Hormonal control of behavior: amines and the biasing of behavioral output in lobsters.

Hormones and neurohormones act on the nervous system to produce important changes in behavior. Amine actions in the lobster nervous system and their possible relations to aggressive behavior in lobsters were studied in order to explore how such changes might come about.

Ornithine decarboxylase stimulation in rat ovary by luteinizing hormone.

In normal albino rats with a 4-day estrous cycle, the activity of ovarian ornithine decarboxylase undergoes a transitory rise on the evening of proestrus and only at that time. The response could be elicited by the administration of either luteinizing hormone or human chorionic gonadotrophin. When antiserum to luteinizing hormone was injected at 2 p.m. on the day of proestrus, the induction of ornithine decarboxylase was blocked, an indication that the enzyme is under luteinizing hormone control. The strategic positioning of the induction of ornithine decarboxylase between the normal release of luteinizing hormone and ovulation impties that putrescine is associated with the ovulatory process, and opens a new avenue of research on the control of ovulation.

Histochemical protein markers of monoamine cell bodies in man.

Neurons in brainstem and hypothalamus of postmortem, formaldehyde-fixed tissue of 25 healthy controls were studied with a double-staining procedure for the consecutive demonstration of Nissl material and of cytoplasmic spherical bodies, which are rich in basic proteins. The investigation established that the protein bodies are located in cells that correspond to the aminergic neurons demonstrable by histofluorescence. Protein bodies were also found in the neurons of the inferior olive, which are not as a rule included in the aminergic cell groups. The localization of protein bodies is perikaryal and dendritic and, thus, parallels the distribution of monoamines and monoamine-synthesizing enzymes reported in experimental animals. The invariable presence of protein bodies in all aminergic perikarya of control human brains and their absence from nonaminergic neurons permits us to consider them markers of monoamine neurons in man.

Effect of endogenous vasoconstrictors on maternal intramyometrial and fetal stem villous arteries in pre-eclampsia.

The contractile responses to various endogenous vasoactive agents were investigated in isolated human uteroplacental arteries from normotensive (NT) patients and patients with pre-eclampsia (PE) undergoing caesarian section. Tissue samples were obtained from the uterine incision and from macroscopically normal cotyledons. Vascular ring preparations of intramyometrial and stem villous arteries (length 1.0-1.3 mm, outer diameter 400-600 microns) were dissected and mounted in organ baths and isometric tension was recorded. Concentration-response relationships for vasopressin (VP), oxytocin (OX), angiotensin II (Ang II), noradrenaline (NA), 5-hydroxytryptamine (5-HT), prostaglandin F2 alpha (PGF2 alpha) and prostaglandin E2 (PGE2) were assessed. For each compound, the mean maximum contractile effect (Emax) and the drug concentration producing half-maximal response (EC50) were determined. In intramyometrial arteries from NT and PE patients, VP, Ang II, NA, 5-HT and PGF2 alpha induced contraction while OX and PGE2 produced weak or no responses. Preparations from PE patients showed higher Emax values, while no differences in EC50 were found between the two groups. In fetal stem villous arteries, Ang II, 5-HT, PGF2 alpha and PGE2 induced contractions, while VP, NA and OX produced weak responses. No differences in Emax or EC50 values were found between the fetal vessels of PE and NT patients. No qualitative differences were demonstrated in response to the agents tested between the vessels (fetal and maternal) from NT women at term and PE patients. However, the results may reflect quantitative differences, suggesting increased contractility of maternal uteroplacental arteries from women with PE.

Evidence that hypoxic pulmonary vascular remodeling in rats is polyamine dependent.

This study tested the hypothesis that the polyamines, a family of low-molecular-weight organic cations with documented regulatory roles in cell growth and differentiation, are mediators of chronic hypoxia-induced pulmonary vascular remodeling. Relative to room air controls, chronically hypoxic animals (inspired O2 fraction = 0.1; 21 days) exhibited higher pulmonary arterial pressures (measured in room air), thicker medial layers in pulmonary arteries of 50-100 microns diam, increased hematocrits, and right ventricular hypertrophy. In addition, lung contents of the polyamines, putrescine, spermidine, and spermine were greater in hypoxic animals than in controls. alpha-Difluoromethylornithine (DFMO), an inhibitor of polyamine synthesis, attenuated the hypoxia-induced elevations in lung putrescine and spermidine content and blunted the increases in pulmonary arterial pressure and medial thickness. Neither the increased hematocrit nor right ventricular hypertrophy associated with chronic hypoxia were abrogated by DFMO. In addition, DFMO failed to influence vasoconstrictor responses provoked by acute hypoxic ventilation in isolated, buffer-perfused rat lungs. These observations suggest that depression of polyamine biosynthesis with DFMO blunts the sustained increase in pulmonary arterial pressure by attenuating hypoxia-induced medial thickening.

The A-B-C (Allocortex-Brainstem-Core) circuitry of endocrine-autonomic integration and regulation: a proposed hypothesis on the anatomical-functional relationships between estradiol sites of action and peptidergic-aminergic neuronal systems.

A sex steroid hormone sensitive brainstem-allocortex axis of neuronal cell groups and projections is recognized with convergent pathways of aminergic-peptidergic messenger systems, which subserves the adjustment for varying reproductive and environmental conditions and the coordination of endocrine-autonomic functions. Main stations in the A-B-C (Allocortex-Brainstem-Core) periventricular axis include the substantia gelatinosa, nucleus (n.) tractus solitarii-dorsal vagal nucleus-area postrema complex, locus ceruleus, n. parabrachialis, central gray and associated raphe nuclei, ventral tegmental area, lateral and periventricular hypothalamus, n. paraventricularis, bed nucleus of the stria terminalis, preoptic-septal nuclei and n. centralis amygdalae with associated amygdaloid nuclei, as well as the ventral and dorsal allocortex. All of these stations and their periventricular and medial forebrain bundle projections contain estradiol sites of action and represent elements of earlier defined periventricular estradiol-target neuron systems. Results from colocalization of 3H estradiol by thaw-mount autoradiography and aminergic and peptidergic messengers by immunohistochemistry or other histochemical techniques indicate direct nuclear effects of estradiol on certain noradrenalin, dopamine, gamma aminobutyric acid, somatostatin, and neurophysin neurons. Additional data about correspondence of estradiol-target neuron accumulations with neuronal sites of peptide messenger production suggest direct effects of estradiol on certain enkephalin, endorphin, corticotropin releasing hormone, adrenalin, serotonin, cholecystokinin, pancreatic polypeptide and gonadotropin releasing hormone neurons--and probably others. As documented for the pituitary, and as an approach to understand varying and dual effects, it is postulated that estradiol activation of brain messenger systems parallels the heterogeneous estradiol binding in the A-B-C- system. This is expressed in the concept of differential Multiple Activation of Heterogeneous Systems (MAHS).(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiological assessment of monoamine synaptic function in neuronal circuits of seizure susceptible brains.

The following report reviews evidence suggesting a role for the monoamines, norepinephrine (NE) and serotonin (5-HT), in the pathophysiology of seizure disorders and outlines a strategy for electrophysiologically evaluating monoaminergic function at the synaptic level in central neuronal circuits of two animal models of epilepsy.

Transglutaminase may mediate certain physiological effects of endogenous amines and of amine-containing therapeutical agents.

Transglutaminase mediation of the effects of certain primary amines and alcohols may be important in receptor coupling to physiological responses. Many of the therapeutic and toxic side effects of drugs also may be related to their covalent linkage of glutamine residues of key regulatory proteins through the catalytic action of transglutaminase. This paper suggests that important therapeutic agents such as digoxin, tetracycline, adriamycin, and actinomycin D may have some effects related to transglutaminase action.