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P Karli

Publications and source records attributed to P Karli.

At least 19 recordsLinked to original sources

[Cognition, memory and affect].

The flow of information within the brain and the sequence of operations which process it get enriched through a twofold mediation, that of the current affective states and that of the references made to an individual life-history. Affectivity and memory are closely linked in the elaboration of action (thought acts, speech acts, behaviours) since it is especially through the mediation of affective states and emotions that the current action is both a partial reactualization of the past and one of the major determinants of future action. Whenever the processing of information derived from the present real world induces a certain affective state, the latter acts in return so as to filter, reorient and focalize the reading of the real, while it further facilitates the memorizing--and later on the recalling--of the very information that induced it. In the elaboration of the historical and affective dimensions of mental life and of the behaviours that express it, one may distinguish--within the brain--three levels of integration, organization and adaptation. It matters to know the role played by each of these functional levels. Indeed, though the latter closely interact with one another under normal conditions, various pathological processes are likely to provoke a dissociation, together with a possibly resulting functional "regression".

Affect

Perception, cognition and action: the mediating role of affective states.

When facing and evaluating the present state of the world, the brain generates predictions and expectancies together with some specific emotional state which imposes on any given situation - or rather on the individual relationship to that situation - its essential meaning that basically orients the choice of an appropriate behavioural strategy. This general notion is exemplified by concrete data concerning brain mechanisms which underlie aggressive behaviour.

Affect

Modulation by morphine of aversive-like behavior induced by GABAergic blockade in periaqueductal gray or medial hypothalamus.

Pretreatment with "analgesic" doses (15 nmoles) of morphine injected either into the periaqueductal gray (PAG) or into the medial hypothalamus (MH) were found to modulate flight behavior elicited by bicuculline injected into the same brain sites. When injected into the MH, morphine always suppressed bicuculline-induced flight, while PAG injections paradoxically either suppressed or facilitated the behavioral effects produced by bicuculline. Whenever a facilitation of the bicuculline-induced effects had been observed following pretreatment with 15 nmoles of morphine into the PAG, the infusion of lower doses (6 nmoles) did no longer induce facilitation but clear suppression. In those animals that had shown suppression of the aversive-like effects of bicuculline following the same 15 nmoles pretreatment, infusion of higher doses (24 nmoles) of morphine into the PAG still produced the same kind of suppression. And yet, when injected into the PAG, very high doses of morphine (50 nmoles) were found to induce, by themselves, flight behavior known as explosive motor behavior. In contrast, such high doses of morphine never induced comparable explosive motor behavior when injected into the MH. These data can be explained by the involvement of different types of receptors in the neural mechanisms subserving and controlling the generation of aversion in periventricular brain regions (PAG and MH).

Animals

Potential and limitations of the offense-defense dichotomy in aggression research, considering the complex and evolving interactions of biological, psychological and social determinants of aggression.

The offense-defense dichotomy undeniably proved to be of heuristic interest in that it allowed relevant distinctions between specific behaviour patterns, to establish correlations between situations in which either "offensive" or "defensive" patterns are likely to be displayed, and to uncover differential drug effects on those distinct behavior patterns. But for a number of reasons, the author is led to conclude that even though the offense-defense dichotomy indeed helps in many instances to describe and to distinguish, it has rather limited potential really to explain in depth what it distinguishes at a phenomenological level of investigation.

Aggression

Mapping of jumping, rearing, squealing and switch-off behaviors elicited by periaqueductal gray stimulation in the rat.

Rats readily learn to escape from a stimulation applied to most mesencephalic periaqueductal gray (PAG) sites. In the present study, we tried to find out to what extent the differential effects induced by such stimulations actually reflect the existence of intraPAG functional subdivisions. To that end, a row of five electrodes was implanted into the PAG of each of 29 rats. Two kinds of effects were analyzed, the stimulation-elicited overt behaviors and the generalization of switch-off responding from one stimulation site to the others. Further, switch-off latency versus interpulse interval (IPI) relationships were established and both the threshold IPIs and the ceiling switch-off latencies were determined. The most commonly elicited behaviors (jumping, rearing and squealing) as well as the threshold IPIs and the ceiling switch-off latencies were mapped within the PAG. Switch-off behavior was elicited from all the stimulation sites studied. However, in the dorsal PAG the switch-off latency was found to decrease more steeply with decreasing IPI than it did in the ventral PAG. Switch-off generalization was less frequently observed between dorsally located stimulation sites. Jumps were most often elicited from dorsally and rostrally located PAG sites while squeals were more frequently elicited from the caudal part of the PAG and rearings from PAG subareas surrounding the aqueduct.

Animals

Unit activity alterations induced in the mesencephalic periaqueductal gray by local electrical stimulation.

In the framework of a series of investigations concerning the neural substrate of aversion, electrophysiological methods were used in order to specify, within the rat's periaqueductal gray (PAG), functional properties, viz. conduction velocity and refractory period, of PAG neurons already assessed in previous studies by means of behavioral methods, and to gather data on their local synaptic relationships. Unit activities were recorded from the periaqueductal gray with the aim of analyzing those alterations that would be induced by locally applying an electrical stimulation with parameters shown to elicit escape behavior. An implanted row of electrodes allowed the application of a stimulation to several sites aligned along a mediolateral or a rostrocaudal axis through the periaqueductal gray. The results indicate that an electrical stimulation applied to the periaqueductal gray may induce its effects through the activation of a number of dendrites and many slow conducting fibers running in a great variety of directions and branching within the periaqueductal gray. Their refractory period was surprisingly low (0.6 ms) for slow conducting fibers (below 1 m/s). The local circuitry appears to include many inhibitory connections. Their organization is assumed to be partly recurrent. Stimulation-induced inhibition becomes predominant when the stimulation is moved away from the recorded neuron along the mediolateral axis, but not along the rostrocaudal axis.

Animals

Morphine injected into the periaqueductal gray attenuates brain stimulation-induced effects: an intensity discrimination study.

A discrimination situation was used to study the effects of morphine microinjected into the periaqueductal gray (PAG) on the aversive effects induced by PAG or medial hypothalamic (MH) electrical stimulation. Rats were trained in a T-maze to interrupt a high intensity (HI) stimulation inducing a short escape latency by pressing the lever (HI lever) located in one arm of the maze and a low intensity (LI) stimulation inducing a longer escape latency by pressing the lever (LI lever) located in the other arm. Microinjections of 15 nmol (5 micrograms) or 40 nmol (13 micrograms) of morphine both lengthened the escape latencies and shifted towards the LI lever the animal's choice in order to interrupt HI stimulations. This effect of morphine showed a similar time course as regards both escape latency and lever choice; it was more marked on PAG than on MH stimulation-induced aversive effects. The data are discussed in terms of morphine microinjections into PAG lengthening the escape latency by decreasing the aversiveness of PAG or MH stimulation rather than by affecting the animals' ability to respond to such stimulations.

Animals

Ventral tegmental stimulation modulates centrally induced escape responding.

Electrical stimulation of the ventromedial tegmentum (VT) exerts a dual effect on escape responding, induced by stimulating either the medial hypothalamus (MH) or the dorsal part of the central gray matter (CG), namely a suppressant effect which reduces MH or CG induced escape responses and a facilitating one which increases these same responses. The relative magnitude of these effects appears to depend on both the location of the VT stimulation site and the stimulation intensity applied. Furthermore, VT stimulation is often more effective in suppressing escape responding induced by MH as opposed to CG stimulation. VT stimulation has clear rewarding effects but seems to have also aversive effects. The VT sites whose stimulation induces escape suppression seem to yield less marked aversive effects than those sites whose stimulation induces escape facilitation. Furthermore, a negative correlation was found to exist between the escape rate induced by a combined CG/VT or MH/VT stimulation and the self-stimulation rate yielded by these VT sites. These results suggest that the effects of a VT stimulation on escape responding induced by electrical brain stimulation are somehow related to the rewarding and/or aversive effects of this same VT stimulation.

Animals

Flight induced by microinjection of D-tubocurarine or alpha-bungarotoxin into medial hypothalamus or periaqueductal gray matter: cholinergic or GABAergic mediation?

Microinjections of various doses (50-300 ng) of the nicotinic antagonist D-tubocurarine (TUBO) into the rat's medial hypothalamus (MH) or dorsal periaqueductal gray (PAG) produced flight reactions characterized by jumps. Two different types of flight reactions were produced depending on whether the drug was injected into the MH or into the PAG. MH injections provoked an increase in both locomotor activity and rearing together with well-oriented jumps. PAG injections provoked either freezing reactions or running with explosive jumps, but no increase in rearing. In addition, the rat exhibited an asymmetry in responsiveness to tactile stimulation. These reactions also differed depending on whether the drug was injected into the dorsal or ventral PAG. Behavioral reactions similar to those produced by TUBO were also produced by microinjection of the GABA receptor antagonist bicuculline into the same brain sites. Among the 4 putative cholinergic antagonists tested under the same conditions only alpha-bungarotoxin produced effects that were qualitatively similar to those induced by D-tubocurarine or bicuculline. Gallamine and hemicholinium produced tremor when injected into sites located near the ventricular system at either the MH or the PAG level, while vocalizations were only produced by PAG injections. Hexamethonium produced no marked effect. The hypothesis that flight reactions induced by D-tubocurarine or alpha-bungarotoxin do not result from their antinicotinic action but rather from a direct effect on GABAergic transmission is discussed.

Acetylcholine

Behavioral effects of microinjections of SR 95103, a new GABA-A antagonist, into the medial hypothalamus or the mesencephalic central gray.

The behavioral effects of unilateral microinjections of SR 95103, a new GABA-A receptor antagonist, into periventricular structures were studied. When injected into the medial hypothalamus (MH) or into the dorsal part of the mesencephalic central gray (CG), SR 95103 produced a dose-dependent behavioral activation together with jumps. However, the characteristics of this behavioral activation differed according to whether SR 95103 was injected into the MH or into the CG. The behavioral activation was found to be attenuated by pretreatment with THIP, a GABA receptor agonist. When injected into the CG or into the deep layers of the superior colliculus, SR 95103 proved to affect the rat's reactivity to tactile stimuli as evidenced by ipsilateral 'neglect' combined with contralateral hyperreactivity expressed as withdrawal reactions and jumping. Similar results were obtained following microinjections of bicuculline methiodide at the same sites. These data confirm that in both the MH and the CG, GABA-A receptors are involved in the neural control of the generation and/or expression of aversive effects. The data further suggest that at the level of the CG and the deep layers of the superior colliculus, GABA is also involved in the gating of sensory information towards the substrate underlying the generation of such aversive effects.

Animals

Enhanced sensory convergence to the visual cortex in the rodless (rd/rd) mouse.

The rd/rd mutation provokes a specific degeneration of the photoreceptive cells in the mouse retina, without affecting other neuronal elements. This degeneration starts 8 to 10 days after birth. Discriminative learning experiments have shown the degenerated retina to remain light-sensitive, the sensitivity being reduced to 10(-5) of normal with a peak still at 500 nm. An ontogenetic study showed a progressive vanishing of visual potentials (electroretinogram and visual evoked potentials) during the third week of life. Potentials of auditory origin, which can be recorded from the visual cortex in normal mice, were found to be clearly facilitated by the absence of the visual input either because of retinal degeneration in rd mouse or provoked by enucleation at birth.

Animals

High-energy phosphate compounds in slow-twitch and fast-twitch muscle fibres. Changes during exercise in some neuromuscular diseases.

Concentrations of the high-energy phosphates, ATP and creatine phosphate, were investigated in slow-twitch (ST) and fast-twitch (FT) muscle fibres of patients with myotonia congenita (n = 6), dystrophia myotonica (n = 5), myopathia ocularis (n = 2) and hyperornithinemia with gyrate atrophy (HOGA) (n = 3) and compared with those of normal subjects (n = 4). At rest, the patients with HOGA had lower values of ATP in ST muscle fibres than the controls (P less than 0.05). They also had lower values of creatine phosphate in these fibres than the patients with dystrophia myotonica (P less than 0.03) and myotonia congenita (P less than 0.05). After 30 s bicycle ergometer exercises there was an increase in ATP in the ST muscle fibres of the patients with myotonia congenita, but in all other patient groups there was a decrease.

Adenosine Triphosphate

Effects of hypothalamic lesions on central gray stimulation induced escape behavior and on withdrawal reactions in the rat.

The effects of unilateral--medial or lateral--hypothalamic lesions were studied with regard to both switch-off (i.e., escape) responding induced by central gray (CG) stimulation and responsiveness of the same animals to peripherally-applied electrical or thermal stimulation. Medial hypothalamic (MH) lesions were found to reduce--but not abolish--the efficiency of CG stimulations applied on the side of the MH lesion, while the efficiency of contralaterally applied CG stimulations remained unchanged. Furthermore, such lesions enhanced the responsiveness to peripheral nociceptive stimuli on whatever body side they were applied. Lateral hypothalamic lesions were found to only slightly--or not at all--affect the efficiency of CG stimulations, while they enhanced the responsiveness to peripheral nociceptive stimuli on either side of the body. These results suggest that the hypothalamus does not exert a univocal control over both centrally induced escape behavior and peripherally induced withdrawal reactions.

Animals

Morphine applied to the ventral tegmentum differentially affects centrally and peripherally induced aversive effects.

In the rat, a microinjection of 15 nmoles of morphine into the ventral tegmentum (VT) was found to suppress escape responding induced by electrical stimulation applied to the dorsal part of the mesencephalic central gray. This suppressant effect could be reversed by a systemic injection of naloxone and was unlikely to be due to gross motor impairment since morphine injected into the VT provoked a behavioral activation. A similar microinjection of morphine into the VT did not induce analgesic effects since it did not affect the reaction thresholds to a nociceptive stimulus. The mechanisms underlying these differential effects of morphine applied to the VT are discussed.

Animals

Hereditary recurrent brachial plexus neuropathy with dysmorphic features.

A Finnish pedigree comprising 13 members in 3 generations with recurrent brachial plexus neuropathy is described. The disease was characterized by repeated attacks of pain in the upper limb/shoulder region, followed by muscle weakness and atrophy. The first episode usually occurred in childhood after a mild infection. Symptoms varied in intensity and seldom left marked neurological deficiencies. Patients had typical features including hypotelorism, small palpebral fissures and a small oral opening. The distribution of the affected members in the pedigree was compatible with autosomal dominant inheritance with high penetrance. Despite the limitation of the symptoms to the upper limbs, sural nerve biopsy showed tomaculous neuropathy in an affected member of the family. The structural changes of tomaculous neuropathy probably reflect a genetically determined generalized abnormality of the Schwann cells predisposing the patients to the recurrent palsies by exogenous factors.

Abnormalities, Multiple

Central gray and medial hypothalamic stimulation: correlation between escape behavior and unit activity.

A chronic experiment and an acute one were carried out in the same rat in order to get information on the neuronal events correlated with the escape latency (EL) induced by an electrical stimulation in the mesencephalic central gray (CG) or in the medial hypothalamus (MH). Escape latencies as well as unitary MH and CG neuronal responses (104 units in 25 rats) were studied as functions of the intensity and the pulse duration of a 50 pulses/sec stimulation train. The CG and/or the MH neuronal firing rate was either synchronized or diffusely altered, either inhibited or activated, by the CG or the MH stimulations. Many neuronal firing rate alterations were highly correlated with the escape speed (ES = 1/EL) induced by the same stimulation. Intensity duration trade-off functions were computed from both the EL and the unit recordings. Chronaxie determinations were performed from these data: the behaviorally determined chronaxies did not differ from the unitary ones (limit values: 0.05-0.42 msec). The discussion bear on the possible role of the observed neuronal alterations induced by CG or MH stimulations in relation to their behavioral effects.

Animals