Cerebrolysin treatment improved short-term memory deficits while simultaneously increasing hippocampal spine density

Ivette Espinoza1, Ma de Jesús Gómez-Villalobos2, Leonardo Aguilar-Hernández2

  • 1Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla (BUAP), Puebla, Mexico; Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Unidad Tlaxcala, Mexico; Maestría en Ciencias Biológicas, Universidad Autónoma de Tlaxcala, Mexico.

PubMed

Hypertension, if untreated, can disrupt the blood-brain-barrier (BBB) and reduce cerebral flow in the central nervous system (CNS) inducing hippocampal atrophy, potentially leading to cognitive deficits and vascular dementia. Spontaneous hypertensive rats (SHR) demonstrated neuroplastic alterations in the hippocampus, hyperlocomotion and memory deficits in males. Cerebrolysin (CBL), a neuropeptide preparation, induces synaptic and neuronal plasticity in various populations of neurons and repairs the integrity of the BBB. This research aims to investigate the behavioral outcomes in locomotion and recognition memory in the Novel Object Recognition Test (NORT) and assess the neuroreparative effect of CBL on the cytoarchitecture of neurons and the spine density in pyramidal neurons of the prefrontal cortex (PFC), the entorhinal cortex (EC) and the CA1 region of the dorsal hippocampus, as well as spheroidal neurons of the dentate gyrus (DG). Our findings indicate that SHR exhibited elevated diastolic and systolic pressures, and increased locomotion. Importantly, CBL treatment improved recognition memory in SHR strain. Hypertension led to reduced arborization in the EC, CA1, and DG regions. Moreover, CBL treatment increased arborization in both normotensive and hypertensive rats in the CA1, and DG regions of hippocampus and EC and selectively increased spine density in the hippocampus of hypertensive rats. These findings suggest that CBL neurotrophic treatment enhances recognition memory and promotes dendritic growth or spine density, depending on the neurochemical environment within the brain.