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M E Calcagnotto

Publications and source records attributed to M E Calcagnotto.

7 recordsLinked to original sources
PubMed2001

High-pass filtering of corticothalamic activity by neuromodulators released in the thalamus during arousal: in vitro and in vivo.

The thalamus is the principal relay station of sensory information to the neocortex. In return, the neocortex sends a massive feedback projection back to the thalamus. The thalamus also receives neuromodulatory inputs from the brain stem reticular formation, which is vigorously activated during arousal. We investigated the effects of two neuromodulators, acetylcholine and norepinephrine, on corticothalamic responses in vitro and in vivo. Results from rodent slices in vitro showed that acetylcholine and norepinephrine depress the efficacy of corticothalamic synapses while enhancing their frequency-dependent facilitation. This produces a stronger depression of low-frequency responses than of high-frequency responses. The effects of acetylcholine and norepinephrine were mimicked by muscarinic and alpha(2)-adrenergic receptor agonists and blocked by muscarinic and alpha-adrenergic antagonists, respectively. Stimulation of the brain stem reticular formation in vivo also strongly depressed corticothalamic responses. The suppression was very strong for low-frequency responses, which do not produce synaptic facilitation, but absent for high-frequency corticothalamic responses. As in vitro, application of muscarinic and alpha-adrenergic antagonists into the thalamus in vivo abolished the suppression of corticothalamic responses induced by stimulating the reticular formation. In conclusion, cholinergic and noradrenergic activation during arousal high-pass filters corticothalamic activity. Thus, during arousal only high-frequency inputs from the neocortex are allowed to reach the thalamus. Neuromodulators acting on corticothalamic synapses gate the flow of cortical activity to the thalamus as dictated by behavioral state.

Acetylcholine↗
PubMed2000

Hippocampus-entorhinal cortex loop and seizure generation in the young rodent limbic system.

Application of the convulsant 4-aminopyridine (4AP, 50 microM) to adult mouse combined hippocampus-entorhinal cortex (EC) slices induces interictal and ictal discharges originating from CA3 and EC respectively. In this model of limbic seizures, ictal discharges disappear over time and are reestablished after Schaffer collateral cut, a procedure that blocks interictal propagation from CA3 to EC. Here we tested whether this form of network plasticity is operant in hippocampus-EC slices obtained from young (10-25 day-old) mice. In these experiments 4AP elicited interictal (duration = 100-250 ms; interval = 0.7 +/- 0.2 s, mean +/- SD, n = 20) and ictal (duration = 267 +/- 37 s; interval = 390 +/- 37 s, n = 20) discharges in both CA3 and EC. However, in young mouse slices the ictal events occurred throughout the experiment, whereas Schaffer collateral cut abolished CA3-driven interictal discharges in EC without influencing ictal activity (n = 10). Perforant path lesion prevented the spread of EC-driven ictal events to CA3, where interictal and short ictal discharges (duration = 32 +/- 11 s; interval = 92 +/- 9.7 s, n = 8) continued to occur. Hence, two independent forms of ictal activity were seen in CA3 and in EC after separation of these structures. In intact hippocampus-EC slices, ictal discharges were reduced by an N-methyl-D-aspartate receptor antagonist (n = 10). Under these conditions, Schaffer collateral cut abolished ictal activity in EC, not in CA3 (n = 6). Thus the young mouse hippocampus-EC loop has different properties as compared with adult tissue. These differences, which include the inability of hippocampal outputs to control ictal discharge generation in EC and the ability of the loop to sustain ictal activity, may contribute to the low-seizure threshold seen in young individuals.

4-Aminopyridine↗
PubMed1999

Presynaptic long-term potentiation in corticothalamic synapses.

The thalamus and neocortex are two highly organized and complex brain structures that work in concert with each other. The largest synaptic input to the thalamus arrives from the neocortex via corticothalamic fibers. Using brain slices, we describe long-term potentiation (LTP) in corticothalamic fibers contacting the ventrobasal thalamus. Corticothalamic LTP is input-specific, NMDA receptor-independent, and reversible. The induction of corticothalamic LTP is entirely presynaptic and Ca(2+)-dependent. The expression of corticothalamic LTP is associated with a decrease in paired-pulse facilitation (PPF) and blocked by an inhibitor of the cAMP-dependent protein kinase A (PKA). Consistent with an involvement of cAMP and PKA, activation of adenylyl cyclase induced a synaptic enhancement that was associated with a decrease in PPF and occluded LTP. Corticothalamic LTP may serve to enhance the efficacy of cortico-cortical communication via the thalamus and/or to mediate experience-dependent long-term modifications of thalamocortical receptive fields.

Animals↗
PubMed1999

[Neuropathology of hard to control epilepsy. Study of 300 consecutive cases].

We report histopathological findings in 300 consecutive surgical specimens from epilepsy surgery during 6 years. Our material was mainly from temporal lobe epilepsy (70.33%). In 44% the diagnosis was hippocampal sclerosis. There were tumors in 15% of cases and neuronal migration disorders in 10%. The most common tumors were gangliogliomas (42.22%) and dysembryoplastic neuroepithelial tumors (20%). We review the more frequent diagnosis in epilepsy surgery based on this series and comparing with literature.

Cerebral Cortex↗
PubMed1997

Frequency of the different mutations causing spinocerebellar ataxia (SCA1, SCA2, MJD/SCA3 and DRPLA) in a large group of Brazilian patients.

Spinocerebellar ataxia type 1 (SCA1), spinocerebellar ataxia type 2 (SCA2) and Machado-Joseph disease or spinocerebellar ataxia type 3 (MJD/SCA3) are three distinctive forms of autosomal dominant spinocerebellar ataxia (SCA) caused by expansions of an unstable CAG repeat localized in the coding region of the causative genes. Another related disease, dentatorubropallidoluysian atrophy (DRPLA) is also caused by an unstable triplet repeat and can present as SCA in late onset patients. We investigated the frequency of the SCA1, SCA2, MJD/SCA3 and DRPLA mutations in 328 Brazilian patients with SCA, belonging to 90 unrelated families with various patterns of inheritance and originating in different geographic regions of Brazil. We found mutations in 35 families (39%), 32 of them with a clear autosomal dominant inheritance. The frequency of the SCA1 mutation was 3% of all patients; and 6% in the dominantly inherited SCAs. We identified the SCA2 mutation in 6% of all families and in 9% of the families with autosomal dominant inheritance. The MJD/SCA3 mutation was detected in 30% of all patients; and in the 44% of the dominantly inherited cases. We found no DRPLA mutation. In addition, we observed variability in the frequency of the different mutations according to geographic origin of the patients, which is probably related to the distinct colonization of different parts of Brazil. These results suggest that SCA may be occasionally caused by the SCA1 and SCA2 mutations in the Brazilian population, and that the MJD/SCA3 mutation is the most common cause of dominantly inherited SCA in Brazil.

Adolescent↗
PubMed1994

Value of immunologic testing in stroke patients. A prospective multicenter study.

BACKGROUND AND PURPOSE: The aims of this prospective and multicenter study were to determine the frequency of anticardiolipin and antinuclear antibodies in an unselected ischemic and hemorrhagic stroke population and to evaluate the clinical significance of these autoantibodies. METHODS: Over a 1-year period, we collected plasma from 481 consecutive patients with ischemic or hemorrhagic stroke attending four different hospitals. Blood (10 mL) was drawn from each subject into a citrated glass tube. Plasma was obtained immediately by centrifugation and was stored at -70 degrees C until use. Concentrations of IgM and IgG anticardiolipin antibodies were measured at room temperature in normal (not heat-treated) plasma by standardized enzyme-linked immunosorbent assay. All sera were treated by indirect immunofluorescence on mouse liver and kidney sections for antinuclear antibodies. RESULTS: A total of 481 patients (325 men, 156 women) 16 to 90 years in age (mean age, 61 years) were studied. Anticardiolipin antibodies were present in 5 of 481 (1.04%) patients. One patient was IgG positive and four patients were IgM positive. Of 481 patients, 35 (7.2%) were positive for antinuclear antibodies. Anti-DNA antibodies were not demonstrable in any patient. CONCLUSIONS: The frequency of anticardiolipin antibodies in a heterogeneous stroke population is possibly lower than reported. The routine screening of anticardiolipin and antinuclear antibodies in a stroke population is of questionable value.

Adolescent↗