Biomedical subjects

I González-Burgos

Publications and source records attributed to I González-Burgos.

18 recordsLinked to original sources

PubMed2006

Prenatal-through-postnatal exposure to moderate levels of ethanol leads to damage on the hippocampal CA1 field of juvenile rats: a stereology and Golgi study.

Experimental paradigms conducted to assess the neurotoxic effects of ethanol exposure on hippocampus development have yielded controversial findings. Hippocampal CA1 population and some cytoarchitectural parameters of pyramidal cells were studied after exposure to ethanol during early development, in rats. Examination of 30-day-old offspring of rats exposed to moderate levels of ethanol during gestation through lactation showed an increased volume of the hippocampal CA1 field compared to untreated or pair-fed control pups, as well as a reduced number of pyramidal neurons. In addition, the number of spines from surviving CA1 pyramidal neurons was reduced. Furthermore, stubby and wide spines were proportionally increased, while the proportion of mushroom and ramified spines was reduced; no variation in the proportion of thin spines was observed. Because alcoholic women usually drink alcohol before, during, and after pregnancy, a broad-range experimental model of alcohol exposure was used in this study. The present findings show that experimental exposure to moderate levels of ethanol, resembling the human situation in alcoholic mothers, leads to loss of hippocampal CA1 pyramidal neurons, along with several pathological and plastic events in the dendritic arborization of these neurons. Some ethanol-induced excitotoxicity-related mechanisms, which may be underlying these effects, are discussed.

Animals↗

PubMed2005

Neonatal exposure to monosodium glutamate disrupts place learning ability in adult rats.

The activation of glutamatergic NMDA receptors of the hippocampus is closely associated with expression of place learning. Neonatal exposure to monosodium glutamate leads to abnormal expression of NMDA receptor subunits in the hippocampus, but its effect on place learning is unknown. Place learning acquisition and retrieval were assessed in mature adult rats after subcutaneous injection of monosodium glutamate (4 mg/g body weight) in eight neonatal rat pups at postnatal days one, three, five, and seven. Eight untreated rats were used as controls. At four months of age, the rats were challenged over a period of nine days with a place learning task. The task used an acquisition-retrieval paradigm in a Morris maze. Place learning acquisition was impaired in the experimental rats, which were unable to reduce their escape latencies during the nine training days. Controls improved between the fifth and ninth days of training. Test trials showed that retrieval of spatial information was also impaired in the experimental animals. These results show that both place learning acquisition and retrieval abilities in mature rats are impaired by neonatal treatment with monosodium glutamate. These findings may be related to the abnormal expression of NMDA receptor subunits in the hippocampus.

Animals↗

PubMed2005

Cerebellar granule cell and Bergmann glial cell maturation in the rat is disrupted by pre- and post-natal exposure to moderate levels of ethanol.

Migration of the external granular layer cells in the cerebellum of rats was delayed after exposure to moderate levels of ethanol during a pre-gestational period, through gestation and lactation until weaning. After ethanol withdrawal, cell soma and dendrites were observed to be larger in granule cells. Likewise, Bergmann glia showed several cytoarchitectonic features suggesting cell immaturity, as well as some apparent compensatory plastic responses after ethanol withdrawal. These effects may be due to ethanol impairing neurotrophin-mediated processes during cerebellar development that could lead to alterations in Purkinje cell structure and activity, and thereafter in the psychoneural functions in which the cerebellar cortex is involved.

Aging↗

PubMed2004

Density, but not shape, of hippocampal dendritic spines varies after a seizure-inducing acute dose of monosodium glutamate in rats.

Dendritic spines are the main postsynaptic neuronal targets of excitatory inputs in cortical neurons, and both spine density and shape possess a well known adaptive synaptic-stimulation-dependent plastic capacity. Eighteen Sprague-Dawley adult male rats were used. Monosodium glutamate-treated rats (4 g/kg of body weight, i.p.) showed tonic and clonic epileptic seizures, as well as less dendritic spines in the apical arborization of their hippocampal CA1 pyramidal cells, compared to both control groups. No changes were seen in the proportional density of thin, stubby, mushroom-shaped, wide, or ramified spines between groups. Excessive glutamate-mediated excitatory activity on receptors could have led dendritic spines to shrink until they disappeared, while the spine-type proportion may be kept balanced as an adaptive response.

Animals↗

PubMed2002

Place-learning, but not cue-learning training, modifies the hippocampal theta rhythm in rats.

Hippocampal theta activity accompanies behaviours such as running, swimming, head movements and spatially orientated responses in the rat. However, whether a relationship between this activity and information processing exists remains unclear. As place-learning depends on hippocampal integrity, whereas cue-learning does not, the hippocampal theta activity underlying each test was evaluated. Local CA1 hippocampal electroencephalograms (EEGs) were recorded over 6 days in a Morris maze for one place-learning test group of rats (n=10) and one cue-learning test group (n=8). The EEG of the corresponding test was taken during waking immobile, searching, and on-platform stages. The relative power (RP) values of EEGs were divided into 4-6.5Hz, 6.5-9.5Hz, and 9.5-12Hz frequency sub-bands. The place-learning training produced a separation of 4-6.5Hz and 6.5-9.5Hz sub-bands in searching and platform stages and a higher activity on the 6.5-9.5Hz sub-band during searching, compared with the basal record, while the cue-learning group did not show differences related either to the training or behavioural stage. As the motor activity and swimming velocity was similar in both groups, the results strongly suggest that the changes observed in theta activity reflect information processing by the hippocampus.

Action Potentials↗

PubMed2001

Cerebral serotonin depletion induces egocentric learning improvement in developing rats.

Egocentric learning ability of developing serotonin (5-HT)-depleted female rats was evaluated in the Morris maze test. 5-HT depletion was accomplished by a unique intracisternal injection of 5,7-dihydroxytriptamine at 21 days-old. A first behavioral test was applied before the lesion procedure. The animals were thereafter challenged to resolve the same test at 40 and 60 days-old. 5-HT depletion caused a dual effect on the rats' egocentric learning ability, i.e. at 40 days; control rats learned the task while the experimental rats were unable to learn it. At 60 days, control animals were unable to learn the test, while the experimental rats showed a successful performance. These results strongly suggest that 5-HT neurotransmission is necessary for egocentric learning establishment and regulation.

5,7-Dihydroxytryptamine↗

PubMed2001

Neonatal exposure to monosodium glutamate induces cell death and dendritic hypotrophy in rat prefrontocortical pyramidal neurons.

Monosodium glutamate was administered subcutaneously to male neonate rats, and the effects on cell number and cytoarchitecture of third-layer pyramidal neurons from the prefrontal cerebral cortex were studied in the adult. Monosodium glutamate treatment (4 mg/g of body weight, on post-natal days 1, 3, 5 and 7) resulted in fewer neurons, and shorter and less ramified dendritic processes, than those observed in control animals. Both density and proportional shapes of dendritic spines were not modified. We propose a dual effect of neonatal exposure to glutamate: an excitotoxic effect leading to cell death, and; a secondary neuroprotective effect, arising from the proliferation of glial cells and their subsequent uptake of glutamate, that favors the survival of the remaining neurons, and leads to a further hypotrophic effect on their dendritic processes.

Animals↗

PubMed2001

A tryptophan-deficient corn-based diet induces plastic responses in cerebellar cortex cells of rat offspring.

Sprague-Dawley male rats, fed with a tryptophan-deficient and 8% protein corn-based diet were compared with a group of animals fed with 8% protein alone, and with a group fed with Chow Purina containing 23% protein. Retardation of Bergmann glial cell maturation and a concomitant retardation in granule cell migration were observed in the corn-fed group at 21 days. At 30 days of age, the dendrites of granule cells of both hypoproteic and corn-fed groups were larger than those of the Chow-fed animals. At 60 days of age, dendritic arborization of Purkinje cells was more profuse in both the hypoproteic and corn-fed rats compared with the Chow-fed group. This retardation in granule cell migration could be partially due to Bergmann glial cell immaturity. Consequently, several plastic and maybe compensatory events in both granule and Purkinje cells could have occurred, due to tryptophan deficiency resulting from the corn-based diet.

Animal Feed↗

PubMed2000

Prenatal and postnatal exposure to ethanol induces changes in the shape of the dendritic spines from hippocampal CA1 pyramidal neurons of the rat.

20%-ethanol was provided to adult female rats since a pregestational stage until weaning of the pups, and percentage proportion of thin, mushroom-shaped, stubby, or wide spines from the apical dendrite of hippocampal CA1 pyramidal cells, was counted at 15, 21, 40, and 90 days of age. By-kind-of-spine analysis revealed higher fluctuation of experimental spines, and less percentage of thin spines was observed in the ethanol-intoxicated rats concomitantly with a higher proportion of stubby or wide spines; through development. Because thin spines may propagate the synaptic potentials more efficiently than stubby or wide spines, this findings suggest that the electrical excitability and thereafter the firing pattern of those cells may be altered, due to the toxic effects of chronic ethanol ingestion.

Age Factors↗

PubMed2000

Prefrontocortical serotonin depletion results in plastic changes of prefrontocortical pyramidal neurons, underlying a greater efficiency of short-term memory.

The prefrontal cortex activity is involved in organizing the short-term memory. Although the involvement of serotonin for an appropriate performance in learning and memory tests is well known, its role is still unclear; as is the cellular basis of short-term memory behavioral performance. Sprague-Dawley rats were stereotactically injected with 1 microg/microl of 5, 7-dihydroxitryptamine to cause a lesion to the dorsal raphe nucleus. Sham-operated or intact rats were also studied as control groups. Before surgery and 20 days post-operatively, each animal was placed in the Biel maze for five consecutive trials. In the pre-treatment test, all three groups decreased significantly the number of errors beginning with the fourth trial. The same occurred in the post-treatment test, except for the experimental group, whose animals committed less errors beginning with the second trial. After behavioral testing, the dorsomedial prefrontal cerebral cortex was dissected out, and the Golgi study of the third-layer pyramidal neurons revealed that the length of both the apical and the basilar dendrites was smaller than that of controls, and that the apical and oblique dendrites had a greater spine density. A major proportion of thin spines was also seen on the basilar and oblique dendrites, and more stubby spines were seen on the apical dendrite. Serotonin depletion in the prefrontal cerebral cortex resulted in cytoarchitectural alterations of the prefrontocortical pyramidal neurons, which may be underlying partially the greater efficiency observed in the short-term memory behavioral performance.

Animals↗

PubMed1998

Effect of tryptophan restriction on short-term memory.

Several brain regions are involved in the learning process that is integrated from sensorial inputs. It is thereafter consolidated in short- (STM) or long-term memory. Serotonin is strongly related to both types of memory, and particularly, to STM, however, its regulatory role is still unclear. In this study, the effects of tryptophan (TRY) restriction on learning and STM were evaluated. Ten Sprague-Dawley female rats were fed with a TRY-restricted diet (0.15g/100g) starting from postnatal Day 21. At 21, 40, and 60 days of age, 5 trials per animal were carried out in a "hard-floor"-Biel maze, after 24 h of water abstinence. The number of errors per trial were registered before reaching the goal. At both 40 and 60 days, experimental rats committed less errors than controls. Likewise, the TRY-restricted group learned the task from the second trial on, whereas controls did not solve it until the third trial. TRY restriction, and therefore brain serotonin reduction, could impair normal cholinergic activity in some areas such as the hippocampus and the cerebral cortex, where involvement in learning and memory is well documented. Morphological and neurochemical plastic events could also be related to the more efficient performance of the task by the TRY-restricted rats.

Aging↗

PubMed1996

Chronic tryptophan restriction disrupts grooming chain completion in the rat.

Tryptophan restriction in the diet leads to low levels of brain serotonin. Serotonin has been implicated in the magnitude of novelty-induced grooming behavior, but its possible role in self-grooming chain completion has not been investigated. A tryptophan-deficient diet produced fewer chain-associated face washings, more face washings alone, fewer number of chains, as well as elementary units into chains. Thereafter, an apparent lower threshold for emotional responsiveness also took place. Impairments of the serotoninergic inhibitory activity of striatal and/or nigral dopaminergic terminals is suggested, because corpus striatum has been proposed to be an organizer structure of both the serial ordering as well as in the completion of the self-grooming chains.

Aging↗

PubMed1996

Tryptophan restriction causes long-term plastic changes in corticofrontal pyramidal neurons.

A Golgi study of third-layer pyramidal neurons from the corticofrontal cortex of tryptophan-restricted rats was carried out. At 40 days of age, dendritic arborization from treated rats was less profuse than that seen in control rats, and enlargement of dendritic processes, as well as an increase of the number of dendritic spines, were observed in 60-day-old rats. These plastic responses could be mediated either by a decrease in serotonin, which acts on the serotoninergic receptors of pyramidal neurons, or through an indirect mechanism mediated by cortical interneurons, or by serotoninergic modulation of the activity of other cortical neurotransmitters such as acetylcholine. Also, it could represent compensatory mechanisms underlying behavioral performance in some paradigms related to several cognitive processes.

Animals↗

PubMed1995

Serotonin involvement in the spontaneous alternation ability: a behavioral study in tryptophan-restricted rats.

Spontaneous alternation (SA) is controlled by septal cholinergic terminals in the hippocampus. Serotoninergic terminals end on cholinergic nerve endings in the hippocampus, and their possible role in SA was investigated in rats fed with a tryptophan-deficient diet, from weaning to 60 days of age. A T-maze was used for the test. At the age of 40 days, an increase in SA occurred in the tryptophan deficient rats, although this effect disappeared by 60 days of age. A modulatory role of serotonin in the psychoneural control of SA is suggested, and it may be through presynaptic inhibition of hippocampal cholinergic terminals.

Aging↗

PubMed1993

Morphometric characterization of the arcuate nucleus neurons of the rat. A Golgi study.

Six types of neurons were identified and characterized by the Golgi technique in the hypothalamic arcuate nucleus of the rat: non-ramified unipolar, ramified unipolar, non-ramified bipolar, ramified bipolar, small multipolar, and large multipolar. All had few spines, both somatic and dendritic spines. Characterization of the neuronal cytoarchitecture of the arcuate nucleus could be useful in developmental studies under specific experimental conditions.

Animals↗

PubMed1992

Ethological categorization of adult rat motor behavior in an open field.

From 100 rats observed during 1 h, elementary behavioral units were identified, characterized, and behavioral boundaries were established. From this, two main categories were established and named a) basic body postures, and b) posture-associated moving actions. Four subcategories concerning posture-associated moving actions were 1) body-directed actions; 2) actions of interaction with the environment; 3) moving actions without locomotion; and 4) displacement actions with locomotion. This ethological characterization in an open field could be applied to the study of motor effect induced by experimental manipulation of the brain function, at maturity.

Animals↗

PubMed1992

Golgi method without osmium tetroxide for the study of the central nervous system.

A variant Golgi technique was developed that consisted of substituting osmium tetroxide with formaldehyde as the initial fixative in intracardiac perfusion, along with the addition of glacial acetic acid to the chromating fluid. This procedure avoids disposal of dangerous waste substances into the environment. Other advantages include 1) reduction of cost, danger to lab workers, and risk of disruption of the tissue slices during their handling by eliminating the osmium tetroxide, 2) clear tissue background, 3) greater quantity of impregnated neurons than in the classical procedure, with distinct morphological details easily identified even in gross sections and 4) reduction in processing time.

Animals↗

PubMedDate not supplied

Neuroprotective effect of melatonin on brain damage induced by acute global cerebral ischemia in cats.

BACKGROUND: Melatonin has been proposed as a neuroprotective agent on the basis of its ability to function as a free radical scavenger, provided that lipoperoxidation and other free radical damage induced by reactive oxygen species resulting from cerebral ischemia are relevant pathophysiologic processes of ischemic neuronal damage. METHODS: The effects of melatonin or vehicle on neurologic deficit scores (Todd scale; maximal deficit score = 100, daily during 7 days after the ischemic episode) and neuronal population of hippocampal CA1-CA4 fields (cresyl violet stain, at the eighth day after the ischemic episode) were evaluated in adult male cats subjected to a 15-min period of acute global cerebral ischemia induced by cardiorespiratory arrest, and in cats subjected to a sham procedure. Continuous intravenous (iv) administration of either melatonin 10 mg/kg/h in 10% ethanol in saline or the vehicle alone (3 mL/kg/h) for 6 h starting 30 min after the end of the period of global cerebral ischemia was used as treatment. RESULTS: Global cerebral ischemia resulted in a severe loss of neurons in hippocampal CA1-CA4 fields (9, 13, 30 and 28% remaining neurons, respectively) of ischemic vehicle-treated cats in comparison with sham cats (100%). By contrast, remaining neurons in these regions were between 81 and 100% in the ischemic melatonin-treated cats, values that are nonsignificantly different as compared with sham cats. Values of remaining neurons in CA1-CA4 fields in ischemic melatonin-treated cats were significantly higher than those in ischemic vehicle-treated cats. Neurologic deficit scores in ischemic vehicle-treated cats (42-77 at day 1, 6-39 at day 7) were significantly higher than those in ischemic melatonin-treated cats (16-38 at day 1, 0-6 at day 7) on the days after the ischemic episode. CONCLUSIONS: Overall, the results support the neuroprotective effect of melatonin against the neuronal cerebral damage induced by acute global cerebral ischemia.

Acute Disease↗