E Soroca-Lucas

Bio: E Soroca-Lucas is an academic researcher. The author has contributed to research in topics: Enkephalinase inhibitor & Enkephalinase. The author has an hindex of 1, co-authored 1 publications receiving 117 citations.

Selective protection of methionine enkephalin released from brain slices by enkephalinase inhibition.

Abstract: Methionine enkephalin release was evoked by depolarization of slices from rat striatum with potassium. In the presence of 0.1 microM thiorphan [(N(R,S)-3-mercapto-2-benzylpropionyl)glycine], a potent inhibitor of enkephalin dipeptidyl carboxypeptidase (enkephalinase), the recovery of the pentapeptide in the incubation medium was increased by about 100 percent. A similar effect was observed with the dipeptide phenylalanylalanine, a selective although less potent enkephalinase inhibitor. Inhibition of other known enkephalin-hydrolyzing enzymes--aminopeptidase by 0.1 mM puromycin or angiotensin-converting enzyme by 1 microM captopril--did not significantly enhance the recovery of released methionine enkephalin. These data indicate that enkephalinase is critically involved in the inactivation of the endogenous opioid peptide released from striatal neurons.

Characterization and inhibition of a cholecystokinin-inactivating serine peptidase

Abstract: A cholecystokinin (CCK)-inactivating peptidase was purified and identified as a membrane-bound isoform of tripeptidyl peptidase II (EC 3.4.14.10), a cytosolic subtilisin-like peptidase of previously unknown functions. The peptidase was found in neurons responding to cholecystokinin, as well as in non-neuronal cells. Butabindide, a potent and specific inhibitor, was designed and shown to protect endogenous cholecystokinin from inactivation and to display pro-satiating effects mediated by the CCKA receptor.

Endogenous opioid regulation of hippocampal function.

Abstract: Publisher Summary This chapter discusses the anatomy and physiology of opioids in the hippocampus It also discusses the roles of opioids in learning and memory processes and epileptogenesis Endogenous opioid peptides modulate neural transmission in the hippocampus Proenkephalin-derived peptides have been demonstrated to act at mu and delta opioid receptors to inhibit GABA release from inhibitory interneurons, resulting in the increased excitability of hippocampal pyramidal cells and dentate gyrus granule cells Prodynorphin-derived peptides primarily act at presynaptic kappa opioid receptors to inhibit excitatory amino acid release from perforant path and mossy fiber terminals Opioid receptors reduce membrane excitability by modulating ion conductances; and in this way, they may decrease voltage-dependent calcium influx and transmitter release Synaptic plasticity in the hippocampus also is modulated by endogenous opioids Enkephalins facilitate long-term potentiation, whereas dynorphins inhibit the induction of this type of neuroplasticity Opioids may play important roles in hippocampal epilepsy Recurrent seizures induce changes in the expression of opioid peptides and receptors Also, enkephalins have proconvulsant effects in the epileptic hippocampus, whereas dynorphins may function as endogenous anticonvulsants

Clinical and biochemical aspects of depressive disorders: II. Transmitter/receptor theories

Abstract: The present document is the second of three parts in a review that focuses on recent data from clinical and animal research concerning the biochemical bases of depressive disorders, diagnosis, and treatment. Various receptor/transmitter theories of depressive disorders are discussed in this section. Specifically, data supporting noradrenergic, serotonergic, cholinergic, dopaminergic, GABAergic and peptidergic theories, as well as interactions between noradrenergic and serotonergic, or cholinergic and catecholaminergic systems are presented. Problems with the data and future directions for research are also discussed. A previous publication, Part I of this review, dealt with the classification of depressive disorders and research techniques for studying the biochemical mechanisms of these disorders. A future publication, Part III of this review, discusses treatments for depression and some of the controversies in this field.