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C Destrade

Publications and source records attributed to C Destrade.

At least 55 records · Page 3Linked to original sources

[Differentiation of the effects of diazepam on self-stimulation behavior as a function of the structure of the stimulated brain].

The effect of diazepam was tested on self-stimulation in 21 mice with a bipolar electrode in lateral hypothalamus (HL), dorsolateral hippocampus (HPC) or lateral entorninal cortex (CEL). Diazepam at 0.5, 1 and 2 mg/kg significantly increased self-stimulation rates in HL while 4 and 8 mg/kg had no significant effect. Similar increases were seen in CEL mice but high doses produced a significant suppression. HPC animals showed a drastic suppression of self-stimulation beginning at 2 mg/kg of diazepam, lower doses having no significant effect. The results demonstrate that entorhinal and hippocampal self-stimulation involve at least partly independent neuronal mechanisms and point to a possible inhibitory influence of HPC and CEL.

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Functional dissociation between lateral and medial entorhinal cortex in memory processes in mice.

The effects of lesions of the medial or the lateral entorhinal cortex in mice were examined on acquisition, retention and extinction of an operant-conditioning task in a Skinner box. Compared with the control animals, lesions in the medial entorhinal had no behavioral effects whereas lesions in the lateral entorhinal enhanced retention and increased resistance to extinction but did not change acquisition of this task. These results suggest a functional dissociation between the two parts of the entorhinal cortex.

Animals↗

Facilitation of memory consolidation by post-training electrical stimulation of the medial septal nucleus: is it mediated by changes in rhythmic slow activity?

Sinusoidal (100 Hz) electrical stimulation was applied at a weak intensity (7.5 muA peak to peak) through bipolar electrodes located in the medial septal nucleus after partial acquisition of an appetitive operant conditioning task in a Skinner box. Analysis of performance in a retention test 24 hr later showed that (i) the presence of stimulation electrodes by itself impaired retention-test performance, and (ii) electrical stimulation applied 30 sec after the end of the acquisition session improves retention; this facilitatory effect disappeared when the treatment was delayed 15 min. Both impairment and facilitation were found to vary (considerably) among subjects. Electrodes located in the center of the medial septal nucleus led to both a greater impairment in unstimulated subjects and a greater facilitation in stimulated subjects than more anterior placements in the vicinity of the diagonal band. Finally, spectral analysis of hippocampal EEG showed that stimulation had no effect on rhythmic slow activity (RSA). These results are discussed in relation to studies showing that RSA is associated with memory-storage processes and our own hypothesis which underlines the importance of activation of septo-hippocampal cholinergic neurons in the early stages of these mnemonic processes.

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[Evidence for transmitter-specific modulation of slow, rhythmic activity of the hippocampus].

In freely moving male Wistar rats the hippocampal EEG was recorded by using chronically implanted "chemitrodes" (combination of guide cannula and bipolar recording electrodes). A part of the animals received additionally stimulating electrodes in the dorsomedial hypothalamus. In order to characterize specific effects of presumable transmitter substances the hippocampal rhythmic slow activity (RSA) was divided into two types: (1.) slow RSA (5.0 to 7.5 Hz) which occurred spontaneously during orienting behaviour of the animals and (2.) fast RSA (7.5-12.0 Hz) which could be evoked by 100-Hz-stimulation of the hypothalamus. The intrahippocampal depletion of norepinephrine, dopamine, and serotonin did not influence both types of RSA. The alpha-adrenergic antagonist phenoxybenzamine depressed the generation of RSA in a frequency range of 7-8 Hz. The muscarinic agonist oxotremorine caused a long-lasting increase of slow RSA. The latter effect was blocked by the muscarinic antagonist scopolamine. In the same way another muscarinolytic drug (QNB) depressed the spontaneous slow RSA. The intrahippocampal activation of nicotinic receptors inhibited RSA generation, whereas the systemic application of nicotine increased the RSA for a short time. Clonidine which is known to be a noradrenergic agonist at presynaptic alpha-receptors induced a long-lasting slow RSA following intrahippocampal injection. This effect can be discussed as a presynaptic regulation of transmitter release in cholinergic terminals. The results described here support the conclusion that the slow RSA is a sign of a activation of hippocampal muscarinic receptors whereas others of the examined non-cholinergic transmission systems are not involved directly in the RSA generation.

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Is a retrosplenial (cingulate) pathway involved in the mediation of high frequency hippocampal rhythmical slow activity (theta)?

In previous experiments we demonstrated that in rats there are two kinds of hippocampal rhythmical slow activity patterns (RSA or theta) as defined by the dominating EEG frequencies. RSA with a frequency of 6-8 Hz appeared during exploratory behavior (locomotion), whereas stimulation of the dorsomedial hypothalamus (DMH) elicited RSA with frequencies of 8-12 Hz. To determine the neural pathways involved in the mediation of these two types of RSA, local injections of tetracaine were made either in the medial septum or in the cingulate cortex in order to reversibly interrupt the functional activity of these loci. Blockade of the medial septum suppressed the 6-8 Hz 'walking-associated' RSA in the hippocampal EEG, but had no effect on the 8-12 Hz DMH-driven RSA. On the other hand, a tetracaine injection into the cingulate cortex selectively blocked the high-frequency RSA elicited by DMH stimulation, but had no effect on the 6-8 Hz 'walking-associated' RSA. Both effects disappeared between 30 and 90 min after tetracaine injection. We conclude that the DMH-driven RSA is mediated by the cingulum and/or fibers traveling through the cingulate cortex (retrosplenial region) and thus, that this type of RSA operates without septal involvement.

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[Posttrial injections of corticosterone in dorsal hippocampus of the BALB/c mouse facilitate extinction of appetitive operant conditioning in the Skinner box].

Corticosterone was injected bilaterally into the dorsal hippocampus of BALB/c Mice immediately after the first extinction session of an operant conditioning in a Skinner box. Compared with the control animals the Mice that received 1 or 0.1 microgram corticosterone exhibited 24 hrs. later, faster extinction of this conditioning. With a 0.01 microgram dose of corticosterone in each hippocampus we obtained an accelerated extinction during the session. These data suggest that corticosterone modulates hippocampal mechanisms involved in memory processes.

Animals↗

[Facilitation of memory consolidation induced by electrical stimulation of the medial septal nucleus in BALB/c mice (author's transl)].

Sinusoidal (100Hz) electrical stimulation was applied at a weak intensity (7.5microA peak to peak) to the medial septal nucleus after partial acquisition of an appetitive operant conditioning task in a Skinner box. Analysis of performance recorded 24 hrs later during a retention session shows that (i) implantation alone impaired performance; (ii) electrical stimulation applied 30 sec. after the end of the acquisition session improves retention; this facilitatory effect disappears when the treatment is delayed 15 min. Furthermore spectral analysis of hippocampal EEG showed that there was no significant modification of theta rhythms. These results are discussed in relation to studies in the literature which demonstrate that RSA (rhythmical slow activity) is associated with memory-storage processes and our own hypothesis which underlines the importance of activation of septo-hippocampal cholinergic neurons in the early stages of these mnemonic processes.U

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Late post-learning participation of entorhinal cortex in memory processes.

Mice of the BALB/c strain were bilaterally implanted with electrodes in the lateral entorhinal cortex (EC) in order to study the influence of post-trial EC stimulation on memory. The learning task was a food reinforced operant conditioning. At one of several time intervals after a first learning session, the experimental groups were stimulated for 80 s with subseizure current intensity. Testing was carried out 24 h later. In the first experiment, a continuous reinforcement schedule was used. EC stimulation had no effect when applied at the 30-s or 3-h intervals, but surprisingly a 30-min delayed stimulation greatly improved retention compared to performance of non-stimulated animals. In the second experiment, the same paradigm was used in a discriminative operant conditioning task. The same facilitation on retention was observed only with the 30-min delayed stimulation. Compared to previous data with hippocampal or hypothalamic stimulation, the present results reveal that EC is lately involved in memory processes.

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[Facilitation of the retention and acceleration of operant conditioning extinction after cingulate cortex lesions in BALB/c mice].

One week after receiving bilateral electrolytic lesions of the cingulate cortex, BALB/c Mice underwent acquisition, retention and extinction of an appetitive operant-conditioning task in a Skinner box. There was no significant difference between lesioned and control animals in acquisition; however, lesioned mice exhibited improved retention and faster extinction. These results suggest a possible involvement of the cingulate cortex in memory processes.

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[Memory facilitation induced by delayed electric stimulation of the entorhinal cortex in mice].

A subconvulsive bilateral stimulation of the lateral entorhinal cortex has been applied in BALB/c mice at different time intervals after an appetitive operant conditioning task. 24 hrs later, compared to the control subjects, the performance was improved only in animals stimulated 30 min. after the first learning session. No change was observed in animals stimulated 30 sec. or 3 hrs. post-trial. These results suggest that entorhinal cortex is involved rather late in memory processes.

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Changes in hippocampal cholinergic activity following learning in mice.

A short bar-press operant conditioning acquisition session with food reward on continuous reinforcement was shown to induce a decrease (13.5%) of hippocampal choline acetyltransferase activity in mice. Such an effect seems to be specific to this kind of learning since no change was observed in several control groups, including a group of mice submitted to another type of conditioning in the same apparatus. It is suggested that these enzymatic modifications might be responsible for the delayed improvement of performance observed on retention of this task.

Acetylcholinesterase↗

Blockade of high frequency rhythmical slow activity by intrahippocampal injection of a glutamic acid antagonist.

Intrahippocampal injections of glutamic acid diethylester (GDEE) were performed in rats in order to study a possible implication of glutamate in the mediation of high frequency (8-12 Hz) rhythmical slow activity (RSA) elicited by 100 Hz electrical stimulation of the dorsomedial hypothalamus. This 8-12 Hz RSA was selectively and reversibly suppressed in hippocampal EEG 6 min and 15 min after 150 micrograms or 400 micrograms of GDEE, whereas no modifications were found in the low frequency RSA (6-8 Hz) evoked in hippocampus during exploratory behavior.

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