Search PubMed⌕ Search

Biomedical subjects

F Pellicer

Publications and source records attributed to F Pellicer.

24 records · Page 2Linked to original sources

Habituation and dehabituation of the spinal polysynaptic reflex responses: modification by naloxone and opiates and their anatomical correlates.

The sustained inhibitory action of spinal endorphins could be responsible for the habituation of polysynaptic responses in the spinal cord. To test this hypothesis, acute spinalized unanesthetized cats (decerebrated and curarized) were used. Sural nerve electrical stimulation (0.2 Hz) was provided and a progressive decrease in the reflex response was found. Conversely, the field potential (lamina V) progressively increased during stimulation, reaching its maximum amplitude when ventral root response showed maximum habituation. The administration of naloxone (0.8-10.0 mg/kg) produced dehabituation or prevented habituation. The immunohistological results showed leu-enkephalin-like immunoreactive dot-like structures in close proximity to neurons of laminae VII, VIII and IX in the lumbo-sacral segment of the spinal cord. Our results suggest an involvement of opioid peptides in the habituation process.

Animals↗

Massed amygdaloid kindling in encéphale isolé cats: its facilitation by naloxone.

The effect of repetitive administration of naloxone on the development of massed amygdaloid kindling in 'encéphale isolé' cats was studied. Electrical amygdaloid kindling was carried out with a 15 min inter-stimulus interval (ISI) in a control situation with intravenous (i.v.) naloxone administration (2, 4, and 8 mg/kg), 5 min prior to amygdaloid stimulation. It was found that it was possible to complete the amygdaloid kindling process in the encéphale isolé preparation reaching generalized electrographic tonic-clonic self-sustained seizures. The enhancement of the duration, frequency, and propagation of the after-discharge (AD) was accentuated by naloxone which also induced a progressive amplitude increment of the first potential evoked by the onset of the tetanus. The number of trials needed to achieve seizure generalization was reduced in dose-dependent manner by naloxone. The ability of naloxone to accelerate the development of amygdaloid kindling may be related to an inhibitory role of opioid peptides in this process.

Amygdala↗

Epileptogenesis and muscular hypertonic postictal phenomena induced by naloxone in intact cats.

Epileptogenesis produced by repeated i.p. administration of naloxone chloride and sensory stimulation (photoacoustic stimulation at 1, 3, 10, and 15 Hz) every 15 min was studied in freely moving cats. The repeated administration of naloxone provoked some behavioral manifestations that resemble those produced by electrical amygdaloid kindling. Photoacoustic stimulation accentuated the manifestations. All the animals presented generalized behavioral seizures when total naloxone administration reached 80 mg/kg. None of the animals demonstrated postictal depression. These results suggest an inhibitory role of endogenous opioids and/or GABA in epileptogenesis.

Acoustic Stimulation↗

[Jugular phlebectasia. Apropos a case].

We present a case of 6-years-old male with an internal jugular phlebectasia, diagnosed at our Hospital. Review of the bibliography, and complementary examination, like doppler, echography and digital intravenous angiography subtraction (DIVAS) was made.

Angiography, Digital Subtraction↗

[Non-syndromic familial deafness. Review and genetic study].

Many cases of hearing impairment are of genetic origin. Non-syndromic recessive transmission is the most frequent form. A genetic study was made of cases of non-syndromic familial hearing impairment seen in our service. The pattern of Mendelian inheritance was studied in the disorders associated with deafness. Four families had non-syndromic deafness and autosomal inheritance (3 dominant and one recessive) and one had a probable sex-linked inheritance. Genetic counseling was given and guidelines were created after reviewing the literature.

Adolescent↗