The frequency of spontaneous seizures in rats correlates with alterations in sensorimotor gating, spatial working memory, and parvalbumin expression throughout limbic regions

Wolf, Daniele C.; Bueno-Júnior, Lézio Soares; Lopes-Aguiar, Cleiton; Silva, R.A. Do Val Da; Kandratavicius, Ludmyla; Leite, João Pereira

doi:10.1016/j.neuroscience.2015.11.008

Cited by 40 publications

(37 citation statements)

References 80 publications

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“…Patients and an animal model of MTLE often present neurodegenerative damage in different brain areas (Araujo et al, 2006; Diniz et al, 2011; Kandratavicius et al, 2015; Peixoto-Santos et al, 2015; Wolf et al, 2016). In particular, severe loss of hilar interneurons and pyramidal neurons in CA3 and CA1 is commonly seen in the hippocampus of MTLE patients and animal models (Turski et al, 1983a; Leite et al, 1996; Covolan et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…An activity monitor apparatus (Insight, Brazil) was used to analyze total distance explored, the number of vertical activities (the number of times an animal rises in its hind limbs), time explored on the borders and center of the arena ( Supplementary Figure S3 ). The testing protocol consisted of placing the animal in the center of the box (habituation) for 3 min and then test for 8 min, according to previously tested protocols (Wolf et al, 2016). After each test, open field was cleaned with acetic acid (0.1% v/v).…”

Section: Methodsmentioning

confidence: 99%

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Protective Effects of Cannabidiol against Seizures and Neuronal Death in a Rat Model of Mesial Temporal Lobe Epilepsy

et al. 2017

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The present study reports the behavioral, electrophysiological, and neuropathological effects of cannabidiol (CBD), a major non-psychotropic constituent of Cannabis sativa, in the intrahippocampal pilocarpine-induced status epilepticus (SE) rat model. CBD was administered before pilocarpine-induced SE (group SE+CBDp) or before and after SE (group SE+CBDt), and compared to rats submitted only to SE (SE group), CBD, or vehicle (VH group). Groups were evaluated during SE (behavioral and electrophysiological analysis), as well as at days one and three post-SE (exploratory activity, electrophysiological analysis, neuron density, and neuron degeneration). Compared to SE group, SE+CBD groups (SE+CBDp and SE+CBDt) had increased SE latency, diminished SE severity, increased contralateral afterdischarge latency and decreased relative powers in delta (0.5–4 Hz) and theta (4–10 Hz) bands. Only SE+CBDp had increased vertical exploratory activity 1-day post SE and decreased contralateral relative power in delta 3 days after SE, when compared to SE group. SE+CBD groups also showed decreased neurodegeneration in the hilus and CA3, and higher neuron density in granule cell layer, hilus, CA3, and CA1, when compared to SE group. Our findings demonstrate anticonvulsant and neuroprotective effects of CBD preventive treatment in the intrahippocampal pilocarpine epilepsy model, either as single or multiple administrations, reinforcing the potential role of CBD in the treatment of epileptic disorders.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Protective Effects of Cannabidiol against Seizures and Neuronal Death in a Rat Model of Mesial Temporal Lobe Epilepsy

et al. 2017

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“…1a). Photomicrograph samples were analyzed using ImageJ software (NIH), and the number of PV-immunoreactive cells was quantified using macros written to automate particle counting within each region [41,53]. An example of the ImageJ analysis can be seen in figure 1c.…”

Section: Methodsmentioning

confidence: 99%

Developmental Age Differentially Mediates the Calcium-Binding Protein Parvalbumin in the Rat: Evidence for a Selective Decrease in Hippocampal Parvalbumin Cell Counts

Ganguly

Keary²,

Kania³

et al. 2016

Dev Neurosci

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Local circuit GABAergic neurons, including parvalbumin (PV)-containing basket cells, likely play a key role in the development, physiology, and pathology of neocortical circuits. Regionally selective and well-defined decreases in PV have been described in human postmortem schizophrenic brain tissue in both the hippocampus and prefrontal cortex. Animal models of schizophreniform dysfunction following acute and/or chronic ketamine treatment have also demonstrated decreases in PV expression. Conflicting reports with respect to PV immunoreactivity following acute and chronic ketamine treatments in rodents question the utility of using PV as a biological marker of pathology-related dysfunction. The current literature lacks sufficient and systematic characterization of normative PV expression in pharmacologically and behaviorally naïve rodent tissue. In order to understand developmental changes in PV and its putative role in neuropathology, we examined the baseline distribution of the number of cells expressing this protein at distinct developmental ages. The present study examined PV cell counts across the septotemporal axis of the CA1, CA3, and dentate gyrus (DG) regions of the hippocampus, as well as within the retrosplenial, somatosensory, and prefrontal cortices, in 1-, 6-, and 12-month-old naïve rats. Our findings suggest that the hippocampal PV+ cell number significantly decreases as a function of age with considerable regional (CA1, CA3, and DG) and septotemporal variation, a finding that was specific to the hippocampus. Additionally, we observed a modest increase in PV cell number within the prefrontal (anterior cingulate) cortex, which is in line with findings indicating a delayed developmental maturation of this region. The present work highlights decreases in PV+ cell counts within the hippocampus across development, and points to the need for a greater understanding of the role of PV and local circuit developmental changes, as well as consideration of their development when modeling developmentally related neuropathological disorders (e.g. schizophrenia, autism).

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“…Five squares of 50 Â 50 lm were randomly placed on each analyzed brain area (right and left hemispheres) from all animals of each group, and then averaged after the counting. We performed neuron counts (neurons per cubic millimeter) estimated at 200Â magnification using a morphometric grid methodology and Abercrombie's correction (Abercrombie, 1946) as previously described and extensively used by our group and others (Andrade-Valenc¸a et al, 2008; Kandratavicius et al, 2013Kandratavicius et al, , 2014Rodrigues et al, 2015;Wolf et al, 2015). Neurons were distinguished from glial cells by their clearly distinct morphological appearance.…”

Section: Cell Density Analysismentioning

confidence: 99%

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

et al. 2017

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Abstract-Brain glucose metabolism is altered in sporadic Alzheimer's disease (sAD), whose pathologies are reproduced in rodents by intracerebroventricular (icv) infusion of streptozotocin (STZ) in subdiabetogenic doses. The icv-STZ model also culminates in central cholinergic dysfunctions, which in turn are known to underlie both the sAD cognitive decline, and synaptic plasticity impairments. Considering the cognitive-enhancing potential of chronic nicotine (Nic), we investigated whether it attenuates icv-STZ-induced impairments in recognition memory and synaptic plasticity in a cognition-relevant substrate: the hippocampal CA1-medial prefrontal cortex (mPFC) pathway. Rats treated with icv-STZ were submitted to a chronic Nic regime, and were evaluated for recognition memory. We then examined long-term potentiation (LTP), paired-pulse facilitation (PPF) under urethane anesthesia, and brains were also evaluated for hippocampus-mPFC cell density. We found that Nic treatment prevents icv-STZ-induced disruptions in recognition memory and LTP. STZ did not precipitate neuronal death, while Nic alone was associated with higher neuronal density in CA1 when compared to vehicle-injected animals. Through combining behavioral, neurophysiological, and neuropathological observations into the Nic-STZ interplay, our study reinforces that cholinergic treatments are of clinical importance against earlystage Alzheimer's disease and mild cognitive impairments.

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The frequency of spontaneous seizures in rats correlates with alterations in sensorimotor gating, spatial working memory, and parvalbumin expression throughout limbic regions

Cited by 40 publications

References 80 publications

Protective Effects of Cannabidiol against Seizures and Neuronal Death in a Rat Model of Mesial Temporal Lobe Epilepsy

Protective Effects of Cannabidiol against Seizures and Neuronal Death in a Rat Model of Mesial Temporal Lobe Epilepsy

Developmental Age Differentially Mediates the Calcium-Binding Protein Parvalbumin in the Rat: Evidence for a Selective Decrease in Hippocampal Parvalbumin Cell Counts

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

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