Broad band spectral EEG parameters correlated with different IQ measurements

The relationship of IQ (measured by WAIS and all its subscales) and EEG broad band spectral parameters were studied in 40 right-handed, male volunteers ranging in age from 20 to 25 years old. EEGs were recorded in 20 derivations during rest with eyes opened. The results obtained reveal positive and negative correlations with abundant frontal participation in all bands. Mean frequency data show a frequency shift in a very narrow range suggesting that more relations in narrow band could be achieved. These results highlight the need of psychological tests that measure more homogeneous abilities and finer measurement technique to reveal clearly explainable correlations and demonstrate that EEG recordings do reflect intellectual abilities.     

Formation of the corticopontine projection in a long-term culture system.

The reestablishment in vitro of the corticopontine projection was studied in organotypic co-cultures of cortex and pons of rats 0 (day of birth) - 3 days old. After 2-3 weeks in vitro, application of the lipophilic tracer DiI in the pontine explant retrogradely stained in layer V of the cortical explant pyramidal neurons which were characterized by large somata and spiny dendrites with an apical dendrite that reached upper cortical layers II/III. The projection developed only in co-cultures from rats 0-2 days old when the pontine explant was placed in close vicinity either to the white matter or the pial surface of the cortical explant. Control experiments demonstrated the specificity of the corticopontine projection in vitro by showing that the projections of the layer V pyramidal cells to the pons did not reflect a non-directed outgrowth pattern with subsequent survival of axons contacting the target explant. Our findings demonstrate that morphology and laminar position of corticopontine projection neurons in vitro are similar to those in vivo and thus support the "organotypic" nature of the explant co-culture system.     

Calcium-binding proteins in the dorsal ventricular ridge of the lizard Psammodromus algirus

The aim of the present work was to study further the intrinsic organization of the dorsal ventricular ridge of lizards. For that purpose, the morphology and distribution of cells and fibers containing the calcium-binding proteins calbindin-D28k, parvalbumin, and calretinin were investigated by using immunohistochemical methods. Colocalization of calcium-binding proteins with the neurotransmitter gamma-aminobutyric acid (GABA) was also studied because they are shown to coexist in many areas of the telencephalon where they define distinct subpopulations of GABAergic local circuit neurons. Neurons containing calcium-binding proteins are limited to the anterior part of the dorsal ventricular ridge (ADVR), whereas the posterior or caudal portion of the ridge is devoid of immunoreactive cells. This result gives further evidence for defining both regions of the dorsal ventricular ridge. Calcium-binding proteins mark three distinct populations of neurons within the ADVR. Two of them, parvalbumin- and calretinin-expressing cells, are GABAergic. On the other hand, calbindin-containing neurons do not express GABA, and the possibility is discussed that these cells are projection neurons. The distribution and overall density of fibers immunoreactive to calcium-binding proteins suggests that most fibers are of extrinsic origin, the thalamic nuclei projecting to the ADVR and the lateral amygdala being good candidates for their origin. The comparison of data on the populations of calcium-binding protein-containing neurons in the reptilian ADVR with those of mammals illustrate the difficulty in finding a mammalian homologue for this controversial region of the reptilian telencephalon.     

Ultrastructural confirmation of neuronal protection by melatonin against the neurotoxin 6-hydroxydopamine cell damage

6-Hydroxydopamine (6-OHDA) is a neurotoxin used in the induction of experimental Parkinson's disease in both animals and cultured neuronal cells. Biochemical and molecular approaches showed previously that low doses of 6-OHDA induced apoptosis in PC12 cells, while high doses of this neurotoxin induced necrosis. Melatonin has been shown to protect against the neuronal programmed cell death induced by 6-OHDA, although it was not able to prevent the massive necrotic cellular death occurring after the addition of high doses of the neurotoxin. In the present work, we demonstrate by ultrastructural analysis that although low doses of 6-OHDA induced apoptosis in PC12 cells, it also damaged the non-apoptotic cells, morphologically corresponding this damage to incipient and reversible necrotic lesions. When the doses of the neurotoxin increase, there are still apoptotic cells, although most of the cells show necrotic irreversible lesions. We also found that melatonin partially prevents the incipient necrotic lesions caused by low doses of 6-OHDA. The fact that melatonin was shown in previous work to prevent apoptosis caused by low doses of 6-OHDA, but not necrosis induced by high doses of the neurotoxin, seemed to indicate that this agent is only able to protect against apoptosis. However, our present results, melatonin preventing also the incipient necrotic neuronal lesions, suggest that this hormone may provide a general protection against cell death, suggesting that higher doses should be tried in order to prevent the necrotic cell death induced by high doses of the neurotoxin.     

Role of nitric oxide in the cerebral circulation during hypotension after hemorrhage, ganglionic blockade and diazoxide in awake goats

The role of nitric oxide in cerebrovascular response to hypotension was analyzed by evaluating the changes in cerebrovascular resistance after inhibition of nitric oxide synthesis with Nw-nitro-L-arginine methyl ester (L-NAME) during three types of hypotension in conscious goats. Blood flow to one brain hemisphere was electromagnetically measured, hypotension was induced by controlled bleeding, and by i.v. administration of hexametonium (ganglionic blocker) or of diazoxide (vasodilator drug), and L-NAME was injected by i.v. route (35 mg kg-1). Under control conditions (13 goats), L-NAME increased arterial pressure from 98 +/- 3 to 123 +/- 4 mmHg and decreased cerebral blood flow from 65 +/- 3 to 40 +/- 3 ml min-1 (all P < 0.001); cerebrovascular resistance increased from 1.52 +/- 0.04 to 3.09 +/- 0.013 mmHg ml-1 min-1 (P < 0.01) (delta = 1.59 +/- 0.12 mmHg ml-1 min-1). After bleeding (five goats), mean arterial pressure decreased to 60 +/- 4 mmHg and cerebral blood flow decreased to 37 +/- 4 ml min-1 (all P < 0.01); cerebrovascular resistance did not change (1.56 +/- 0.14 vs. 1.54 +/- 0.12 mmHg ml-1 min-1, P > 0.05). During this hypotension, L-NAME increased arterial pressure to reach the normotensive values an did not affect the hypotensive values for cerebral blood flow; cerebrovascular resistance increased from the hypotensive values to 2.91 +/- 0.19 mmHg ml-1 min-1 (P < 0.01) (delta = 1.37 +/- 0.16 mmHg ml-1 min-1), and this increment is comparable to that under control conditions (P > 0.05). Ganglionic blockade (six goats) decreased arterial pressure to 67 +/- 2 mmHg) and did not affect significantly cerebral blood flow; cerebrovascular resistance decreased from 1.71 +/- 0.11 to 1.05 +/- 0.09 mmHg ml-1 min-1 (P < 0.01). During this hypotension, L-NAME increased arterial pressure to 103 +/- 6 mmHg (P < 0.001), and did not affect cerebral blood flow; cerebrovascular resistance increased from the hypotensive values to 1.68 +/- 0.18 mmHg ml-1 min-1 (P < 0.01) (delta = 0.63 +/- 0.10 mmHg ml-1 min-1), and this increment was lower than under control conditions (P < 0.01). Diazoxide (six goats) decreased arterial pressure to 69 +/- 5 mmHg (P < 0.01) without changing cerebral blood flow; cerebrovascular resistance decreased from 1.89 +/- 0.11 to 1.16 +/- 0.14 mmHg ml-1 min-1 (P < 0.01). During this hypotension, L-NAME increased arterial pressure to 87 +/- 6 mmHg (P < 0.05) and did not affect the hypotensive values for cerebral blood flow (P > 0.05); cerebrovascular resistance increased from the hypotensive values to 1.53 +/- 0.13 mmHg ml-1 min-1 (P < 0.05) (delta = 0.36 +/- 0.06 mmHg-1 ml-1 min-1), and this increment was lower than under control conditions (P < 0.01). Therefore, the role of nitric oxide in cerebrovascular response to hypotension may differ in each type of hypotension, as this role during hemorrhagic hypotension may not change and during hypotension by ganglionic blockade or diazoxide may decrease. These differences may be related to changes in nitric oxide release as stimuli on the endothelium (shear stress and sympathetic activity) may vary in each type of hypotension.     

Characterization of membrane melatonin receptor in mouse peritoneal macrophages: inhibition of adenylyl cyclase by a pertussis toxin-sensitive G protein

Melatonin binding sites were characterized in mouse peritoneal macrophages. Binding of 2-[125I]melatonin by macrophages fulfills all criteria for binding to a receptor site. Thus, binding was dependent on time, temperature and cell concentration, stable, reversible, saturable and specific. Stoichiometric studies showed a high-affinity binding site with a Kd of 0.58-0.71 nM. These data are in close agreement with data obtained from kinetic studies (Kd = 0.29 nM). The affinity of these binding sites suggests that they may recognize the physiological concentrations of melatonin in serum. Moreover, binding experiments using macrophage crude membranes showed that melatonin bound specifically to the membranes. Additionally, in competition studies we observed a low-affinity binding site (Kd = 2.02 microM). Melatonin inhibited significantly forskolin-stimulated cyclic AMP accumulation in a dose-dependent manner. This effect was blocked by luzindole, an antagonist of the melatonin membrane receptor. Pretreatment of macrophages with pertussis toxin blocked the inhibitory effect of melatonin. Pertussis toxin ADP-rybosilation and Western blot experiments demonstrated both alpha(i1/2) and alpha(i3/o) G protein subunits expression in mouse peritoneal macrophages membranes. Our results demonstrate the existence of melatonin receptors in mouse peritoneal macrophages, and a pertussis toxin-sensitive melatonin signal transduction pathway that involves the inhibition of adenylyl cyclase.     

Growth factors effects on the expression of morphological and biochemical properties of avian embryonic sympathetic cells. Emphasis on NGF

Growth factors are known to be important agents in the differentiation and modulation of neuronal phenotypes. We have analyzed the effect of several growth factors on the modulation of morphological and biochemical properties of avian embryonic sympathetic neurons. The growth factors studied include: nerve growth factor (NGF), neurotrophin-3 (NT-3), brain derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF), basic fibroblast growth factor (bFGF) and transforming growth factor beta-1 (TGF-beta1). Morphological properties were analyzed by immunocytochemistry to neurofilament proteins and visualization of fibers after glyoxylic acid-induced fluorescence. Biochemical modulation was determined by radioimmunoanalysis for the peptides enkephalin (ENK), somatostatin (SS) and neuropeptide Y (NPY) and by HPLC-electrochemistry quantification of catecholamines. Similar to previous results using chromaffin cell cultures [R. Ramírez-Ordó?ez, J.E. García-Arrarás, Peptidergic, catecholaminergic and morphological properties of avian chromaffin cells are modulated distinctively by growth factors, Dev. Brain Res., 87 (1995) 160-171], we found a dissociation in the modulation of biochemical and morphological properties, however, the effect of specific factors differed between the chromaffin and sympathetic cultures. We have focused on NGF to analyze its effect on the sympathetic peptide phenotypes and its lack of an effect on the chromaffin cell peptide phenotypes. The results presented here, establish interesting differences between chromaffin cells and sympathetic neurons that are of importance to studies of cell lineage and differentiation.     

The developing profile of cerebral ischemia

Cerebral ischemia, which may be silently manifested as transitory ischemia attacks or cerebral infarction, is not a stable, but rather, a moving process. In cerebral infarctions the initial ischemic area may change or move in a high percentage of patients and may involve a significant volume (mean of 32%) of neuronal tissue. The negative changes of initial cerebral ischemia which produce a worsening of the same may be due to the progression of the thrombus, appearance of new embolisms, cerebral edema, hemorrhage, blood reperfusion and systemias causes. These changes may determine the conversion of the shaded ischemic area into a definitive, irreversible infarction. The negative changes may also be produced some distance from the initial ischemic area, either because of microthromboembolisms or diaschisis. The positive changes of initial cerebral ischemia which produce as improvement of the same, may be due to collateral circulation, lysis or fragmentation of the embolism and a decrease in cerebral edema. Clinical changes with no evident clinical manifestations may also be produced and may be diagnosed with the use of clinical scales, imaging techniques, ultrasound and hematological and biochemical markers. Acknowledgement of these cerebral ischemia changes in the acute phase may determine the salvation of a part of the brain, and thereby modify the future clinical situation of the patient.     

Encephalopathy with focal lesions due to Mycoplasma pneumoniae

Mycoplasma pneumoniae infections usually produce respiratory symptoms, that only exceptionally involve the nervous system. In this case, the infection generally causes an encephalitic picture characterized by impaired consciousness and seizures, and by normal or non-specific neuroradiological findings. However, four cases of M. pneumoniae infection associated with symmetrical lesions in the putamen and its external surrounding areas, and with extrapiramidal symptoms, have been recently published. We present the case of a patient with a clinical picture characterized by confusion, fever, and seizures, associated with a M. pneumoniae infection. The MRI study showed two symmetrical lesions that involved the areas just outside the putamen and disappeared coinciding with her clinical improvement. The present case would support that the encephalopathy associated with the M. pneumoniae infection shows a tendency to involve a particular region of the brain. Our case might represent the minimal expression of these characteristic lesions, which in the most benign cases would involve the areas immediately outside the putamen, and in other instances the putamen as well.