Brain Disorders & Therapy

Postnatal betamethasone administration produces delayed changes in the immuno histochemical expression of brain-derived neurotrophic factor and the tyrosine kinase B receptor in the rat cerebellar cortex together with an

7^th International Conference on Neurological Disorders & Stroke

September 20-21, 2018 | Rome, Italy

Martina Valencia, Illanes J and Pascual R

Pontifical Catholic University of Valparaiso, Chile

Posters & Accepted Abstracts: Brain Disord Ther

Abstract:

Postnatal synthetic glucocorticoids (GCs) are widely used in the prevention of chronic lung disease in premature infants and their pharmacologic use is associated with neuro developmental delay and various behavioral and brain changes. Using classic Golgi staining methods, we previously showed that the administration of GCs betamethasone (BET), in equivalent doses to those given in cases of human premature birth, generates long term alterations in Purkinje cell (PC) dendritic development in the cerebellar cortex. On the other hand, the brain-derived neurotrophic factor (BDNF) and the tyrosine kinase B receptor (TrkB) are involved in cerebellar PC dendritic development and maintenance and are located predominantly in the cerebellar molecular layer where PC dendritogenesis occurs. Therefore, we hypothesized that reductions in protracted lower PC dendritic arborization could be due, atleast in part, to changes in dendritic expression of BDNF and TrkB. On the other hand, previous studies demonstrated that animals that experience stress, either via chronic maternal stress or exogenous GCs administration, exhibited a significant alteration in the neurotrophic factors regulation and behavioral changes associated with anxious behaviors. For these reasons, in the present study, we evaluated whether postnatal administration of betamethasone alters the immunohistochemical (IHC) expression of BDNF and TrkB in the cerebellar cortex along with anxiety behaviours in infants, adolescent and adult rats. Consistent with our previous studies, we observed that animals postnatal exposed to betamethasone showed long term alterations in the IHC expression of BDNF and TrkB in adolescent and adult rats. Additionally, these protracted molecular changes were accompanied by an increase of anxiety like behaviors in the elevated plus maze and marble burying test in adolescent and adult rats. Recent Publications 1. Pascual R, Santander O, Cuevas I and Valencia M (2017) Prenatal glucocorticoid administration persistently increased the immunohistochemical expression of type-1 metabotropic glutamate receptor and Purkinje cell dendritic growth in the cerebellar cortex of the rat. Romanian Journal of Morphology and Embryology. 58(1):67-72. 2. Pascual R, Valencia M and Bustamante C (2015) Antenatal betamethasone produces protracted changes in anxiety-like behaviors and in the expression of microtubule-associated protein 2, brain-derived neurotrophic factor and the tyrosine kinase B receptor in the rat cerebellar cortex. International Journal of Developmental Neuroscience. 43:78-85. 3. Pascual R, Valencia M and Bustamante C (2015) Purkinje cell dendritic atrophy induced by prenatal stress is mitigated by early environmental enrichment. Neuropediatrics. 46(1):37-43. 4. Pascual R, Valencia M, Larrea S and Bustamante C (2014) Single course of antenatal betamethasone produces delayed changes in morphology and calbindin-d28k expression in a rat's cerebellar Purkinje cells. Acta Neurobiologiae Experimentalis. 74(4):415-423. 5. Bustamante C et al. (2014) Effects of a single course of prenatal betamethasone on dendritic development in dentate gyrus granular neurons and on spatial memory in rat offspring. Neuropediatrics. 45(6):354-361.

Biography :

Martina Valencia is a part of the research team at the Neuroscience Laboratory of the Pontifical Catholic University of Valparaíso, Chile and has her expertise in university teaching in subjects such as neurophysiology, research methodology and history of science. In parallel and more than seven years ago, she carried out research on the effect of prenatal stress on neurodevelopment. To achieve this goal, the work is based on a problem that occurs in the obstetric clinic: the use of antenatal and postnatal synthetic glucocorticoids in the prevention of chronic lung disease in premature infants and their adverse side effects at the level of the Central Nervous System, such as, neurodevelopmental delay and various behavioral and brain changes observed in the progeny. She has built this model after years of experience in research, evaluation, teaching and administration both in hospital and education institutions.

E-mail: martina.valencia@pucv.cl