Gabriel Roldan | UNAM Universidad Nacional Autónoma de México (original) (raw)

Papers by Gabriel Roldan

Salud ment, 1989

Base de dados : LILACS. Pesquisa : 89526 [Identificador único]. Referências encontradas : 1 [refi... more Base de dados : LILACS. Pesquisa : 89526 [Identificador único]. Referências encontradas : 1 [refinar]. Mostrando: 1 .. 1 no formato [Detalhado]. página 1 de 1, 1 / 1, LILACS, seleciona. para imprimir. Fotocópia. experimental, Documentos relacionados. Id: 89526. ...

Universitas Medica, 2011

Proyecto académico sin fines de lucro, desarrollado bajo la iniciativa de acceso abierto 1 Médico... more Proyecto académico sin fines de lucro, desarrollado bajo la iniciativa de acceso abierto 1 Médico anestesiólogo, candidato a Doctor en Ciencias; profesor titular e investigador, Laboratorio

Neuroscience …, 1997

The effect of three different M1 muscarinic antagonists, pirenzepine, biperiden, and trihexypheni... more The effect of three different M1 muscarinic antagonists, pirenzepine, biperiden, and trihexyphenidyl on memory consolidation was investigated. Rats were trained in a one-trial step-through inhibitory avoidance task and injected intraperitoneally immediately ...

Neurobiology of Learning and Memory, 1996

Disruption of synaptic activity of a number of cerebral structures (e.g., neostriatum, amygdala, ... more Disruption of synaptic activity of a number of cerebral structures (e.g., neostriatum, amygdala, and thalamus) produces marked deficits in retention of instrumentally conditioned behaviors. When animals are given a relatively high number of training trials or high intensities of footshock during learning, however, such disruption is considerably less effective. Since there is a close anatomical and functional relationship between the

Universitas Médica

En el último año, el Laboratorio Experimental de Farmacobiología de la Facultad de Medicina de la... more En el último año, el Laboratorio Experimental de Farmacobiología de la Facultad de Medicina de la Universidad Autónoma de Chiapas (UNACH), ha venido sistematizando pruebas no condicionadas para el estudio de la ansiedad en modelos animales. En este trabajo se efectúa una revisión bibliográfica que actualiza el conocimiento sobre las pruebas útiles en la evaluación de la ansiedad. Estas pruebas las utilizamos en los trabajos de investigación de extractos vegetales con base en hallazgos etnobotánicos de la medicina tradicional chiapaneca, los cuales se han desarrollado con modestos recursos financieros de la Facultad de Medicina de la Universidad y autofinanciamiento por parte de los investigadores, considerando la generación de conocimiento y la posibilidad de ampliar las expectativas terapéuticas con recursos naturales, como el insumo de mayor valor.Además, es de interés para el equipo investigador vincular en este proceso a investigadores de otras universidades e instituciones de s...

Psychopharmacology, Jan 7, 2018

The amygdala plays a paramount role in the modulation of anxiety and numerous studies have shown ... more The amygdala plays a paramount role in the modulation of anxiety and numerous studies have shown that arginine vasopressin (AVP) elicits anxiogenic effects following either its systemic or septal administration. The aim of this paper was to study the involvement of vasopressinergic neurotransmission in the amygdaloid modulation of unconditioned anxiety and to ascertain whether or not AVP receptor subtypes may have a differential role in this modulation. Anxiety behavior was evaluated both in Shock-Probe Burying Test and Light-Dark Box following the bilateral microinfusion of AVP alone or AVP together with either AVP 1a or AVP 1b receptor antagonists into the central amygdala (CeA). AVP microinfusion elicited at low (1 ng/side) but not at high doses (10 ng/side) anxiogenic-like responses in the Shock-Probe Burying Test but not in the Light-Dark Box. SSR149415, an AVP 1b antagonist unlike Manning compound, an AVP 1a antagonist, fully prevented AVP effects in the Shock-Probe Burying Te...

Behav Brain Res, 2001

The present investigation was aimed at elucidating the dose and time dependency of scopolamine-in... more The present investigation was aimed at elucidating the dose and time dependency of scopolamine-induced recovery of inhibitory avoidance after its extinction. Two experiments were conducted: in the first, we analyzed the effects of four doses (1, 2, 4, and 8 mg/kg) of the musacrinic receptor antagonist scopolamine, on the expression of this conditioned response once it had been extinguished. Independent groups of rats were trained in a one-trial, step-through inhibitory avoidance task and submitted to daily retention (extinction) tests. After extinction had occurred, animals were injected intraperitoneally 10 min before retention testing, either with saline or scopolamine. Results show that scopolamine produced a dose-dependent recovery of the avoidance response. The second experiment was carried out in the same animals, which were now tested for retention of inhibitory avoidance at 1, 2, 3, 6, and 9 months after completion of the first experiment. All rats received counterbalanced injections of saline or scopolamine 10 min before testing at each time interval. Reliable recovery of the avoidance response was observed at the 1-month interval with a clear dose dependency while, after the second month, only the groups treated with the two higher doses continued responding. The results indicate that recovery of the extinguished response produced by muscarinic blockade follows dose-and time-dependent curves, and can be achieved long after a single training session. These data suggest that the inhibitory avoidance memory trace is retained in the brain after behavioural extinction of this response, thus supporting the view of extinction as new learning that affects the retrieval of the original memory, but does not modify its storage.

Rats learn to avoid a tasteless odorized solution if they experience visceral malaise after consu... more Rats learn to avoid a tasteless odorized solution if they experience visceral malaise after consuming it. This phenomenon is referred as Conditioned Odor Aversion (COA). It is widely accepted that an odor can only be associated with illness if the inter-stimulus interval (ISI) is shorter than 15 min. However, this conclusion is based on long-term memory tests usually made 48 h after conditioning, thus precluding the possibility to discriminate between a specific failure to make the odor–malaise association rather than the failure to consolidate the short-term association into long-term memory. In the present study, we compared the short-term and long-term memories for COA in rats trained with long ISIs. Independent groups of male rats were conditioned using 5, 15, 30, 60 or 90 min ISIs and tested either 4 or 48 h after conditioning. We found a reliable odor aversion at 5, 15, 30 and 60 min, but not at 90 min ISIs, when tested 4 h after conditioning. In contrast, odor aversion was only found at 5 and 15 min ISIs in the groups tested 48 h after training. Our results show that COA can be acquired when malaise follows the odor CS by at least 60 min. This finding indicates that the lack of aversion at long ISIs is not due to an association failure, but rather to a limitation in consolidating short-term memory into long-term memory of COA.

Artículo original RESUMEN RESUMEN RESUMEN RESUMEN RESUMEN La enfermedad de Parkinson es una condi... more Artículo original RESUMEN RESUMEN RESUMEN RESUMEN RESUMEN La enfermedad de Parkinson es una condición neurológica devastadora que afecta a millones de persona en el mundo; su característica fisiopatológica es la pérdida de las neuronas dopaminérgicas en el mesencéfalo. Se han buscado las causas posibles de ésta enfermedad y se ha encontrado una diversidad que incluye mutaciones genéticas y tóxinas ambientales, pero la causa precisa que conduce a la muerte neuronal aún se desconoce. En la actualidad se han caracterizado algunos mecanismos patogénicos que son básicos para la degeneración de las células dopaminérgicas. Principalmente, la deficiencia en el almacenamientro de la dopamina en las vesículas sinápticas deriva en la generación en el citoplasma de radicales libres y especies reactivas del oxígeno, lo que parece ser el punto de inicio en el proceso de la muerte de estas neuronas, lo que eventualmente progresará a enfermedad de Parkinson. Esto parece ser la vía fisiopatológica c...

Sleep, 1988

Twelve healthy volunteers were included in this study. Baseline curves for melatonin and cortisol... more Twelve healthy volunteers were included in this study. Baseline curves for melatonin and cortisol were obtained after one night of adaptation to laboratory conditions. From 10:00 p.m. to 6:00 a.m., blood samples were drawn every hour. On the third night, the subjects were kept awake at the sleep unit. Curves for the two hormones were then obtained after 36 h of total sleep deprivation (SD). The levels of these hormones were evaluated by calculating the area under the curve at each hour in both situations (basal and after sleep deprivation). It was found that the melatonin levels were increased after sleep deprivation, whereas the cortisol levels remained the same. These results suggest a mechanism by which a reset of abnormal rhythms can occur in depression.

Sleep, 1989

Rapid eye movement sleep (REMS) deprivation is believed to alter the sensitivity of various neuro... more Rapid eye movement sleep (REMS) deprivation is believed to alter the sensitivity of various neurotransmitter systems. In the present article, we studied 20 healthy volunteers divided into three groups. Group A attended the sleep laboratory for three nights: acclimatization, a baseline night, and one night of physostigmine infusion. Group B attended for eight nights; acclimatization, baseline, four nights of REMS deprivation, and two recovery nights. With the exception of the first recovery night, when group C volunteers were administered physostigmine, group C's schedule was identical to group B's. The infusions received by group A and C were composed of 1.0 mg of physostigmine, dissolved in 100 ml of saline solution. These were administered 5 min after sleep onset and thereafter every hour, except when the subjects were either awake or in REMS. All of the subjects receiving the cholinomimetic infusion were given a peripheral anticholinergic. Group A experienced a great numb...

Efecto de la exposición al pesticida rotenona sobre el desarrollo del sistema dopaminérgico nigro... more Efecto de la exposición al pesticida rotenona sobre el desarrollo del sistema dopaminérgico nigro-estriatal Vol. 36, No.

Behavioral and Neural Biology, 1994

It was recently reported that administration of relatively high intensities of footshock (overrei... more It was recently reported that administration of relatively high intensities of footshock (overreinforcement) during training of passive avoidance protected animals against the amnesic effect of scopolamine, injected 5 min after training. This was interpreted in terms of a lesser involvement of acetylcholine in memory consolidation. An alternative explanation was that overreinforcement accelerated the consolidation process, which could have taken place before the injection of scopolamine. To test for this possibility, male Wistar rats were injected with 4, 8, or 12 mg/kg of scopolamine, 5 min before training with low or high levels of footshock and then tested for retention of the task. Scopolamine induced the expected memory deficit after the low-intensity footshock; after overreinforcement the higher doses of scopolamine induced state dependency, while no deficits were produced with the lower dose. It was concluded that: (a) acetylcholine is indeed involved in memory consolidation of passive avoidance; (b) scopolamine interacts with high footshock levels to produce state dependency; and (c) when relatively low doses of scopolamine are used in conditions of overreinforcement, protection against scopolamine-induced amnesia becomes evident.

Physiology & Behavior, 1994

of extinction by scopolamine. PHYSIOL BEHAV 56(1) 27-30, 1994.--The aim of this experiment was to... more of extinction by scopolamine. PHYSIOL BEHAV 56(1) 27-30, 1994.--The aim of this experiment was to determine the effects of muscarinic blockade on extinction of passive avoidance conditioning. Rats were trained with a foot shock of 2.5, 3.0, or 6.0 mA and were tested for retention for 8 weeks (once weekly). Five minutes before the seventh test they were injected with 8 mg/kg scopolamine. The groups that had been trained with 2.5 and 3.0 mA showed extinction, which was reversed by the scopolamine; the overreinforced group (6.0 mA) did not show extinction and the scopolamine did not alter the conditioned response. The data support the hypothesis that extinction represents the learning of a new response sustained by a set of cholinergic neurons, different from that which mediated original passive avoidance learning.