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Biomedical subjects

R Soto-Moyano

Publications and source records attributed to R Soto-Moyano.

15 recordsLinked to original sources
PubMed1991

Yohimbine early in life alters functional properties of interhemispheric connections of rat visual cortex.

It has been shown that noradrenaline (NA) is an important regulator of normal regressive processes occurring during synaptogenesis such as cell death, axonal pruning and synaptic elimination. The present study was designed to investigate whether enhanced NA release induced by chronic yohimbine administration early in life may alter in the rat the normal pattern of functional interhemispheric connections of the visual cortex. Yohimbine administration to rats between days 5 and 16 of postnatal life (2.5 mg/kg, IP, daily) resulted in changes in the pattern of transcallosal responses evoked in the visual cortex, characterized by a reduction in the peak-to-peak amplitude as well as a reduction of the extent of projecting fields of maximal activity, when examined at 30-35 days following termination of the drug treatment regimen. The results indicate that yohimbine treatment early in life induces functional alterations in the interhemispheric connectivity of the visual areas, probably by disrupting the normal trophic role of NA during synaptogenesis.

Animals↗
PubMed1990

Analgesia produced by intrathecal administration of the kappa opioid agonist, U-50,488H, on formalin-evoked cutaneous pain in the rat.

The antinociceptive activity of the selective kappa opioid agonist U-50,488H, given intrathecally (i.t.) against chemically induced cutaneous pain in rats, was assessed from cumulative dose-response experiments and the formalin test. Three successive i.t. doses of 5, 10 and 35 nmol of U-50,488H produced a gradual reduction of pain scores which was statistically significant at all observation periods. This effect was antagonized significantly by 3 mg/kg i.p. of the opiate antagonists, naloxone and WIN 44,441-3. The analgesia profile showed a clear dose-response relationship. A dose producing 50% 'maximum possible analgesia' of 6.20 nmol (95% confidence interval: 3.05-12.59 nmol) was calculated. The results indicated that cutaneous pain of a chemical/inflammatory nature is highly sensitive to activation of kappa receptors of the spinal cord dorsal horn.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1990

Kappa opioid receptor-mediated depression of activity evoked in convergent dorsal horn cells by thermal and non-thermal noxious stimulation.

The response of convergent dorsal horn cells to tonic and phasic noxious heating and to noxious pinching was studied before and after topical application of a solution (30 nmol) of the kappa agonist U-50,488H to the dorsal surface of the spinal cord. U-50,488H depressed the discharge of convergent units evoked by thermal and mechanical nociceptive stimuli. The opiate antagonist WIN 44,441-3 reversed the effect of U-50,488H. It is concluded that kappa opioids are effective in preventing the depolarization of convergent dorsal horn neurons evoked by either thermal or non-thermal noxious stimuli.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1990

Asymmetry of interhemispheric responses evoked in the prefrontal cortex of the rat.

Interhemispheric responses of anesthetized rats were evoked in the prefrontal cortex of both cerebral hemispheres by electric stimulation of the homologous contralateral cortical region. Fatigability of interhemispheric responses to repetitive stimulation was lower in the right prefrontal cortex. Besides, responses recorded in the right hemisphere exhibited greater amplitude increments to double-shock stimulation. No significant differences in rheobase, chronaxie, and threshold current were observed when comparing responsiveness of both prefrontal cortices to single stimuli. Results suggest that brain lateralization in the rat could depend, in part, on synaptic functional asymmetries of the prefrontal cortex.

Animals↗
PubMed1989

Effect of clonidine early in life on brain morphofunctional deficits induced by neonatal malnutrition in the rat.

A great body of evidence indicates that malnutrition early in life induces central noradrenergic hyperactivity (CNH). On the other hand, it is known that noradrenaline (NA) is an important regulator of the regressive processes occurring during synaptogenesis such as cell death, axonal pruning and synaptic elimination. This leads to the hypothesis that some of the morphofunctional modifications induced by malnutrition on the brain could be due, at least in part, to an increase of NA activity during the period of accelerated brain growth. This study evaluates whether early reduction of CNH by the alpha-2 presynaptic adrenoreceptor agonist clonidine, prevents long-term morphofunctional deficits induced by protein-energy malnutrition in the rat. Results of experiments performed on 45 day-old malnourished animals that received clonidine during the suckling period, show that the pharmacological treatment prevented: (i) deficits in both NA levels and NA release in the visual cortex; (ii) deficit in brain weight but not in body weight; and (iii) reduction of the normal brain interhemispheric asymmetry of visual cortical evoked potentials. It is suggested that administration of clonidine early in life prevents brain morphofunctional deficits by malnutrition, by restoring the normal tropic role of NA during synaptogenesis.

Animals↗
PubMed1988

Topical application of morphine to the rat somatosensory cortex produces analgesia to tonic pain.

Topical application of 0.01 or 0.1% morphine solution to the somatosensory SI area of the rat cerebral cortex significantly decreased the pain intensity rating in the formalin test without producing motor side effects or sensory deficits. Naloxone partially antagonizes this effect. Topical application of morphine to the striate cortex did not induce analgesia. It is suggested that the primary somatosensory SI area of the cerebral cortex plays a role in opiate pain control.

Animals↗
PubMed1987

Early malnutrition and changes in the induced release of noradrenaline in the prefrontal cortex of adult rats.

The influence of early protein-energy malnutrition on the induced release of noradrenaline in the rat prefrontal cortex was studied: (i) by evaluating in vivo the release of the neurotransmitter as revealed by changes in the ability of pyramidal cells to integrate transient transmembrane currents generated by discrete packets of noradrenaline released by repetitive electrical stimulation of the locus coeruleus; and (ii) by measuring in vitro the potassium-induced release of 3H-noradrenaline in slices obtained from the brain frontal pole. Both electrophysiological and neurochemical data show that, in malnourished rats, weak stimulation produces an increased release, whereas strong stimulation results in a decreased release of the neurotransmitter. The results provide direct evidence that malnutrition alters the release of noradrenaline at the cortical level. Since the prefrontal cortex is involved in cognitive processing, the present results could provide functional evidence linking nutritional and behavioral deficits.

Age Factors↗
PubMed1986

Effect of morphine-induced cortical excitation on spinal sensory transmission.

Bioelectrical responses evoked in the ventrolateral funiculus (VLF) of the spinal cord by electrical stimulation of the contralateral hind limb were studied following topical application of 1% morphine solution to the somatosensory SI area of the rat cerebral cortex. After morphine, a typical pattern was observed in the electrocorticogram, characterized by the appearance of rhythmic spiking activity. Time-related with each cortical spike, a significant reduction in the amplitude of VLF responses was observed. It is concluded that cortical excitation induced by morphine generates descending influences having the ability to inhibit spinal sensory transmission.

Afferent Pathways↗
PubMed1986

Prefrontal cortex excitability in early postnatally malnourished rats.

The effect of early postnatal malnutrition on the responsiveness of the rat prefrontal cortex was studied by determining excitability thresholds and fatigability to direct cortical stimulation. Malnutrition imposed during the period of rapid brain growth caused a significant increase of cortical chronaxie values as well as increased fatigability of direct cortical responses, indicating a detrimental effect on the axodendritic synapses. Since the prefrontal cortex plays an important role in the temporal organization of behavior, a dysfunction of this cortical area could be a causal link between nutritional and behavioral deficits.

Animal Population Groups↗
PubMed1985

Effect of morphine-induced cortical excitation on somatosensory responses evoked in the periaqueductal grey matter.

The somatosensory cortex responses and periaqueductal grey matter responses evoked by electric peripheral nerve stimulation were studied following topical application of 1% morphine solution to the primary somatosensory area of rat cerebral cortex. Cortically applied morphine increased the negative component of cortical potentials and enhanced the peak-to-peak amplitude of the periaqueductal grey responses. It is suggested that cortical excitation induced by morphine generates descending bioelectrical impulses modulating neuronal activity at this mesencephalic level.

Animals↗
PubMed1985

Malnutrition-induced changes of responses evoked in the rat prefrontal cortex as revealed by sensitivity to strychnine.

Susceptibility to strychnine of somatosensory responses evoked in the prefrontal cortex was studied in normal and protein-malnourished rats in three groups. (a) The normal group was from mothers fed a 21% casein diet. (b) The prenatally malnourished group was from mothers fed a 6% casein diet during 5 weeks prior to mating and throughout gestation. (c) The postnatally malnourished group born from dams fed a 6% casein diet throughout the nursing period. At 45 days of age, sensitivity of the responses to 0.5% strychnine sulfate solution was tested by measuring changes in peak-to-peak amplitude. The results showed that cortical neurons of the postnatally protein-restricted group had decreased susceptibility to strychnine, indicating functional disturbances of glycinergic synapses.

Animals↗
PubMed1978

Differential effect of pentazocine on primary cortical evoked potentials elicited by stimulation of the trigeminal tract and spinal cord pathways.

The influence of pentazocine on primary cortical evoked potentials was studied in guinea pigs under pentobarbital anesthesia. Pentazocine (10 mg/kg, i.v.) increased the latency time of evoked responses to posterior limb stimulation, more than that of response to lip stimulation. This result suggests that pentazocine decreases the velocity of nervous conduction.

Animals↗