Development of evoked responses into self-sustained activity within amygdalo-hippocampal circuitsDéveloppement des réponses evoquées en activité auto-entretenue à l'intérieur des circuits amygdalo-hippocampiens

Spontaneous brain oscillations during states of vigilance are associated with neuronal plasticity due to rhythmic spike bursts and spike trains fired by thalamic and neocortical neurons during low-frequency rhythms that characterize slow-wave sleep and fast rhythms occurring during waking and REM sleep. Intracellular recordings from thalamic and related cortical neurons in vivo demonstrate that, during natural slow-wave sleep oscillations or their experimental models, both thalamic and cortical neurons progressively enhance their responsiveness. This potentiation lasts for several minutes after the end of oscillatory periods. Cortical neurons display self-sustained activity, similar to responses evoked during previous epochs of stimulation, despite the fact that thalamic neurons remain under a powerful hyperpolarizing pressure. These data suggest that, far from being a quiescent state during which the cortex and subcortical structures are globally inhibited, slow-wave sleep may consolidate memory traces acquired during wakefulness in corticothalamic networks. Similar phenomena occur as a consequence of fast oscillations during brain-activated states.

During various states of vigilance, brain oscillations are grouped together through reciprocal connections between the neocortex and thalamus. The coherent activity in corticothalamic networks, under the control of brainstem and forebrain modulatory systems, requires investigations in intact-brain animals. During behavioral states associated with brain disconnection from the external world, the large-scale synchronization of low-frequency oscillations is accompanied by the inhibition of synaptic transmission through thalamocortical neurons. Despite the coherent oscillatory activity, on the functional side there is dissociation between the thalamus and neocortex during slow-wave sleep. While dorsal thalamic neurons undergo inhibitory processes due to the prolonged spike-bursts of thalamic reticular neurons, the cortex displays, periodically, a rich spontaneous activity and preserves the capacity to process internally generated signals that dominate the state of sleep. In vivo experiments using simultaneous intracellular recordings from thalamic and cortical neurons show that short-term plasticity processes occur after prolonged and rhythmic spike-bursts fired by thalamic and cortical neurons during slow-wave sleep oscillations. This may serve to support resonant phenomena and reorganize corticothalamic circuitry, determine which synaptic modifications, formed during the waking state, are to be consolidated and generate a peculiar kind of dreaming mentation. In contrast to the long-range coherent oscillations that occur at low frequencies during slow-wave sleep, the sustained fast oscillations that characterize alert states are synchronized over restricted territories and are associated with discrete and differentiated patterns of conscious events.

The state of resting sleep is associated with a series of oscillations generated in cortical and thalamic networks. A newly discovered rhythm groups the spindle and delta sleep oscillations within slowly recurring (<1 H₂) sequences. Multi-site, extra- and intracellular recordings provide evidence for synchronization of various classes of cell in the neocortex and thalamus during sleep oscillations that might reach paroxysmal levels similar to epileptic states. Sleep oscillations and the underlying synchronizing processes are disrupted during transition to brain arousal.

Neurons become dependent on a supply of target-derived neurotrophins for survival when their axons reach their targets in development. Because the distance axons have to grow varies from one population of neurons to another, the timing of dependence on neurotrophins likewise varies. Although it would be expected that the simplest way of getting the timing right would be for the target to provide a suitable signal to the arriving axons, detailed studies on developing cranial sensory neurons suggest that these neurons are programmed, before differentiation, to acquire dependence at the correct time independently of external signals. Neurons not only partly compensate for different target distances by extending axons more rapidly the further they have to grow, but possess an intrinsic clock that switches on dependence at the right time in accordance with the time it normally takes their axons to reach their targets. Here the experimental evidence for these intrinsic programmes of growth and survival is reviewed, the rationale that might have favoured their evolution is discussed, and parallels are drawn with other developing neuronal systems.

During stereotaxic explorations of patients suffering from intractable temporal or non-temporal epilepsies, isolated electrical shocks could be delivered through depth electrodes to either the amygdaloid nucleus or the hippocampus, recording of the elicited response being performed from hippocampus or amygdala, respectively, on the same side.

All patients displayed hippocampal responses to amygdala stimulation, whatever the type of epilepsy diagnosed. On the other hand, amygdala responses to hippocampal single shocks were only observed in a majority of patients suffering temporal epilepsy, while such back to forth activation could seldom be assessed in a group of patients not clearly characterized as temporal epileptics.

It is suggested that subtle changes in excitability of an (indirect) pathway from hippocampus to amygdala are revealed through this procedure of low intensity, short-lasting stimulation, as a correlate of the temporal epileptic process.

Au cours d'explorations stéréoélectroencéphalographiques effectuées chez des patients souffrant d'épilepsie réfractaire aux thérapeutiques médicamenteuses, on a procédé à des stimulations par choc isolé, du noyau amygdalien ou de la corne d'Ammon ipsilatérale, l'enregistrement s'effectuant dans la corne d'Ammon ou le noyau amygdalien, respectivement. Il est montré que l'hippocampe développe toujours une réponse d'allure assez constante, lors de la stimulation amygdalienne, quel que soit le type d'épilepsie caractérisé par ailleurs chez le sujet. En revanche, des résponses amygdaliennes à la stimulation hippocampique n'ont été observées que chez des patients atteints d'épilepsie temporale; de telles activations n'ont en effet été que rarement notées dans un groupe de patients caractérisés comme épileptiques non-temporaux.

Il est suggéré que l'utilisation de la stimulation électrique isolée révèle ainsi de discrètes modifications d'excitabilité d'une liaison (indirecte) de l'hippocampe vers l'amygdale chez des épileptiques temporaux.

Hippocampus-mammillary body evoked potentials were recorded in awake, unrestrained cats. Electrical stimulation of the basal amygdala with intensities eliciting behavioral reactions depressed the amplitude of the evoked responses. This effect, shown in 31 experiments, lasted for 20 min up to more than 4 hr. The induction of epileptic seizures (n = 5) due to amygdaloid stimulation did not modify the duration of this depression. The effect was specific for the basal amygdala, because stimulation of central amygdala and mesencephalic reticular formation did not alter the hippocampus-mammillary body evoked potentials. Lesions within both basal and central amygdala had no constant effect on the hippocampus-mammillary body evoked potentials. The mechanism underlying the suppression of the hippocampus-mammillary body evoked potentials due to electrical stimulation of the basal amygdala is not dependent on paroxysmal activity within hippocampus and mammillary body, as was shown by depth recordings. It is speculated that this mechanism might have a protective function in the propagation of ictal discharges originating within the hippocampus.