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

Abstract

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.

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

“…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, ).…”

“…This study demonstrated that Cbl administration increases the dendritic length and number of dendritic spines of the pyramidal neurons from dorsal hippocampus and PFC of aged SH rats, without changes in the BLA neurons. 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, ).…”

Juvenile stress causes reduced locomotor behavior and dendritic spine density in the prefrontal cortex and basolateral amygdala in Sprague–Dawley rats

“…However, there are many studies that suggest the participation of other neurotransmitters, such as serotonin, GABA, and glutamate (for review see Moe et al, ; Flores, Morales‐Medina, & Diaz, ). There are also several reports suggesting the participation of limbic structures, such as the PFC, the VH, the BLA, and the NAcc (Flores, Flores‐Gómez, & Gómez‐Villalobos, ; Flores, Morales‐Medina, & Diaz, ). Animals subjected to prenatal stress showed an increase in this behavior at prepubertal and adult stages (Peters, 1986, Deminiére et al, 1992, Martinez‐Tellez et al, ).…”

“…The latter sends inhibitory GABAergic projections to the limbic thalamus, especially to the dorsomedial nucleus, which sends glutamatergic projections to the PFC. All of these structures belong to the limbic system, which is responsible for the management of emotions (for review see Flores, Morales‐Medina, & Diaz, ; Flores, Flores‐Gómez, & Gómez‐Villalobos, ).…”

Chronic administration of resveratrol prevents morphological changes in prefrontal cortex and hippocampus of aged rats

“…Aging is a progressive decline in cognitive processes associated with morphological brain changes, such as a decrease in neurogenesis, dendritic spine density (Burke and Barnes, ; Flores et al, ), and neurotransmission (del Arco et al, ; Segovia et al, ), which, causes neuronal dysfunction that correlates with a loss of cognitive and motor skills. It is reported that during aging, there is a decrease in motor activity in both, animal experimental models and in humans (Segovia et al, ).…”