Search PubMed⌕ Search

Biomedical subjects

H Akil

Publications and source records attributed to H Akil.

At least 271 records · Page 15Linked to original sources
PubMed1980

Enkephalinase: selective inhibitors and partial characterization.

There are at least two types of enzymes in brain, endopeptidases and aminopeptidases, which metabolize enkephalins. Evidence is presented to suggest that enkephalinase, an endopeptidase cleaving at the Gly-Phe bond, is specific for the endogenous enkephalinergic system. Selective inhibitors are described for each enzyme. These are parachloromercuriphenylsulfonic acid and puromycin in the case of aminopeptidases and various enkephalin fragments in the case of enkephalinase. Some characteristics of the two types of enzymes are described. Enkephalinase has many properties in common with the well-characterized brain angiotensin-converting enzyme. These two enzymes, however, behaved differently when tested for chloride dependence, for activity in several buffers and for susceptibility to specific inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1979

Some observations on the opiate peptides and schizophrenia.

With the discovery of the opiate peptides, several major avenues of research became apparent. These peptides produced a great deal of focused attention on their anatomy, biochemistry, and physiology. In this article, we present an overview of some of the main research issues and recent findings in the field of opiate peptides. The possible relationship of the opiate peptide neuronal systems to schizophrenia is discussed in light of attempts to alter schizophrenic symptoms with opiate antagonists, beta-endorphin, and dialysis. It is hypothesized that if the opiate peptides are involved in schizophrenia, then their involvement with dopamine systems and/or with stress responses may be critical.

Administration, Oral↗
PubMed1978

Enkephalin-like material elevated in ventricular cerebrospinal fluid of pain patients after analgetic focal stimulation.

Enkephalin-like activity has been measured in the ventricular cerebrospinal fluid of patients with intractable pain. Electrical stimulation of periventricular brain sites resulted in significant decrease in persistent pain in these subjects. This analgesia, which was blocked by naloxone in 80% of the cases, was accompanied by a significant rise in ventricular enkephalin-like activity, as measured by two different methods. The results present evidence of in vivo release of enkephalin-like material in humans and suggest that stimulation analgesia may be partially due to this release.

Brain↗
PubMed1978

Effects of naloxone on schizophrenia: reduction in hallucinations in a subpopulation of subjects.

Endogenous opiate-like peptides (endorphins) are putative neuroregulators located throughout the mammalian brainstem. There is some evidence for their role in pain, stress, and affect. We report that the opiate antagonist, naloxone, alters some schizophrenic symptoms. In a double-blind, cross-over study, naloxone produced decreases in auditory hallucinations in some schizophrenic patients. This finding supports the hypothesis that the endorphins may play a roll in modulating hallucinations in a highly selected subgroup of chronically hallucinating schizophrenic patients.

Adult↗
PubMed1978

Behavioral neurochemistry: neuroregulators and behavioral states.

There is compelling evidence that behavioral events after neurochemical function and that altered neurochemical function can change behavior. Such processes have been related both to neurotransmitters and to neuromodulators, together termed neuroregulators. Available research tools and theoretical constructs have begun to permit studies of certain types of behavior, primarily those related to emotional states and drives. This work is changing long-held concepts about severe mental disorders and the treatment of them.

Animals↗
PubMed1978

Appearance of beta-endorphin-like immunoreactivity in human ventricular cerebrospinal fluid upon analgesic electrical stimulation.

beta-Endorphin-like immunoreactivity in human ventricular cerebrospinal fluid was measured with a specific radioimmunoassay. The subjects were undergoing a surgical procedure for relief of chronic intractable pain. This procedure involved the focal stimulation of a medial thalamic site adjacent to the wall of the third ventricle. Samples were collected before and during the analgesic stimulation. No beta-endorphin-like immunoreactivity could be detected prior to stimulation, suggesting that baseline levels are below 25 fmol/ml of cerebrospinal fluid. Electrical stimulation led to substantial increases (13- to 20-fold) in immunoreactive material in every subject. These results suggest that beta-endorphin-like material can be released into the ventricular system and may contribute to the pain blockade that results from periventricular stimulation.

Analgesia↗