Biomedical subjects

J De Felipe

Publications and source records attributed to J De Felipe.

6 recordsLinked to original sources

PubMed2005

Vesicular glutamate transporter 1 immunostaining in the normal and epileptic human cerebral cortex.

Glutamate is the main excitatory neurotransmitter in the brain where, due to the activity of specific vesicular glutamate transporters, it accumulates in synaptic vesicles. The vesicular glutamate transporter 1 is found in the majority of axon terminals that form asymmetrical (excitatory) synapses in the rat neocortex. However, since there is no information available regarding the distribution of vesicular glutamate transporter 1 in the human neocortex, we have used correlative light and electron microscopy to define its expression in this tissue. We found that the distribution of vesicular glutamate transporter 1-immunoreactivity is virtually identical to that found in the rat neocortex, both at the light and electron microscope levels. Therefore, we assessed whether vesicular glutamate transporter 1 immunostaining might be a useful tool to study the pathological alterations of glutamatergic transmission in the epileptic cerebral cortex. We analyzed the distribution of vesicular glutamate transporter 1 in the peritumoral neocortex of patients with epilepsy secondary to low-grade tumors. In these regions, we found alterations in the pattern of vesicular glutamate transporter 1-immunoreactivity that perfectly matched the neuronal loss and gliosis, as well as the decrease in the number of asymmetrical synapses identified by electron microscopy in this tissue. Thus, vesicular glutamate transporter 1 immunostaining appears to be a reliable and simple tool to study glutamatergic synapses in the normal and epileptic human cerebral cortex.

Adolescent↗

PubMed2001

Dendritic but not somatic GABAergic inhibition is decreased in experimental epilepsy.

Impaired inhibition is thought to be important in temporal lobe epilepsy (TLE), the most common form of epilepsy in adult patients. We report that, in experimental TLE, spontaneous GABAergic inhibition was increased in the soma but reduced in the dendrites of pyramidal neurons. The former resulted from the hyperactivity of somatic projecting interneurons, whereas the latter was probably due to the degeneration of a subpopulation of dendritic projecting interneurons. A deficit in dendritic inhibition could reduce seizure threshold, whereas enhanced somatic inhibition would prevent the continuous occurrence of epileptiform activity.

Action Potentials↗

PubMed1980

New contribution on the oesophageal mucous innervation in certain monkeys (Cercopithecidae).

Spindle-shaped, barrel-like, or bush-like corpuscular neural structures situated in the mucous epithelium of the upper third of the oesophagus are described. These structures are not homogeneously distributed in this area. Some are very close to the pharyngooesophageal sphincter, spanning the thickness of the epithelium and communicating with the basal membrane by means of a thin pedicle and with the lumen by a small hilus or pore, their morphology being that of a taste bud. The others are situated deeper in the mucous epithelium of the upper third, communicating with the basal membrane only by means of either a thin pedicle or a thicker one, and separated from the lumen by a thick layer of epithelial cells. The bush-like apparatuses lie closely adjacent to the basal membrane of the epithelium.

Animals↗

PubMed1980

Sensorivagal nature of oesophageal submucous layer nerve endings. Determination of surgical degeneration methods.

Two types of surgery were performed on domestic cats to establish the source and functional significance of the apparatuses we have denominated perivascular, perifascicular and free endings of the oesophageal submucous layer. After extirpation of the cranial regions of the sympathetic ganglionic chain, of all the cervical ganglia and of the four proximal thoracic ganglia, no Wallerian degeneration of the concerned nerve endings was observed, thus ruling out their dependence on this neural pathway. After ablation of the central portion of the nodose ganglion, of the vagal nerve. Wallerian degeneration was observed in these nerve-ending apparatuses, thus demonstrating: (i) that these nerve apparatuses depend on perikarya situated in the nodose ganglion and (ii) that they are sensory receptors.

Animals↗

PubMed1979

Spinous leafy nerve endings in the feline stomach wall.

The Champy-Maillet ZIO technique has been applied to the study of the muscular tunic of the stomach. In the corpus and antrum pyloricum some nerve fibres end in non-capsulated expansions owning thorn-like protrusions. Their morphology is studied and a possibly functional sensory significance is proposed, on the basis of previous experimental results.

Animals↗

PubMedDate not supplied

Inhibitory synaptogenesis in mouse somatosensory cortex.

It is widely believed that inhibitory synapses are not present or present in only small numbers in the rodent cerebral cortex during the early postnatal period when the cortex is being innervated by thalamocortical fibers. Quantitative electron microscopy was carried out on the posteromedial barrel subfield of mouse somatosensory cortex from postnatal day 4 (P4) when thalamocortical innervation of the barrels is becoming established, through to sexual maturity (>P32), and in adulthood. Both asymmetrical (putatively excitatory) and symmetrical (putatively inhibitory) synapses were present in all layers from P4. The symmetrical synapses were immunoreactive for GABA at all ages. There was a progressive increase in both asymmetrical and symmetrical synapses up to P32, density in all layers increasing 16-fold, with the production of asymmetrical synapses leading and greatly outstripping that of symmetrical. From P32 to P120, the oldest age studied, synaptic numbers declined by 18% to 13 times the P4 level, but this affected predominantly layers II/III, IV and V, and mainly involved asymmetrical synapses. The relative percentage of asymmetrical to symmetrical synapses from P4 to P8 was 57%/43% but at P32 it was 89.5%/10.5% and in adulthood 85.4%/14.6%. These data indicate that inhibitory synaptogenesis in the rodent cortex begins earlier than previously thought, a basis for inhibition being present from the earliest period. Pruning of all synapses occurs well after thalamocortical innervation is established and inhibitory synapses are less affected by the pruning process.

Aging↗