Biomedical subjects

José Javier Miguel-Hidalgo

Publications and source records attributed to José Javier Miguel-Hidalgo.

3 recordsLinked to original sources

PubMed2006

Withdrawal from free-choice ethanol consumption results in increased packing density of glutamine synthetase-immunoreactive astrocytes in the prelimbic cortex of alcohol-preferring rats.

Excess activation of glutamatergic neurotransmission in the cerebral cortex following ethanol withdrawal is considered to contribute to significant behavioural disturbances, and to alcohol craving. Astrocytes may play a role in these manifestations because astrocytes are essential in the regulation of released glutamate and its conversion to glutamine through the enzyme glutamine synthetase (GS). However, it is unclear if withdrawal from free-choice ethanol drinking causes changes in the numbers of astrocytes expressing GS or the cytoskeletal protein of astrocytes glial fibrillary acidic protein (GFAP). Alcohol-preferring (P) rats exposed to free-choice ethanol drinking were either maintained without forced interruption of ethanol drinking, subjected to a 3-day withdrawal period at the end of 2 months, or subjected to three 3-day withdrawal periods along 6 months. At 2 months, P rats were also compared with alcohol-naïve alcohol non-preferring rats (NP) rats. Packing density of GS and GFAP-immunoreactive (IR) astrocytes was measured in sections from the prelimbic cortex (PLC) using the optical disector probe. An alcohol deprivation effect was observed in P rats with withdrawals during a 6-month ethanol drinking period. Ethanol withdrawal significantly increased the packing density of GS- and GFAP-IR astrocytes in the PLC of P rats as compared with P rats with continuous access to ethanol. In addition, there was a positive correlation between the pre-withdrawal ethanol consumption and the packing density of GS-IR astrocytes. The present results suggest the involvement of astrocytes in the regulation of the glutamatergic activation associated with withdrawal from free-choice ethanol consumption and point to differential adaptations of GS and GFAP to prolonged alcohol drinking in the PLC of P rats.

Alcoholism↗

PubMed2002

Glia pathology in the prefrontal cortex in alcohol dependence with and without depressive symptoms.

BACKGROUND: Reductions in glial density and enlargement of glial nuclei have been reported in the dorsolateral prefrontal cortex (dlPFC) in mood disorders. In alcohol dependence, often comorbid with depression, it is unclear whether there are changes in the density and size of glial cells in the dlPFC. METHODS: The packing density and size of Nissl-stained glial cell nuclei were analyzed postmortem in the cortical layers of the dlPFC from 21 control and 17 alcohol-dependent (Alc) subjects without Wernicke or Korsakoff syndromes. Eight Alc subjects had depressive symptoms. The density of glial cells was measured with a three-dimensional cell counting method, and the areal fraction of glial fibrillary acidic protein immunoreactivity (GFAP) was also determined. RESULTS: Glial density was reduced by 11-14% in layers V and VI and in all layers combined in the Alc group. The size of glial nuclei was decreased by 3.2% in Alc subjects. The Alc subjects with depressive symptoms showed the lowest values of density and size. There was no difference in GFAP immunoreactivity, although the lowest values were in the Alc group. CONCLUSIONS: Alcohol dependence is characterized by decreases in both density and size of glia in the dlPFC. Glial pathology may be more severe in Alc subjects with depressive symptoms.

Adolescent↗

PubMed2002

Morphological brain changes in depression: can antidepressants reverse them?

Structural neuroimaging and postmortem histopathological studies of the brain have revealed morphological changes in cortical and subcortical regions in individuals diagnosed with depression. Moreover, these regions are known to be functionally altered in mood disorders. This indicates that the morphological changes might be directly involved in the pathophysiology of depression, and implies that antidepressants may be able to regulate or reverse the detected structural abnormalities. Work with animal models has shown that antidepressants are capable of inducing structural alterations in dendrites and axons and changes in the numbers of neural cells. However, there have been no studies in the human brain that have directly addressed whether antidepressant treatment can reverse or regulate the depression-related structural changes. Nevertheless, experience with lithium in bipolar disorder and antipsychotics in schizophrenia suggests that treatment with psychotropic drugs can result in structural changes that are consistent with reversion towards normal values. Clearly, ascertaining the role of the reversal of structural changes in the therapeutic actions of antidepressants will require further longitudinal studies and careful comparisons between those patients with mood disorder who are treated with antidepressants and those who are not.

Animals↗