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J Micheau

Publications and source records attributed to J Micheau.

28 records · Page 2Linked to original sources
PubMed1993

Relationships between testing-induced alterations of hippocampal cholinergic activity and memory performance on two spatial tasks in mice.

Alterations in hippocampal cholinergic activity associated with different types and/or stages of learning were explored using measures of sodium-dependent high-affinity choline uptake (SDHACU) in the hippocampus of C57BL/6 mice. Animals were divided into 'active' subjects submitted to memory testing before being killed and 'quite' controls. 'Active' subjects were trained in a radial-arm maze on either a discrimination task (mixed Working Memory (WM)-Reference Memory (RM) task) or a Delayed-Non-Matching-To-Place task (more selective WM-task). In the discrimination task mice were sacrificed after either the 1st, 2nd, 3rd or 9th daily session of training and at intervals of either 30 s, 15 min, 24 h or 9 days post-test. In the DNMTP-task all subjects of the 'active' groups were sacrificed after 12 days of training at either 30 s or 24 h post-test. Results showed that: (1) Both types of training induced an immediate (30 s post-test) increase of hippocampal SDHACU as compared to 'quite' control condition. (2) In the discrimination task, this immediate increase in SDHACU was followed by a decrease leading to a long-lasting (24 h and 9 days) inhibition of this cholinergic marker. This secondary decrease in SDHACU occurred earlier (15 min post-test) at the end (9th session) than at the beginning (1st-3rd sessions) of training. Thus, as training progressed there was a shortening of the testing-induced cholinergic activation. (3) By contrast, in the DNMTP-task, SDHACU was still increased at the interval of 24 h following the last session of DNMTP-training. (4) The amplitudes of both the immediate (30 s) increase and subsequent secondary (15 min) decrease in SDHACU after the last (9th) session of discrimination training were significantly related to the rate of acquisition and behavioural profile for individual animals. Subjects that had displayed better response accuracy across the 9 days of training exhibited the highest SDHACU at 30 s post-test and the lowest at 15 min post-test. These results are discussed in the context both of previous findings on the effects of training on cholinergic activity, and of contemporary models of hippocampal function. It is suggested that (1) an increase in hippocampal cholinergic transmission during testing would facilitate the acquisition of a 'relational' kind of informations (spatial WM and RM); (2) the post-training consolidation (spatial RM) of information would be facilitated by a decrease and long-lasting inhibition of hippocampal cholinergic activity.

Animals↗
PubMed1992

Age-related changes in cortico-releasing factor, somatostatin, neuropeptide Y, methionine enkephalin and beta-endorphin in specific rat brain areas.

We investigated the age-related changes in the tissular protein, cortico-releasing factor (CRF), somatostatin (SOM), neuropeptide Y(NPY), methionine enkephalin (M-ENK) and beta-endorphin (beta-END) levels in frontal cortex, hippocampus, striatum and hypothalamus of young (4-month-old), mature (18-month-old) and senescent (26-month-old) Wistar male rats, bred in a specific pathogen free environment. Between the age of 4 and 18 months, the tissular protein levels increased in all 4 structures studied. The CRF and SOM levels increased in the hippocampus, while the NPY levels decreased. During this time, the NPY content increased in the striatum, whereas the SOM and M-Enk striatal levels decreased. Concomitantly, the NPY and beta-End levels decreased in the hypothalamus. Interestingly, no significant variations were found to occur in the frontal cortex whatever the neuropeptide studied. Between the age of 18 and 26 months, no significant changes in the tissular protein levels were detected, except in the hippocampus. The changes in the neuropeptide concentrations observed during this period depended on the neuropeptide and the brain structure studied. The CRF and beta-End levels decreased in the frontal cortex and the hypothalamus, respectively. The NPY peptidergic systems seem to be preferentially affected by aging processes since 3 out of the 4 structures studied--the frontal cortex, the striatum and the hypothalamus--showed a decrease in their tissular NPY content. During the same period, none of the 5 neuropeptides studied were affected in the hippocampus.

Aging↗
PubMed1992

Memory deficits following chronic alcohol consumption in mice: relationships with hippocampal and cortical cholinergic activities.

Chronic ethanol consumption (12% v/v for 12 months) produced an accelerated decay of T-maze spontaneous alternation (SA) rates as the interval that elapsed between forced trials, used as acquisition, and a free test trial, used as a retention test, increased. Thus, alcohol-treated mice that exhibited normal SA rates at a short interval (5 min) were impaired at the longer one (6 h) relative to controls. This alcohol-induced deficit was almost completely reversed by physostigmine (0.05 mg/kg, IP) given only before the test trial. Parallel neurochemical analysis showed that chronic alcohol intake produced a significant decrease in hippocampal and cortical sodium-dependent high-affinity choline uptake. In particular, the significant cholinergic activation produced by a T-maze exploration in controls was attenuated in experimental subjects so that the between-groups differences already present in the quiet condition were amplified in the active (exploration) state. These findings suggest that the memory deficits induced by chronic ethanol consumption stem from a failure of some cholinergic-dependent retrieval processes. An attempt is made to relate the present results with our previous ones that emphasized the importance of diencephalic damage in alcohol-induced retrieval deficits.

Acetylcholine↗
PubMed1986

The effects of acute intraseptal injection of haloperidol in vivo on hippocampal cholinergic function in the mouse.

Acute injection of haloperidol into the lateral septum in mice produced an immediate and long-lasting increase in hippocampal sodium-dependent high-affinity choline uptake. Parallel electrophysiological investigations revealed that the increased septo-hippocampal cholinergic activity augmented CA1 pyramidal cell excitability and also accelerated the extinction of a conditioned reinforcement. These results constitute further evidence that septal dopaminergic terminals, via their control of septo-hippocampal cholinergic activity play a significant role in the modulation of hippocampal function.

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↗
PubMed1982

[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↗