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Papers by Soledad de Olmos

Research paper thumbnail of Developing the theory of the extended amygdala with the use of the cupric-silver technique

Journal of the History of the Neurosciences

Research paper thumbnail of Fear-context association during memory retrieval requires input from granular to dysgranular retrosplenial cortex

Neurobiology of Learning and Memory, 2019

Research paper thumbnail of Chronic restraint stress and acute binge ethanol intoxication induce apoptosis in the adolescent brain

Research paper thumbnail of Restraint stress exacerbates cell degeneration induced by acute binge ethanol in the adolescent, but not in the adult or middle-aged, brain

Behavioural Brain Research, 2019

HighlightsStress caused neurotoxicity in dorsal CA1 of adolescent, but not adult or aged, rats.Et... more HighlightsStress caused neurotoxicity in dorsal CA1 of adolescent, but not adult or aged, rats.Ethanol caused neurotoxicity in dorsal CA2, and ventral CA3 and DG of adolescents.Ethanol induced neurotoxicity at dorsal CA3 and DG.Stress + ethanol increased neurotoxicity at ventral CA1 and CA2 in adolescents only.The results highlight the vulnerability of the adolescent brain. &NA; Restraint stress (RS) induces neurotoxicity in the hippocampus, yet most of the studies have employed protracted RS (i.e., ≈ 21 days). Binge ethanol can induce brain toxicity, an effect affected by age. It could be postulated that RS may facilitate ethanol‐induced neurotoxicity, perhaps to a greater extent in adolescent vs. older subjects. We analyzed whether adolescent, adult or middle‐aged male rats exposed to five episodes of RS followed, 72h later, by binge ethanol (i.e., two administrations of 2.5 g/kg ethanol) exhibited hippocampal neurotoxicity. Adolescents, but not adult or middle‐aged rats, exhibited sensitivity to the neurotoxic effects of ethanol at dorsal CA2, ventral CA3 and ventral DG, and a neurotoxic effect of stress at dorsal CA1. Moreover, the combination of ethanol and stress exerted a synergistic effect upon cell degeneration at ventral CA1 and CA2, which was restricted to adolescents. Ethanol also increased cell degeneration, irrespective of age or stress, in dorsal CA3 and in dorsal DG; and ethanol and stress had, across all ages, a synergistic effect upon cell degeneration at the dorsal CA1. The greater neurotoxic response of adolescents to ethanol, stress, or ethanol+stress can put them at risk for the development of alcohol problems.

Research paper thumbnail of The offspring of rats selected for high or low ethanol intake at adolescence exhibit differential ethanol-induced Fos immunoreactivity in the central amygdala and in nucleus accumbens core

Pharmacology Biochemistry and Behavior, 2018

Research paper thumbnail of Long-term ethanol self-administration induces ΔFosB in male and female adolescent, but not in adult, Wistar rats

Progress in Neuro-Psychopharmacology and Biological Psychiatry, 2017

Research paper thumbnail of El Uso Del Modelo Farmacológico Basado en La Administración Experimental De MK-801, Para La Revisión y Re-Definición Del Sistema Límbico en El Contexto De La Anátomo-Patología

Ciencias Psicológicas, 2015

El efecto neurotóxico inducido en el sistema límbico de ratas por el tratamiento agudo con MK-801... more El efecto neurotóxico inducido en el sistema límbico de ratas por el tratamiento agudo con MK-801, afecta a todas las áreas del lóbulo límbico, como la corteza olfatoria, la amígdala baso-lateral, el sistema hipocampal, la corteza del cíngulo y regiones específicas de la corteza frontal e insular (allo-corticales y meso-corticales). En contraste, los núcleos sub-corticales habitualmente incluidos en el sistema límbico, como la amígdala extendida, el sistema estriado-palidal ventral, el área septal, el tálamo y el hipotálamo, no evidencian muerte neuronal. Los resultados anátomo-patológicos sugieren que las áreas del lóbulo límbico comparten características comunes, y soporta la idea de una unidad funcional que es diferente, dentro del sistema límbico, de otras regiones “límbicas” sub-corticales. Esto apoya la consideración de un lóbulo límbico compuesto estrictamente por áreas allo-corticales y meso-corticales del telencéfalo e implica la necesidad de re-definir el clásico y amplio ...

Research paper thumbnail of Sex differences and influence of gonadal hormones on MK801-induced neuronal degeneration in the granular retrosplenial cortex of the rat

Brain Structure and Function, 2008

Research paper thumbnail of Selective neuronal degeneration in the retrosplenial cortex impairs the recall of contextual fear memory

Brain Structure and Function, 2015

The retrosplenial cortex (RSC) is one of the largest cortical areas in rodents, and is subdivided... more The retrosplenial cortex (RSC) is one of the largest cortical areas in rodents, and is subdivided in two main regions, A29 and A30, according to their cytoarchitectural organization and connectivities. However, very little is known about the functional activity of each RSC subdivision during the execution of complex cognitive tasks. Here, we used a well-established fear learning protocol that induced long-lasting contextual fear memory and showed that during evocation of the fear memory, the expression of early growth response gene 1 was up-regulated in A30, and in other brain areas implicated in fear and spatial memory, however, was down-regulated in A29, including layers IV and V. To search for the participation of A29 on fear memory, we triggered selective degeneration of neurons within cortical layers IV and V of A29 by using a non-invasive protocol that takes advantage of the vulnerability that these neurons have MK801-toxicity and the modulation of this neurodegeneration by testosterone. Application of 5 mg/kg MK801 in intact males induced negligible neuronal degeneration of A29 neurons and had no impact on fear memory retrieval. However, in orchiectomized rats, 5 mg/kg MK801 induced overt degeneration of layers IV-V neurons of A29, significantly impairing fear memory recall. Degeneration of A29 neurons did not affect exploratory or anxiety-related behavior nor altered unconditioned freezing. Importantly, protecting A29 neurons from MK801-toxicity by testosterone preserved fear memory recall in orchiectomized rats. Thus, neurons within cortical layers IV-V of A29 are critically required for efficient retrieval of contextual fear memory.

Research paper thumbnail of Strain and colony differences in the neurotoxic sequelae of MK-801 visualized with the amino-cupric-silver method

Experimental and Toxicologic Pathology, 2003

Research paper thumbnail of Comparative analyses of the neurodegeneration induced by the non-competitive NMDA-receptor-antagonist drug MK801 in mice and rats

Neurotoxicology and Teratology, 2010

Research paper thumbnail of Neurodegeneration and prolonged immediate early gene expression throughout cortical areas of the rat brain following acute administration of dizocilpine

Research paper thumbnail of Neuronal Degeneration in Mice Induced by an Epidemic Strain of Saint Louis Encephalitis Virus Isolated in Argentina

Frontiers in Microbiology

Research paper thumbnail of Use of an amino-cupric-silver technique for the detection of early and semiacute neuronal degeneration caused by neurotoxicants, hypoxia, and physical trauma

Research paper thumbnail of Developing the theory of the extended amygdala with the use of the cupric-silver technique

Journal of the History of the Neurosciences

Research paper thumbnail of Fear-context association during memory retrieval requires input from granular to dysgranular retrosplenial cortex

Neurobiology of Learning and Memory, 2019

Research paper thumbnail of Chronic restraint stress and acute binge ethanol intoxication induce apoptosis in the adolescent brain

Research paper thumbnail of Restraint stress exacerbates cell degeneration induced by acute binge ethanol in the adolescent, but not in the adult or middle-aged, brain

Behavioural Brain Research, 2019

HighlightsStress caused neurotoxicity in dorsal CA1 of adolescent, but not adult or aged, rats.Et... more HighlightsStress caused neurotoxicity in dorsal CA1 of adolescent, but not adult or aged, rats.Ethanol caused neurotoxicity in dorsal CA2, and ventral CA3 and DG of adolescents.Ethanol induced neurotoxicity at dorsal CA3 and DG.Stress + ethanol increased neurotoxicity at ventral CA1 and CA2 in adolescents only.The results highlight the vulnerability of the adolescent brain. &NA; Restraint stress (RS) induces neurotoxicity in the hippocampus, yet most of the studies have employed protracted RS (i.e., ≈ 21 days). Binge ethanol can induce brain toxicity, an effect affected by age. It could be postulated that RS may facilitate ethanol‐induced neurotoxicity, perhaps to a greater extent in adolescent vs. older subjects. We analyzed whether adolescent, adult or middle‐aged male rats exposed to five episodes of RS followed, 72h later, by binge ethanol (i.e., two administrations of 2.5 g/kg ethanol) exhibited hippocampal neurotoxicity. Adolescents, but not adult or middle‐aged rats, exhibited sensitivity to the neurotoxic effects of ethanol at dorsal CA2, ventral CA3 and ventral DG, and a neurotoxic effect of stress at dorsal CA1. Moreover, the combination of ethanol and stress exerted a synergistic effect upon cell degeneration at ventral CA1 and CA2, which was restricted to adolescents. Ethanol also increased cell degeneration, irrespective of age or stress, in dorsal CA3 and in dorsal DG; and ethanol and stress had, across all ages, a synergistic effect upon cell degeneration at the dorsal CA1. The greater neurotoxic response of adolescents to ethanol, stress, or ethanol+stress can put them at risk for the development of alcohol problems.

Research paper thumbnail of The offspring of rats selected for high or low ethanol intake at adolescence exhibit differential ethanol-induced Fos immunoreactivity in the central amygdala and in nucleus accumbens core

Pharmacology Biochemistry and Behavior, 2018

Research paper thumbnail of Long-term ethanol self-administration induces ΔFosB in male and female adolescent, but not in adult, Wistar rats

Progress in Neuro-Psychopharmacology and Biological Psychiatry, 2017

Research paper thumbnail of El Uso Del Modelo Farmacológico Basado en La Administración Experimental De MK-801, Para La Revisión y Re-Definición Del Sistema Límbico en El Contexto De La Anátomo-Patología

Ciencias Psicológicas, 2015

El efecto neurotóxico inducido en el sistema límbico de ratas por el tratamiento agudo con MK-801... more El efecto neurotóxico inducido en el sistema límbico de ratas por el tratamiento agudo con MK-801, afecta a todas las áreas del lóbulo límbico, como la corteza olfatoria, la amígdala baso-lateral, el sistema hipocampal, la corteza del cíngulo y regiones específicas de la corteza frontal e insular (allo-corticales y meso-corticales). En contraste, los núcleos sub-corticales habitualmente incluidos en el sistema límbico, como la amígdala extendida, el sistema estriado-palidal ventral, el área septal, el tálamo y el hipotálamo, no evidencian muerte neuronal. Los resultados anátomo-patológicos sugieren que las áreas del lóbulo límbico comparten características comunes, y soporta la idea de una unidad funcional que es diferente, dentro del sistema límbico, de otras regiones “límbicas” sub-corticales. Esto apoya la consideración de un lóbulo límbico compuesto estrictamente por áreas allo-corticales y meso-corticales del telencéfalo e implica la necesidad de re-definir el clásico y amplio ...

Research paper thumbnail of Sex differences and influence of gonadal hormones on MK801-induced neuronal degeneration in the granular retrosplenial cortex of the rat

Brain Structure and Function, 2008

Research paper thumbnail of Selective neuronal degeneration in the retrosplenial cortex impairs the recall of contextual fear memory

Brain Structure and Function, 2015

The retrosplenial cortex (RSC) is one of the largest cortical areas in rodents, and is subdivided... more The retrosplenial cortex (RSC) is one of the largest cortical areas in rodents, and is subdivided in two main regions, A29 and A30, according to their cytoarchitectural organization and connectivities. However, very little is known about the functional activity of each RSC subdivision during the execution of complex cognitive tasks. Here, we used a well-established fear learning protocol that induced long-lasting contextual fear memory and showed that during evocation of the fear memory, the expression of early growth response gene 1 was up-regulated in A30, and in other brain areas implicated in fear and spatial memory, however, was down-regulated in A29, including layers IV and V. To search for the participation of A29 on fear memory, we triggered selective degeneration of neurons within cortical layers IV and V of A29 by using a non-invasive protocol that takes advantage of the vulnerability that these neurons have MK801-toxicity and the modulation of this neurodegeneration by testosterone. Application of 5 mg/kg MK801 in intact males induced negligible neuronal degeneration of A29 neurons and had no impact on fear memory retrieval. However, in orchiectomized rats, 5 mg/kg MK801 induced overt degeneration of layers IV-V neurons of A29, significantly impairing fear memory recall. Degeneration of A29 neurons did not affect exploratory or anxiety-related behavior nor altered unconditioned freezing. Importantly, protecting A29 neurons from MK801-toxicity by testosterone preserved fear memory recall in orchiectomized rats. Thus, neurons within cortical layers IV-V of A29 are critically required for efficient retrieval of contextual fear memory.

Research paper thumbnail of Strain and colony differences in the neurotoxic sequelae of MK-801 visualized with the amino-cupric-silver method

Experimental and Toxicologic Pathology, 2003

Research paper thumbnail of Comparative analyses of the neurodegeneration induced by the non-competitive NMDA-receptor-antagonist drug MK801 in mice and rats

Neurotoxicology and Teratology, 2010

Research paper thumbnail of Neurodegeneration and prolonged immediate early gene expression throughout cortical areas of the rat brain following acute administration of dizocilpine

Research paper thumbnail of Neuronal Degeneration in Mice Induced by an Epidemic Strain of Saint Louis Encephalitis Virus Isolated in Argentina

Frontiers in Microbiology

Research paper thumbnail of Use of an amino-cupric-silver technique for the detection of early and semiacute neuronal degeneration caused by neurotoxicants, hypoxia, and physical trauma