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H Laborit

Publications and source records attributed to H Laborit.

At least 73 records · Page 4Linked to original sources

[The mechanism of releasing and bio-behavioral significance of the hypothalamo-hypophyso-adrenal gland reaction to the environment (alarm reaction)].

Laboratory experimentation has demonstrated the large increase in the rate of circulating norepinephrin (N.E.), in a parallel with an improvement in cardiovascular dynamism of suprarenalectomized rabbits under the action of injection IV of hydrocortisone. As from this ascertainment, the author attempts to make a synthesis of known experimental facts demonstrating that next to a regulation in constancy (with negative retroaction) of the C.R.F. leads to A.C.T.H. leads to cortisol system, there exists a servomechanism (control external to the system) as from the activity of the nervous systems as compared with environment. Hydrocortisone favouring passive avoidance, and extinction facilitating the activity of the cholinergic inhibiting system of action (I.S.A.). A.C.T.H. facilitates active avoidance and the catecholaminergic activating system of action (A.S.A.). Now, it has already been demonstrated in the same laboratory that stimulation of I.S.A. or inhibition of the A.S.A. freed N.E. from the peripherous nerves of a adrenalectomized animal. It, therefore, seems that the early freeing of A.C.T.H. following aggression is capable of favouring locomotive activity (flight or fight). Should the latter be efficient, there is a return to the prior behavioural and endocrinal balance. On the other hand, should they be inefficient, there arises a vicious circle (regulation with tendency, positive retroaction) because secondary secretion of glucocorticoids will maintain inhibition of action and the secondary freing of the mineralocorticoids are discussed as well as the central mechanism of illness so called "psychosomatic".

Adrenal Glands↗

The action of arachidonic acid on the locomotive activity of mice.

The intraperitoneal administration of methyl or sodium arachidonate (100 and 200 mg-kg causes, in mice, a significant decline in locomotive activity 30 min later, and is able to oppose completely the antagonistic action of D-amphetamine (2.5 and 5 mg-kg). This effect seems to be related to increased synthesis of prostaglandins, for it disappears partially after pretreatment with acetylsalicylic acid, which alone has no effect on the spontaneous activity of mice. Oleic acid, an unsaturated fatty acid not involved in prostaglandin synthesis does not give significant results in the same conditions.

Amphetamine↗

The action of arachidonic acid on experimental hypertension in the rat.

Keeping in mind the vasodilator action of prostaglandins, the control that they exercise over the vascular supply of kidneys and the sympathetic activity, research was conducted in order to establish the effect of arachidonic acid, the precursor of PGE2, on experimental hypertension in the rat. The experimental hypertension was induced by unilateral nephrectomy, followed by the administration of DOCA and the elevated sodium diet. The treatment was short in one group, long in the other, and both groups were compared to a control hypertensive group which received no treatment at all. Arachidonic acid worsened the experimental hypertension by 37% in the long treatment, and by 25% in the short treatment. The administration of lysine-acetylsalicylate diminished this hypertension. A non-saturated acid, oleic acid, which is not involved in prostaglandin synthesis, has no action. The authors would like to emphasize that in one of the previous experiments, L-tyrosine, the precursor of catecholamines, diminished the experimental hypertension in the rat, and also that L-DOPA and IMAO (MAOI) have comparable effects. It seems, therefore, that the depression of the central catecholaminergic activity, which is supposed to be the action of arachidonic acid via an increase in the PGE2 synthesis, appears to increase hypertension. It is noteworthy that the medial forebrain bundle (MFB) is catecholaminergic and that the periventricular system (PVS) is cholinergic. Thus hypertension may represent the peripheral vascular response to anguish which results from the activation of PVS and from the depression of MFB.

Administration, Oral↗

[Neurophysiological and biological bases of active and passive avoidance behaviors. Somatic consequences. Behavioral level. Semantic problems].

After a discussion concerning the semantic contents of terms such as: emotions, pulsions, motivations, as much from the physiological as from the psychological point of view as well as with regard to the role of the processes of memory and learning in their elaboration, the neurophysiological plane of fundamental behaviour patterns is approached. The role of the dorsomedian amygdala and of the lateral hypothalamus in the processes of behavioural activation as well as that of the septal area, of the hippocampus, of the lateral amygdala, of the ventro-median hypothalamus in the processes of inhibition are recalled. The action upon the environment and the reaction to the environment (conditioned or unconditioned) of this system are studied. Anxiety is considered as resulting from the inhibition of action and its endogenous or exogenous causes, as well as the mechanisms of its disappearance, are examined. The distinction between hypophyso-corticoadrenal alarm reaction and sympatho-adrenergic defence reaction is recalled. Basing himself upon the experimental work of his laboratory, the author shows that in the defence reaction it is necessary to make the distinction between the sympathetic reaction, noradrenergic, brrenergic reaction, medullo-adrenal, controlled by the system of behavioural activation. He shows the interest of such a distinction on the physio-pathological plane. Finally he approaches the biochemical level, that of the neuro-modulators and of their central role. He suggests that the effect alpha of catecholamines and the nicotinic effect of acetylcholine indeed seem to have a direct role in the control of synaptic activity, while the beta effect and the muscarinic effect could have a secondary role through the intermediary of the synthesis of cAMP and cGMP respectively. The second messengers would intervene principally in the neuronal protein synthesis and the long term memory. The work ends with a rapid summary concerning the biochemical and neurophysiological mechanisms of drugs which act upon behaviour patterns. This summary is based on the outline previously elaborated.

Animals↗