Biomedical subjects

M T Abellán

Publications and source records attributed to M T Abellán.

7 recordsLinked to original sources

PubMed2000

GABAB-RI receptors in serotonergic neurons: effects of baclofen on 5-HT output in rat brain.

The activation of GABAB receptors hyperpolarizes 5-HT neurons and reduces cell firing. In situ hybridization showed the presence of the GABAB-RI receptor transcript in virtually all 5-HT neurons of the dorsal and median raphe nuclei (DR and MnR, respectively) whereas the GAD transcript was present mainly outside these nuclei. The systemic administration of baclofen increased the in vivo 5-HT release in the DR, MnR and several projection areas. As shown previously in the DR, the application of baclofen in the MnR increased the local 5-HT output. Thus, although 5-HT neurons contain inhibitory GABAB-RI receptors, baclofen increased 5-HT release in some brain areas, likely by a preferential action on terminal GABAB autoreceptors in inhibitory inputs to 5-HT neurons. The scarcity of GAD-expressing cells in the DR and MnR suggests that these inputs originate mainly outside these nuclei.

Animals↗

PubMed2000

Dual control of dorsal raphe serotonergic neurons by GABA(B) receptors. Electrophysiological and microdialysis studies.

We assessed the role of GABA(B) receptors in the control of serotonergic (5-HT) neurons of the dorsal raphe nucleus (DRN) by using microdialysis in vivo and intra- and extracellular recording in vitro in the rat. The GABA(B) agonist R(+)baclofen (but not the inactive S(-)enantiomer) enhanced the 5-HT output in the DRN (4. 7-fold at 15 mg/kg s.c.) and, to a much lesser extent, striatum of unanesthetized rats. Phaclofen (2 mg/kg s.c.) antagonized the effects of 6 mg/kg R(+)baclofen in dorsal striatum. Using dual-probe microdialysis, R(+)baclofen (0.1-100 microM) applied in the DRN enhanced the local 5-HT output (4.5-fold at 100 microM) but decreased that in striatum at 100 microM. At concentrations higher than 100 microM there was a moderate decrement in the elevation of 5-HT in the DRN. In midbrain slices, bath R(+)baclofen exerted a biphasic effect on DRN 5-HT neurons. Consistent with a reduced striatal 5-HT release when infused in the DRN, R(+)baclofen (0.1-30 microM) induced an outward current in 5-HT neurons (IC(50) = 1.4 microM). Lower R(+)baclofen concentrations (0.01-1 microM) preferentially reduced GABAergic inhibitory postsynaptic currents induced by N-methyl-D-aspartate (20 microM) in 5-HT neurons (IC(50) = 72 nM). Using extracellular recordings, R(+)baclofen (300 nM) enhanced the ability of NMDA to induce firing in a subpopulation of serotonergic neurons. These results are consistent with a preferential activation by a low concentration of R(+)baclofen of presynaptic GABA(B) receptors on GABAergic afferents that could disinhibit 5-HT neurons and increase 5-HT release.

Animals↗

PubMed2000

Local modulation of the 5-HT release in the dorsal striatum of the rat: an in vivo microdialysis study.

Using in vivo microdialysis in freely moving rats, we examined the involvement of major striatal transmitters on the local modulation of the 5-HT release. Tetrodotoxin reduced the striatal 5-HT output to 15-20% of baseline. The selective 5-HT(1B) receptor agonist CP 93129 (50 microM) reduced (50%) and the 5-HT(2A/2C) receptor agonist DOI (1-100 microM) increased (220%) the 5-HT output. Neither GABA nor baclofen (100 nM-100 microM) altered the 5-HT output. The glutamate reuptake inhibitor L-trans-PDC (1-4 mM) raised 5-HT to 280% of baseline. This effect was not antagonized by the NMDA receptor antagonist MK-801 (0.5 mg/kg i.p.). Local MK-801 (10-100 microM) did not significantly alter the 5-HT output. Finally, neither carbachol (10-100 microM) nor quipirole (10 microM-1 mM) affected 5-HT. These data suggest that the striatal 5-HT release is influenced by local serotonergic and glutamatergic (but not GABAergic) inputs.

Animals↗

PubMed1996

[Contralateral hyperhidrosis secondary to the pontine infarct].

Unilateral hyperhydrosis due to a cerebral infarct is a clinical sign rarely described in the literature, the significance of which is unknown and may be due to a lesion of the crossed sympathetic inhibitory tract. We describe the case of a patient with contralateral hyperhydrosis due to a hemipontine infarct.

Cerebral Infarction↗

PubMed1995

Hemostatic disturbances in acute ischemic stroke: a study of 86 patients.

The relevance of coagulation abnormalities in ischemic stroke remains uncertain. The purpose of this study was to identify abnormal patterns of coagulation in established ischemic stroke. We measured coagulation parameters in 86 patients with acute ischemic stroke: 10 lacunar, 55 atherothrombotic and 21 cardioembolic. Statistical comparisons were made between different stroke groups and between all stroke patients and 60 healthy controls. A decrease in functional antithrombin III and plasminogen and an increase in thrombin-antithrombin III complexes, total protein S, tissue plasminogen activator, plasminogen activator inhibitor and D-dimer were observed in the stroke group (p < 0.05). A positive correlation was found between tissue plasminogen activator and thrombin-antithrombin III levels in cardioembolic stroke (p < 0.05). Protein C levels showed significant differences between the three groups, and in the cardioembolic group they were lower than in controls (p < 0.05). Antiphospholipid antibodies were positive in two cases. We conclude that activation of coagulation and fibrinolytic pathways was observed during the acute phase of ischemic stroke. Protein C activity is different in the three types of strokes analyzed, and higher levels seem to be associated with lacunar lesions. Antiphospholipid antibodies do not seem to play an important role in the pathogenesis of stroke in a nonselected population.

Aged↗

PubMedDate not supplied

[Latency in the hospital admittance of stroke].

OBJECTIVE: the hospital referral of 200 patients with cerebrovascular disorders in order to evaluate the possibility of treating acute cerebral infarction. METHOD: by means of a personalized interview an evaluation was made of the time that had passed between the start of the symptomatology and the time the patient went into hospital. The results were then grouped into intervals and compared to the different nosological entities of cerebral vascular pathology. The data were analysed using non-parametrical statistical tests (chi 2). RESULTS: of the 200 patients examined, 79.5% had cerebral ischemy (15.1% AIT, 84.9% infarction) and 20.5% intercranial haemorrhage (92.7% intercerebral haemorrhage). Of the patients suffering from cerebral infarction, 27.4% involved lacunary infarctions, 22.2% cardio-embolic infarctions, and 50.4% atherothrombotic infarctions. In 57% of cases the pathology was located in the carotid region and in 35.5%, in the vertebrobasilar region. 46.5% of the patients suffering from cerebrovascular disorders went into hospital less than 3 hours since the start of the symptomatology. 60.7% of the patients with cerebral infarction arrived within 6 hours. When the latency between the different nosological entities was compared, significant statistical differences were only detected between cardio-embolic infarctions and the other infarctions (p = 0.04) and between carotid and vertebrobasilar pathology (p = 0.01). CONCLUSIONS: based on the hospital referral time, the design of new clinics in our field for the treatment of patients suffering acute cerebral infarction is viable, above all as far as those of cardio-embolic origin and located in the carotid region are concerned.

Acute Disease↗

PubMedDate not supplied

[Hematological changes and cerebrovascular disorders].

Stroke is due to abnormalities in the vascular wall, heart disease or hematological abnormalities. This last cause has a low causal rate in stroke but despite this its importance is self evident given that there still exists a number of stroke patients where etiology cannot be established. An exhaustive check was carried out on the different hematological phenomena which may play a part in the etiology of ischaemic or hemorrhagic strokes. We analyzed abnormalities in the red series, white series and blood cells; coagulapathies; discrasias of the plasmic cells and antiphospholipid antibodies. For each of the hematological entities, conceptual criteria, their role in brain hemorrhage or ischaemia, and therapeutic measures were established.

Antibodies, Antiphospholipid↗