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C Destrade

Publications and source records attributed to C Destrade.

At least 37 records · Page 2Linked to original sources
PubMed1991

Time-dependent sequential increases in [14C]2-deoxyglucose uptake in subcortical and cortical structures during memory consolidation of an operant training in mice.

Previous results have suggested that memory processing may involve the sequential activation of subcortical and cortical structures. To study this phenomenon, we have examined the immediate (15 min) and delayed (220 min) metabolic changes produced in BALB/c mice by a partial training session in a bar-pressing appetitive task, using the [14C]-2-deoxyglucose (2-DG) relative glucose uptake method. These relative metabolic changes were compared to the ones produced in several control groups: untrained animals, sham-conditioned animals, overtrained animals, and animals forced to walk on a moving belt (immediate and delayed condition). Animals were given a single intrajugular injection (5 microCi) of 2-DG either 5 min before or 3 h (delayed condition) after the second training session. Forty minutes after the 2-DG injection, the animals were sacrificed and their brains processed for autoradiography. At the 15-min delay, a large 2-DG labeling increase was found in partially trained animals for various subcortical areas (septum, diagonal band, hippocampus, thalamus, and mammillary bodies) while a much smaller increase was found in four cortical areas (frontal, cingulate, parietal, and sensory motor cortices). At the 220-min delay, we observed a large 2-DG labeling increase in cortical (frontal, pyriform, and cingulate cortices) and subicular areas while a moderate 2-DG labeling increase was observed in entorhinal cortex and the diagonal band. These results show that, shortly after training, subcortical structures are preferentially activated while cortical structures are much less activated. Three hours later, at a time when retention performances have been shown to improve spontaneously in the same strain of mice and in the same task, cortical structures are highly activated.

Animals↗
PubMed1991

Locomotor bias produced by intra-accumbens and intracaudate injection of polyclonal dopamine anti-idiotypic antibodies.

The preceding article described anti-idiotypic antibodies to conjugated dopamine (AIDA); results were consistent with the hypothesis that these antibodies contained the internal image of conjugated dopamine (DA-G-BSA) and binded to dopamine (DA) receptors. We further tested these anti-idiotypic antibodies to conjugated dopamine by examining the functional changes produced by unilateral injection of AIDA (or DA-G-BSA) into the nucleus accumbens or into the medio-dorsal caudate in mice. Our results showed that unilateral injection of AIDA (or DA-G-BSA) into the nucleus accumbens or into the medio-dorsal caudate produced an ipsilateral locomotor asymmetry in amphetamine-treated animals which was similar to the one produced by unilateral intra-caudate injection of haloperidol (a non-specific DA antagonist). The asymmetry was site specific: injection of AIDA around the nucleus accumbens or into the anterior caudate was not effective. The asymmetry was also shown not to depend on the peripheral injection of amphetamine. Taken together, the present results and those in the preceding article suggest that the AIDA contains the internal image of DA-G-BSA and that these two substances bind to DA receptors to produce behavioral changes.

Animals↗
PubMed1991

[Analysis of kinetics of consecutive metabolic cerebral activations induced by spatial discrimination testing, using (14C)-glucose, in an eight-arm radial maze in mice].

Regional mapping of relative (14C)-glucose (GLU) uptake was analyzed in Balb/c mice at 3 time intervals (5 min., 1 hr., 3 hrs.) after either the first (Day 1) or the last (Day 9) daily sessions of a spatial discrimination testing procedure in an eight-arm radial maze. On Day 1, increased labelling was found 5 min. post-training in subcortical, hippocampal and cortical regions. Decreased GLU uptake was observed 1 hr. later in the same regions, followed at 3 hrs. post-training by a retarded activation in the above areas and particularly in thalamic and cortical structures. On Day 9, there was only an early (5 min.) post-training increase in metabolic activity followed by a subsequent monotonic decrease over 3 hrs. post-training period.

Animals↗
PubMed1990

Memory-improving action of glucose: indirect evidence for a facilitation of hippocampal acetylcholine synthesis.

The effect of a 3 g/kg glucose injection on the velocity of the sodium-dependent high-affinity choline uptake mechanism in the hippocampus was both measured in quiet control mice and in mice immediately after training in an operant bar pressing task. Glucose did not significantly change high-affinity choline uptake in resting animals. High-affinity choline uptake in the hippocampus was increased by training in the operant bar pressing task. Glucose significantly reduced the amplitude of the increase in high-affinity choline uptake observed in the trained animals. Similarly, a 3 g/kg glucose injection also attenuated the increase in high-affinity choline uptake observed in animals injected with 1 mg/kg scopolamine. Finally, a 3 g/kg glucose injection significantly attenuated the amnesia produced by a post-training 1 mg/kg scopolamine injection in mice trained for an operant bar pressing task. These results provide additional evidence for an action of glucose on hippocampal cholinergic activity under conditions of high acetylcholine demand. This action may be mediated via an increase in acetyl coenzyme A availability, one of the precursors of acetylcholine. This facilitative effect of glucose on hippocampal acetylcholine synthesis may constitute the physiological basis for its facilitative action on memory and its attenuation of scopolamine amnesia.

Acetylcholine↗
PubMed1989

Quantitative [14C]2-deoxyglucose study of a functional dissociation between anterior and posterior cingulate cortices in mice.

We have previously shown that lesion of the posterior cingulate cortex (CCP) but not of the anterior cingulate cortex (CCA), produced learning and memory deficits. As a first evaluation of the functional anatomical basis of this dissociation, we used the quantitative [14C]2-deoxyglucose method and electrical brain stimulation to determine the functional connections of the CCA and CCP in mice. CCP stimulation (but not CCA stimulation) produced significant metabolic increases in the hippocampal formation and in the subicular complex. This result is consistent with the hypothesis that learning and memory deficits following CCP lesion may be due to the disruption of functional neural pathways between the CCP and hippocampal structures.

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PubMed1989

[Circling behavior produced by the unilateral intra-accumbens injection of dopaminergic agonist and two dopaminergic antagonists in mice].

Unilateral intra-accumbens injection of apomorphine, a dopaminergic agonist, produced circling contralateral to the site of injection in Balb/c mice. Unilateral intra-accumbens injection of haloperidol and metoclopramide, two dopaminergic antagonists, produced ipsilateral circling. These results support the hypothesis that the dopaminergic receptors in the nucleus accumbens also contribute to the direction of locomotor activity.

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PubMed1988

Improvement of memory for an operant response by post-training glucose in mice.

Previous experiments have shown that a post-training glucose injection can retroactively and non-contingently improve the retention of a previously learned association. To date, the memory-improving action of glucose has only been demonstrated in rats for negatively-motivated tasks. The present experiment sought to generalize these previous results by examining the effects in mice of post-training glucose injections on the retention of an operant bar-pressing response. The results show that post-training glucose can retroactively and non-contingently improve the retention of an appetitively motivated task in mice. There was a U-shaped relationship between the dose of glucose and the effect on memory similar to the ones already observed in rats using negatively motivated training. The implications of these results for an endogenous memory modulation mechanism are discussed.

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PubMed1988

Electrolytic but not ibotenic acid lesions of the posterior cingulate cortex produce transitory facilitation of learning in mice.

The rate of acquisition of 12 Hebb-Williams mazes was studied after restricted bilateral lesions of the anterior (ANT) or posterior (POST) cingulate cortex in BALB/c mice. In a first experiment, animals with electrolytic lesions were tested with the different mazes at 3 time intervals between 19 and 48 days after surgery. The rate of acquisition in POST-lesioned mice was observed to be facilitated at the 2 first time intervals (between days 19-22 and 32-35), but this effect was reversed (impairment) when the test was carried out between 45-48 days postsurgery; no significant effects were observed in ANT-lesioned mice. In a second experiment, the same behavioral paradigm was used in mice with restricted ibotenic acid lesions of the POST cingulate cortex. These lesions had no significant effects on the acquisition of the mazes. A third experiment was carried out to test if the postoperative delay itself contributed to the long latency of the impairment observed in Expt. I. No impairment of acquisition was observed when POST cingulate lesioned animals underwent their first learning session between 45-48 days after surgery; in contrast, a significant facilitation of the performance was observed at this time. These results suggest an involvement of the posterior cingulate cortex, and in particular the cingulum bundle, both in acquisition and long-term memory processes.

Animals↗
PubMed1986

[Anatomico-functional approach to the mechanisms of memory: analysis by deoxyglucose of the limbic activation induced by electric stimulation of the mouse entorhinal cortex].

Previous behavioral studies using post-training electrical stimulation of the brain have suggested that the lateral entorhinal cortex (LEC) is involved in mnemonic processes. In an attempt to characterize in vivo the neural pathways activated by LEC stimulation, regional patterns of uptake of 14C-2-deoxy-D-glucose (2-DG) were assessed in BALB/c mouse brain. The animals were implanted with a bipolar electrode in the LEC and a catheter in the jugular vein. In addition, four animals received an electrolytic lesion of the perforant path (PP) in order to disconnect the LEC from the hippocampus. The LEC was stimulated at subconvulsive intensity for 5 min. before and 30 min. after an injection of 2-DG. Stimulation of the LEC produced significant increases in 2-DG radioactivity in the hippocampus (dentate gyrus, CA3, CA1), subiculum and pre-subiculum. Demonstrable labelling was found in brain areas, beyond the hippocampal formation: piriform cortex, amygdala, cingulate cortex, Diagonal Band of Broca, the medial and lateral septal nuclei and the medial forebrain bundle. After PP lesion, the metabolic activity disappeared ipsilaterally in subiculum, dorsal part of the hippocampus, in some thalamic nuclei and in mammillary bodies, but all other extra-hippocampal labelling was unchanged. These data considered along with our previous behavioral results, suggest that LEC stimulation may act on mnemonic processes by the recruitment of cortical and subcortical extra-hippocampal structures (e.g. amygdala and cingulate cortex) directly or indirectly connected to the entorhinal cortex.

Animals↗
PubMed1986

[Paradoxical transitory facilitation of performance in the Hebb-Williams labyrinth after lesion of the cingulate cortex in mice].

The effects of lesions of the anterior (Ant) or posterior (Post) regions of the cingulate cortex were tested using the closed-field maze tests of Hebb-Williams. Subjects were male BALB/c mice which had received restricted bilateral electrolytic lesions of the Ant or Post cingulate cortex. Their performances in acquisition or retention were compared to those of sham operated mice at different time intervals after the lesion. In a first series of experiments, naive animals were lesioned. The effects of lesions on acquisition were then tested at different time intervals (up to 45 days) after surgery. In a second series of experiments, the animals were lesioned only after prior complete acquisition of the maze tests and tested in a retention paradigm. The results show a differential effect of Ant versus Post cingulate lesions. Ant lesions had no significant effects whereas Post lesions induced a facilitation of performance at time intervals between 19 and 33 days (acquisition paradigm) or 11 and 25 days (retention paradigm). Conversely a reversal (impairment) of the effect was observed when Post animals were tested 28 days (acquisition) or 48 days (retention) after surgery. Taking into consideration the changing nature of the behavioral paradigm used, we suggest that the paradoxical and transitory facilitatory effects of the Post cingulate lesions may indicate that lesioned mice exhibited a greater degree of adaptability in each new learning situation. However, we can also postulate that these facilitatory effects resulted from a difficulty of lesioned mice in addressing long-term memory stores. This would therefore paradoxically protect them from interference generated by the high degree of familiarity in the behavioural testing apparatus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The Hebb-Williams test to assess recovery of learning after limbic lesions in mice.

A scaled-down Hebb-Williams closed-field maze was constructed and adapted for use with mice. In a first experiment, the acquisition performance of the original 12 Hebb-Williams mazes by BALB/c mice was studied in order to re-group the mazes into 3 main groups of difficulty (low, moderate and high). In a second experiment different problems from each class of difficulty were presented at 3 times intervals (between 3 and 7 weeks after surgery) to mice with lesions of the cingulate cortex. The rate of acquisition in lesioned mice was observed to be facilitated between 3 and 5 weeks after surgery for the most difficult mazes. This effect was reversed (impairment) at 7 weeks post-lesion. The observed biphasic behavioral modifications constitute evidence that our present protocol provides a useful tool to evaluate the time-course of changes in learning performance following brain injury.

Animals↗
PubMed1985

Lesion of the temporo-ammonic perforant path facilitates self-stimulation of the lateral entorhinal cortex in mice.

The effect of a lesion of the perforant path (PP) on self-stimulation (SS) of the lateral entorhinal cortex (LEC) was tested in mice between 8 and 21 days after surgery. The current intensities tested ranged between 0 and 80 microA (peak to peak 100 Hz sine-wave). The PP lesion led to a two-fold increase in SS rates at intensities above 30 microA without affecting the baseline SS rates (0 microA) and SS threshold (30 microA). The lesion also led to a significant increase in LEC after-discharge (AD) threshold and eliminated behavioral convulsions during SS testing. The suppression of AD by i.p. Na phenobarbital injection (10 mg/kg) led to a similar increase in SS rates in sham-lesioned mice; there was no difference in PP-lesioned animals. These results might be interpreted as evidence in favor of an independence of the neuronal processes mediating entorhinal and hippocampal reward-related behaviors.

Animals↗
PubMed1985

Chronic administration of sulbutiamine improves long term memory formation in mice: possible cholinergic mediation.

Thiamine deficiency in both man and animals is known to produce memory dysfunction and cognitive disorders which have been related to an impairment of cholinergic activity. The present experiment was aimed at testing whether, inversely, chronic administration of large doses of sulbutiamine would have a facilitative effect on memory and would induce changes in central cholinergic activity. Accordingly mice received 300 mg/kg of sulbutiamine daily for 10 days. They were then submitted to an appetitive operant level press conditioning test. When compared to control subjects, sulbutiamine treated mice learned the task at the same rate in a single session but showed greatly improved performance when tested 24 hr after partial acquisition of the same task. Parallel neurochemical investigations showed that the treatment induced a slight (+ 10%) but significant increase in hippocampal sodium-dependent high affinity choline uptake. The present findings and previous results suggest that sulbutiamine improves memory formation and that this behavioral effect could be mediated by an increase in hippocampal cholinergic activity.

Animals↗
PubMed1985

Physostigmine reverses memory deficits produced by pretraining electrical stimulation of the dorsal hippocampus in mice.

The aim of the present experiments was to test the validity of the hypothesis that presynaptic cholinergic activity has a functional significance for memory formation. The results show that electrical stimulation of the dorsal hippocampus delivered before learning in BALB/c mice which induces a decrease of about 40% in hippocampal choline acetyltransferase (ChAT) activity at the time of learning results in deficits in retention scores in two appetitive learning tasks (operant conditioning in the Skinner box or a spatial memory task using a 4-hole board). In both behavioral tasks intraventricular injection of 1 microgram of physostigmine 20 min before the acquisition session reverses the disruptive effect of pretraining hippocampal stimulation. Our results seem to indicate that the memory deficits produced by pretraining electrical stimulation of the hippocampus result from both a decrease in ChAT activity and a corresponding reduction of acetylcholine availability in the hippocampal formation.

Acetylcholine↗
PubMed1984

Time-dependent effects of posttraining intrahippocampal injections of corticosterone on retention of appetitive learning tasks in mice.

In previous studies we suggested that corticosterone may modulate hippocampal functioning during memory formation. To test this assumption, we studied the effects of posttrial administration of corticosterone (1 microgram) injected bilaterally in the hippocampus. The treatment was applied at different time intervals after the learning session and the retention session took place 24 h later. Using appetitive operant conditioning tasks in a Skinner box, we found that the posttrial treatment 1) did not affect the retention of a continuously reinforced schedule, 2) improved the retention of a successive discrimination learning task, and 3) was still effective when given 3 h after the acquisition of this task, but not after 6 h. Taken together, the results suggest that corticosterone modulates the hippocampal mechanisms involved in behavioral suppression during memory formation.

Animals↗
PubMed1984

Late post-learning effect of entorhinal cortex electrical stimulation persists despite destruction of the perforant path.

In an appetitive learning task in mice, stimulation of the lateral entorhinal cortex (LEC) 30 min after training produced an improvement in retention 24 h later, as well as faster extinction of conditioning. This effect persisted in animals with bilateral lesions of the perforant path. In addition, the threshold for hippocampal after-discharges produced by LEC stimulation was raised significantly in perforant-path lesioned animals. The results indicate a functional dissociation between hippocampal and cortical mechanisms involved in memory consolidation.

Animals↗
PubMed1984

Dissociation of limbic structures by pharmacological effects of diazepam on electrical self-stimulation in the mouse.

The effect of diazepam was tested on self-stimulation (SS) in 21 mice implanted with a bipolar electrode in the lateral hypothalamus (LH), the dorsolateral hippocampus (HPC) or the lateral entorhinal cortex (LEC). Diazepam, injected i.p. in doses of 0.5, 1 and 2 mg/kg, significantly increased SS rates with electrodes in LH while 4 and 8 mg/kg of diazepam had no significant effect. At low doses, similar increases were seen in mice with LEC electrodes but high doses produced a significant suppression. HPC animals showed an almost total suppression of SS beginning at 2 mg/kg of diazepam; lower doses had no significant effect. The results indicate that entorhinal and hippocampal SS are at least partly independent phenomena; in addition, the suppression of SS by moderate doses of diazepam remains specific to the HPC among the brain structures studied to date.

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