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D Beracochea

Publications and source records attributed to D Beracochea.

15 recordsLinked to original sources
PubMed2004

BetaCCM enhances retrieval of serial contextual but not of serial spatial memory in mice.

The effects of inverse agonists of the gamma-aminobutyric acid (GABA)/benzodiazepine receptors such as beta-carboline-3-carboxylate (betaCCM) on retrieval processes have not been studied extensively. This study investigates the effects in mice of an acute betaCCM injection on retrieval of previously acquired serial discriminations, involving distinct contextual cues (Contextual Serial Discrimination, CSD) or identical cues (Serial Spatial Discrimination, SSD) in a four-hole board. Animals submitted to CSD were also evaluated for emotional reactivity in an elevated-plus maze. In both the CSD and the SSD tasks, mice were injected with saline before the learning session began. Twenty-four hours later, mice were replaced on the hole-board following a single dose of saline or betaCCM (0.5 mg/kg or 1.5 mg/kg) injected 20 min before testing. The highest dose of betaCCM improved performance of the first discrimination in the contextual task but not in the spatial task. Moreover, the higher dose of betaCCM produced anxiety-like reactivity in an elevated-plus maze, and scores of 'anxiety' were positively correlated with memory scores. Overall, the data show that the betaCCM enhancement of memory processes depends on: (1) the cues associated with the to-be-remembered information; and (2) the emotional effects of the drug.

Animals↗
PubMed2000

Deficits of spatial and non-spatial memory and of auditory fear conditioning following anterior thalamic lesions in mice: comparison with chronic alcohol consumption.

This study was aimed at determining (i) whether or not bilateral subtotal lesions of the anterior thalamic nuclei (ATH) in rodents produced memory deficits for spatial and/or non-spatial information and of auditory fear conditioning, and (ii) if these eventual deficits resemble those produced by chronic alcohol consumption (CAC). Working memory was assessed using both spatial (spontaneous alternation) and non-spatial (temporal alternation) delayed response tasks. Results showed that ATH lesions induced delay-dependent memory impairments in both spatial and non-spatial alternation tasks, as well as a decreased level of auditory and background contextual fear conditioning compared with respective controls. CAC did not induce accelerated rate of forgetting in the spatial and non-spatial tasks, but increased the vulnerability to interference in the spatial task. CAC impaired only background contextual fear conditioning. We conclude that ATH nuclei are involved in the maintenance of information over time, regardless of the nature (spatial vs. non-spatial) of the information, and play a role in associative processes for both unimodal (the tone) and polymodal (contextual) information. In contrast, ATH dysfunction does not account for the memory disorders induced by the CAC treatment. Our results contribute to showing that the functional overlap between the structures comprising the hippocampo-mamillo-thalamic pathway is only partial.

Acoustic Stimulation↗
PubMed1996

Reduction of regional brain glucose metabolism following different durations of chronic ethanol consumption in mice: a selective effect on diencephalic structures.

The effects of chronic alcohol consumption on regional brain glucose metabolism were examined in Balb/c mice using the [14C]2-deoxyglucose autoradiographic technique. Animals were given a solution of 12% v/v ethanol as their only source of fluid for either 6, 12 or 18 months and compared to control groups receiving either an isocaloric solution or saccharose or tap water. Alterations of cerebral brain glucose metabolism were assessed in mice who were returned to a non-alcoholic diet and allowed to freely explore a T-maze. The results showed that chronic ethanol consumption induced reductions of regional metabolic activity which were functions both of the duration of alcohol treatment and of the structure studied. Whereas a six month period of alcoholization did not induce any significant effects on metabolic activity, 12 months of treatment were necessary to induce the first observable and significant reductions in [14C]2-deoxyglucose labelling. These effects were mainly limited to diencephalic structures such as the lateral mammillary nuclei and the anterodorsal thalamic nuclei. The cerebellum was also affected but to a lesser degree. After 18 months of alcoholization, a generalized spread of the metabolic reduction to the entire mammillary complex (lateral, medial and posterior nuclei) and to the thalamic nuclei was observed. This same duration of treatment was necessary to induce the first detectable decrease of metabolic activity in the hippocampus. In agreement with data from human neuropathology, these findings confirm the particular vulnerability of diencephalic structures to ethanol and suggest that damage limited to diencephalic regions rather than to hippocampal or cortical areas could be primarily responsible for the memory disorders observed in Korsakoff's syndrome.

Alcohol Drinking↗
PubMed1993

Extended temporal gradient for the retrograde and anterograde amnesia produced by ibotenate entorhinal cortex lesions in mice.

Effects of ibotenic entorhinal cortex (EC) lesions on both retrograde and anterograde amnesia in mice were assessed using two-choice discrimination tasks learned at different intervals before surgery in two eight-arm radial mazes. The results indicated that EC-lesioned mice were severely impaired in postoperative retention of discrimination problems learned 3 d or 2 weeks prior to surgery, but showed no deficit on problems learned between 4, and up to 6 weeks before surgery, as compared to sham-operated controls. When trained on a novel two-choice discrimination problem (not acquired preoperatively), experimental subjects demonstrated quite normal rates of acquisition, but were impaired in learning its reversal. Furthermore, they exhibited a faster rate of forgetting (anterograde amnesia) relative to controls over a 2-week retention interval. These results indicate that approximately 4 weeks is required before memory for a two-choice spatial discrimination problem no longer depends on the integrity of the entorhinal cortex, and suggests that, beyond this time, an EC-independent memory storage system is capable of supporting the retrieval of information. The data, together with complementary behavioral results, are discussed in the context of current theories of memory storage.

Amnesia↗
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↗
PubMed1991

Effects of chronic ethanol consumption associated or not with experimental anterior thalamic lesions on spontaneous sequential alternation in mice.

Previous studies from our team have shown that a 12 month ethanol administration induced deficits in a sequential alternation task, whereas a 6 month treatment had no effects. We have already shown that the 12 month treatment induced deficits both in diencephalic and hippocampal structures, whereas the 6 month treatment damaged only the mammillary bodies. Thus, the question remained whether or not increasing selectively the diencephalic damage by lesioning the anterior thalamic nuclei would disrupt sequential alternation in 6 month ethanol-treated mice. Results indicate that alcohol-treated mice exhibiting experimental lesions into the anterior thalamus were significantly impaired in the sequential task as compared to both controls or 6 month ethanol-treated mice. In contrast, anterior thalamic lesions in normal (no alcohol treatment) subjects induced no deficits. The relative contribution of the hippocampo-mammillo-thalamic circuitry in sequential alternation is discussed.

Afferent Pathways↗
PubMed1991

Differential effects of chronic ethanol consumptions or thiamine deficiency on spatial working memory in Balb/c mice: a behavioral and neuroanatomical study.

This study was aimed to compare the effects of either a thiamine deficiency or a chronic ethanol consumption on memory and on neuronal density within the median mammillary nucleus. Results showed that alcohol-treated (48 weeks) mice exhibited a behavioral impairment in a sequential alternation task characterized by a progressive decay of alternation rates as a function of the number of trials; such a deficit was not observed in controls and thiamine-deficient subjects. A quantitative analysis using histological sections showed an important reduction of neuronal density within the mammillary bodies following the alcohol treatment but not following thiamine deficiency.

Alcoholism↗
PubMed1990

Age-related changes in the subcortical afferents to the medial frontal cortex in mice: a WGA-HRP study.

The subcortical afferent projections to the mediodorsal part of the frontal cortex were studied both qualitatively and quantitatively in young (3 months), adult (12 months) and aged (22 months) Balb/c mice by means of the retrograde transport of wheat germ agglutinine-horseradish peroxidase (WGA-HRP). A progressive decrease in the number of afferents was observed during aging with a differential pattern of reduction as a function of the subcortical structures. In adult mice a large reduction of afferents occurs in the diagonal band of Broca, the posterior thalamic nucleus, the zona incerta, the lateral hypothalamic area, the nuclei of amygdaloid complex, the posterior hypothalamic nucleus, the reticular pontine nucleus, the dorsal and medial raphe nuclei and the dorsal tegmental nucleus. In aged animals, only the anteromedial and mediodorsal thalamic nuclei, as well as the locus coeruleus appear to be clearly affected.

Aging↗
PubMed1987

Neuroanatomical effects of chronic ethanol consumption on dorsomedial and anterior thalamic nuclei and on substantia innominata in mice.

Quantitative analysis, using histological sections, showed that chronic ethanol consumption for 7 months produced a weak but significant cellular loss in the dorsomedial thalamic nucleus, anterior thalamus and substantia innominata in the mouse. These results are in agreement with patterns of neuroanatomical damage observed in human alcoholics.

Animals↗
PubMed1987

Build-up and release from proactive interference during chronic ethanol consumption in mice: a behavioral and neuroanatomical study.

Male mice of the BALB/c strain were given a solution of 15% ethanol as their only source of fluid during either 24 or 48 weeks. They were submitted to a sequential alternation (SA) task in a T-maze (6 successive trials). It was found that 48 but not 24 weeks of alcohol administration lead to a deficit as compared to pair-fed or tap-water controls. Whereas experimental mice performed as well as controls on the first 3 choices, they exhibited a gradual decrease in the SA rate on subsequent trials. We suggest that this deficit might result from an exaggerated vulnerability to proactive interference (PI). In order to further test this hypothesis, a second experiment investigated whether a between-trials variation of context of the maze would increase performance. It was found that the SA rate improved as soon as the variation was provided (5th trial). We suggest that the deficit of experimental mice results from an impairment of retrieval processes. A neuroanatomical study was conducted to quantify cell losses resulting from 8, 24 or 48 weeks of ethanol treatment in the mammillary bodies (MM) or the hippocampus (HPC). At the time of appearance of the deficit, MM exhibited a -32% cellular loss, whereas this was only -18% in the HPC. This result emphasises the importance of MM lesion in memory deficits resulting from long-term alcohol consumption.

Alcohol Amnestic Disorder↗
PubMed1986

On the involvement of the central cholinergic system in memory deficits induced by long term ethanol consumption in mice.

Male mice of the BALB/c strain were given a solution of 12% v/v ethanol as their only source of fluid for 7 months. Memory performance was tested after ethanol was omitted from the diet for 3 to 9 weeks, and was compared with performance of control animals (no ethanol) which had been pair-fed or had received tap water. The spontaneous alternation task that was used consisted of two forced trials (acquisition) followed, at varying intervals ranging from 30 sec to 6 hr, by a free test trial (retention). Experimental subjects exhibited an accelerated rate of decay of spontaneous alternation, reaching chance level at 6 hours. All animals were then tested at this 6-hour interval following injections of either physostigmine or neostigmine that were given before both acquisition and retention (0.05 mg/kg IP). Results showed that physostigmine, but not neostigmine, dramatically improved performance of alcohol-treated subjects. Parallel neurochemical analysis showed that chronic ethanol treatment induced a slight (12%) but significant decrease in hippocampal sodium-dependent high affinity choline uptake. Though these findings suggest that the observed memory deficits (i.e., an accelerated rate of forgetting) might be related to a cholinergic dysfunction, alternative explanations are also proposed.

Alcoholism↗
PubMed1985

Memory deficits subsequent to chronic consumption of alcohol in mice: an analysis based on spontaneous alternation behavior.

Male mice of the BALB/c strain were given a solution of 15% ethanol as their only source of fluid for periods varying from 5 weeks to 8 months. For behavioral testing, they were compared with control groups which had received either an isocaloric solution of sucrose or tap water. Memory was tested by using spontaneous alternation behavior in a T maze. Each test consisted of two forced trials (acquisition) followed by a free trial (test) given at different acquisition--test intervals (from 30 s to 24 h). Results from two independent experiments showed that after 25 weeks of ethanol administration there was an accelerated rate of decay of spontaneous alternation as a function of the acquisition--test interval. Such a phenomenon persisted after ethanol was omitted from the diet. A third experiment showed that when tested on two successive sessions separated by a 5 h interval, experimental subjects exhibited a decreased ability to perform normally on the second test. Our data are interpreted as showing that long-term ethanol administration results in accelerated forgetting and increased vulnerability to proactive interference and, as such, they are compared to the memory dysfunctions observed in amnesic patients.

Alcohol Drinking↗
PubMed1984

Chronic ethanol consumption induces neuronal loss in mammillary bodies of the mouse: a quantitative analysis.

Quantitative analysis, using histological sections, showed that chronic ethanol consumption in the mouse produced neuronal loss in the medial mammillary bodies. This cellular loss was not uniform and was more marked in posterior (-30.1%) than in anterior (-8.8%) parts. Moreover, a reduction of the nucleus diameter of the remaining neurons was found. These results are in agreement with patterns of neuroanatomical damage observed in human alcoholics.

Alcoholism↗
PubMed1983

[Accelerated forgetting and increased proactive interference after long-term alcohol consumption in the mouse].

Male Mice of the BALB/c strain were given a solution of 15% ethanol as its only source of fluid for 8 months. 2 months after alcohols was omitted from the diet they were tested for memory and compared to two control groups which received either an isocaloric solution of sucrose or tap water. Memory was tested by using spontaneous alternation (S.A.) in a T maze as a learning paradigm involving two forced trials (acquisition) followed by a free trial (retention). The 1st experiment was aimed at studying the spontaneous alteration rate as a function of the acquisition-test interval. It was found that for a short interval (5 min) the S.A. rate did not differ between the experimental aid control subjects but that it decreases more rapidly over time (1 h and 24 h) in alcohol treated subjects. The second experiment was aimed at determining whether this accelerated forgetting might not be explained by an excess of proactive interference. Results showed that when experimental subjects remembered for 1 h informations associated with a first acquisition, they were no longer able to remember those associated with a second acquisition when the interval between the two acquisitions was 5 h. Such proactive interference was not found in control subjects. These results suggest that, as in humans, prolonged alcohol consumption results in accelerated forgetting and increased proactive interferences.

Alcoholism↗