purkinje neurons to iontophoretic applications of norepinephrine and gamma-aminobutyrate and to the inhibition produced by stimulation of the noradrenergic ceruleo-cerebellar pathway. As previously reported for rat hippocampal neurons, acute exposure to Li produces selective, reversible antagonism of the effects of norepinephrine and the noradrenergic pathway but does not affect inhibitory actions of gamma-aminobutyrate. Collectively, these selective antagonisms of noradrenergic sympatic inhibitions in the cerebellum and hippocampus may indicate a general effect of Li suitable for extended observations in rats exposed to Li for the chronic periods needed to achieve therapeutic effects in man.

Animals↗
PubMed1978

Neurons containing beta-endorphin in rat brain exist separately from those containing enkephalin: immunocytochemical studies.

Well-characterized antisera to porcine beta-endorphin were used to localize immunoreactive sites in cryostat sections of formaldehyde-fixed rat brain by indirect immunohistochemistry. Specificity was established by absorption of immune sera with synthetic peptide fragments. Specific immunoreactivity was localized to neuronal perikarya in the basal tuberal hypothalamus, and to varicose nerve fibers which were distributed to midline nuclear areas throughout the diencephalon and anterior pons. These patterns of reactivity were unaffected by preabsorption of the immune sera with millimolar concentrations of Met5- or Leu5-enkephalin or alpha-endorphin. The beta-endorphin immunoreactive structures were morphologically separate from those cells and fibers reported to react with antisera to the enkephalins. One anti-beta-endorphin serum gave additional immunoreactivity with myelinated axons in limbic cortical zones; when absorbed with purified rat myelin basic protein, only the specific patterns of immunoreactivity remained. Thus, discrete beta-endorphin-containing neuronal circuits exist in rat brain and are anatomically distinguishable from enkephalin-containing nerve cell and fiber pathways.

Animals↗
PubMed1977

beta-Endorphin: endogenous opiate or neuroleptic?

The opiatelike neuropeptide beta-endorphin produces a spectrum of effects that contrasts with that induced by the neuroleptic haloperidol. Rats injected intraventricularly or directly into the periaqueductal gray with beta-endorphin (0.5 to 50 micrograms) exhibited rigid immobility accompanied by the loss of righting reflex; the period of rigidity was preceded or followed (depending upon dose) by a state of hyperactivity. In contrast, no dose of haloperidol tested (0.5 to 12 milligrams per kilogram) produced rigidity, loss of righting reflex, or behavioral excitation. Furthermore, whereas animals injected with haloperidol remained stationary on a vertical grid, rats injected with beta-endorphin typically slid off the grid. Moreover, combined beta-endorphin and haloperidol treatment produced flaccidity in most animals. These results do not support the contention that this opiatelike peptide may be a naturally occurring neuroleptic.

Animals↗
PubMed1977

beta-Endorphin and adrenocorticotropin are selected concomitantly by the pituitary gland.

The opiate-like peptide beta-endorphin and adrenocorticotropin are concomitantly secreted in increased amounts by the adenohypophysis in response to acute stress or long-term adrenalectomy as well as in vitro in response to purified corticotropin releasing factor and other secretagogues. Conversely, administration of the synthetic glucocorticoid dexamethasone inhibits the secretion of both adrenocorticotropin and beta-endorphin. Thus, both hormones possess common and identical regulatory mechanisms and there may be a functional role for circulating beta-endorphin.

Adrenocorticotropic Hormone↗
PubMed1977

Negative naloxone effects in schizophrenic patients.

On the basis of the hypothesis that the opiate-like neuropeptides, such as beta-endorphin, may be involved in the etiology of schizophrenic symptoms, naloxone 1,2 mg and placebo were administered intravenously to 8 schizophrenic patients, using a double-blind, crossover design. Naloxone was not found to be different from placebo in effecting schizophrenic symptoms, including hallucinations and delusions.

Adult↗
PubMed1976

Endorphins: profound behavioral effects in rats suggest new etiological factors in mental illness.

The endogenous morphinomimetic brain peptides Met5-enkephalin and alpha-, beta-, and gamma-endorphins have been evaluated in rats after intracerebrospinal fluid injection. beta-Endorphin produces marked, prolonged muscular rigidity and immobility similar to a catatonic state, counteracted by the opiate antagonist naloxone; this effect occurs at molar doses 1/100 to 1/400 that at which the other peptides or morphine block the response to painful stimuli. All peptides evoked dose-related, naloxone-reversible, wet-dog shakes in rats that had not been exposed to drugs. beta-Endorphin produced hypothermia, whereas gamma-endorphin produced hyperthermia. Such potent and divergent responses to naturally occurring subtances suggest that alterations in their homeostatic regulation could have etiological significance in mental illness.

Animals↗
PubMed1975

Formation of a functional adrenergic input to intraocular cerebellar grafts: ingrowth of inhibitory sympathetic fibers.

The intraocular transplantation technique was used to study the ingrowth of peripheral sympathetic adrenergic nerves from the iris into transplants of fetal rat cerebellum, and the possible function of these nerves. The transplants, grown in oculo for one-half to eight months, were analyzed by fluorescence histochemistry and electrophysiological techniques. Peripheral sympathetic adrenergic fibers from the iris were able to grow into the cerebellar transplants and arborize in a pattern similar to that in situ, appearing in all three cortical layers and the noncortical areas of the transplants. The density of visible nerves without pretreatment and after preincubation in 10(-6) or 10(-5) M alpha-methylnorepinephrine was comparable to mature rat cerebellum. The spontaneous discharge of the Purkinje cells in oculo was inhibited by microiontophoresis of norepinephrine (NE) and amphetamine in sympathetically innervated, as well as sympathectomized transplants denervated by ganglionectomy. The NE response was blocked by the adrenergic beta-receptor blocker MJ-1999. GABA also inhibited the Purkinje cell activity while glutamate accelerated the discharge. Parenteral amphetamine inhibited Purkinje cell activity in sympathetically innervated transplants, but was ineffective in denervated transplants. The Purkinje cell spontaneous activity was inhibited by electrical stimulation of the NE fiber input through the cervical sympathetic trunk. This inhibition could be antagonized by parenteral reserpine or the beta-adrenergic antagonist propranolol. The responses of the Purkinje cells within the transplants to drugs and transmitters mimic those of the adult rat in situ. In view of the fluorescence histochemical evidence for an ingrowth of peripheral sympathetic adrenergic fibers into the cerebellar transplants, and the results of stimulating the sympathetic trunk, it is suggested that peripheral adrenergic fibers may be able to establish functional connections with the Purkinje cells similar to the cerebellar adrenergic synapses normally formed in situ by fibers from the locus coeruleus.

Amphetamine↗