Apamin induces plastic changes in hippocampal neurons in senile Sprague–Dawley rats

Romero-Curiel, Alejandra; López-Carpinteyro, Diana; Gamboa, Citlalli; Cruz, Fidel de la; Zamudio, Sergio; Flores, Gonzalo

doi:10.1002/syn.20938

Cited by 20 publications

(14 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, our previous reports showed that dendritic spines number of the pyramidal neurons of the layers 3 and 5 of the PFC and CA1 are reduced after several months of high blood pressure (Flores et al, ; Sánchez et al, ; Vega et al, ). Moreover, aged animals also showed a reduced dendritic spine density of the pyramidal neurons of the PFC and CA1 of the dorsal hippocampus (Acosta‐Peña et al, ; Alcantara‐Gonzalez et al, ; Flores et al, ; Juárez et al, ; Romero‐Curiel et al, ). In accordance with our previous reports, chronic Cbl treatment results in an enhancement in the dendritic length and dendritic spine density in the cortical regions such as PFC and hippocampus (Alcantara‐Gonzalez et al, ; Juárez et al, ; Sanchez‐Vega et al, ; Vázquez‐Roque et al, ), without effect on dendritic parameters in the pyramidal neurons of the BLA (Vázquez‐Roque et al, ).…”

Section: Discussionsupporting

confidence: 83%

Cerebrolysin improves memory and ameliorates neuronal atrophy in spontaneously hypertensive, aged rats

Solis-Gaspar

Vázquez-Roque

Gómez-Villalobos

et al. 2016

Synapse

Self Cite

View full text Add to dashboard Cite

The spontaneously hypertensive (SH) rat has been used as an animal model of vascular dementia (VD). Our previous report showed that, SH rats exhibited dendritic atrophy of pyramidal neurons of the CA1 dorsal hippocampus and layers 3 and 5 of the prefrontal cortex (PFC) at 8 months of age. In addition, we showed that cerebrolysin (Cbl), a neurotrophic peptide mixture, reduces the dendritic atrophy in aged animal models. This study aimed to determine whether Cbl was capable of reducing behavioral and neuronal alterations, in old female SH rats. The level of diastolic and systolic pressure was measured every month for the 6 first months and only animals with more than 160 mm Hg of systolic pressure were used. Female SH rats (6 months old) received 6 months of Cbl treatment. Immediately after the Cbl treatment, two behavioral tests were applied, the Morris water maze test for memory and learning and locomotor activity in novel environments. Immediately after the last behavioral test, dendritic morphology was studied with the Golgi-Cox stain procedure followed by a Sholl analysis. Clearly, SH rats with Cbl showed an increase in the dendritic length and dendritic spine density of pyramidal neurons in the CA1 in the dorsal hippocampus and layers 3 and 5 of the PFC. Interestingly, Cbl improved memory of the old SH rats. Our results support the possibility that Cbl may have beneficial effects on the management of brain alterations in an animal model with VD. Synapse 70:378-389, 2016. © 2016 Wiley Periodicals, Inc.

show abstract

Section: Discussionsupporting

confidence: 83%

Cerebrolysin improves memory and ameliorates neuronal atrophy in spontaneously hypertensive, aged rats

Solis-Gaspar

Vázquez-Roque

Gómez-Villalobos

et al. 2016

Synapse

Self Cite

View full text Add to dashboard Cite

show abstract

“…These results may suggest that dendritic spine atrophy could be interpreted as maladaptive plasticity. Several reports have demonstrated that aging‐induced dendritic length hypotrophy and spine loss are accompanied by cognitive deficits in tasks mediated by the hippocampus and the PFC (Acosta‐Peña et al, ; Alcantara‐Gonzalez et al, ; Duan et al, ; Juarez et al, ; Romero‐Curiel et al, ). In addition, reduced spinogenesis in the PFC‐, hippocampus‐pyramidal and NAcc‐medium spiny neurons has been reported in animal models of VD (Sanchez et al, ; Vega et al, ).…”

Section: Relevance Of Neuronal Morphology In Vascular Dementiamentioning

confidence: 99%

Neuronal changes after chronic high blood pressure in animal models and its implication for vascular dementia

Flores

Flores-Gómez²,

Gómez-Villalobos

2016

Synapse

Self Cite

View full text Add to dashboard Cite

Vascular dementia is a devastating disorder not only for the patient, but also for the family because this neurocognitive disorder breaks the patient's independence, and leads to family care of the patient with a high cost for the family. This complex disorder alters memory, learning, judgment, emotional control and social behavior and affects 4% of the elderly world population. The high blood pressure or arterial hypertension is a major risk factor for cerebrovascular disease, which in most cases leads to vascular dementia. Interestingly, this neurocognitive disorder starts after long lasting hypertension, which is associated with reduced cerebral blood flow or hypoperfusion, and complete or incomplete ischemia with cortical thickness. Animal models have been generated to elucidate the pathophysiology of this disorder. It is known that dendritic complexity determines the receptive synaptic contacts, and the loss of dendritic spine and arbor stability are strongly associated with dementia in humans. This review evaluates relevant data of human and animal models that have investigated the link between long-lasting arterial hypertension and neural morphological changes in the context of vascular dementia. We examined the effect of chronic arterial hypertension and aged in vascular dementia. Neural dendritic morphology in the prefrontal cortex and the dorsal hippocampus and nucleus accumbens after chronic hypertension was diskussed in the animal models of hypertension. Chronic hypertension reduced the dendritic length and spine density in aged rats.

show abstract

“…In contrast to this result, in mice with partial hippocampal-lesions, mimicking the pathophysiological hallmark also observed in AD, blocking K Ca 2 channels by apamin could alleviate the impairment in spatial reference memory and working memory (Ikonen and Riekkinen, 1999). Due to these findings, apamin has been proposed as a therapeutic agent in AD treatment (Romero-Curiel et al, 2011). It is of interest to determine whether K Ca 2.2 channel protein expression increases with age and whether blocking K Ca 2.2 channels can limit age-related memory impairment (Stackman et al, 2008).…”

Section: Alzheimer’s Diseasementioning

confidence: 99%

KCa2 and KCa3 Channels in Learning and Memory Processes, and Neurodegeneration

Kuiper¹,

Nelemans²,

Luiten³

et al. 2012

Front. Pharmacol.

View full text Add to dashboard Cite

Calcium-activated potassium (KCa) channels are present throughout the central nervous system as well as many peripheral tissues. Activation of KCa channels contribute to maintenance of the neuronal membrane potential and was shown to underlie the afterhyperpolarization (AHP) that regulates action potential firing and limits the firing frequency of repetitive action potentials. Different subtypes of KCa channels were anticipated on the basis of their physiological and pharmacological profiles, and cloning revealed two well defined but phylogenetic distantly related groups of channels. The group subject of this review includes both the small conductance KCa2 channels (KCa2.1, KCa2.2, and KCa2.3) and the intermediate-conductance (KCa3.1) channel. These channels are activated by submicromolar intracellular Ca2+ concentrations and are voltage independent. Of all KCa channels only the KCa2 channels can be potently but differentially blocked by the bee-venom apamin. In the past few years modulation of KCa channel activation revealed new roles for KCa2 channels in controlling dendritic excitability, synaptic functioning, and synaptic plasticity. Furthermore, KCa2 channels appeared to be involved in neurodegeneration, and learning and memory processes. In this review, we focus on the role of KCa2 and KCa3 channels in these latter mechanisms with emphasis on learning and memory, Alzheimer’s disease and on the interplay between neuroinflammation and different neurotransmitters/neuromodulators, their signaling components and KCa channel activation.

show abstract

Apamin induces plastic changes in hippocampal neurons in senile Sprague–Dawley rats

Cited by 20 publications

References 54 publications

Cerebrolysin improves memory and ameliorates neuronal atrophy in spontaneously hypertensive, aged rats

Cerebrolysin improves memory and ameliorates neuronal atrophy in spontaneously hypertensive, aged rats

Neuronal changes after chronic high blood pressure in animal models and its implication for vascular dementia

KCa2 and KCa3 Channels in Learning and Memory Processes, and Neurodegeneration

Contact Info

Product

Resources

About