We are interested on the molecular mechanisms underlying learning and memory storage, more precisely in the role of transcriptional and epigenetic mechanisms in neuronal plasticity. We also investigate how the malfunction of these mechanisms may cause pathological situations in the nervous system.
To investigate these questions, we use a multidisciplinary approach that combines mouse genetics and genomics, molecular biology, physiology and behavioral
Our research focuses on the following two areas:
1. Role of activity-dependent transcription in neuronal plasticity.
Alterations in patterns of gene expression are thought to underlie the long-lasting changes in the strength of synaptic connections between neurons responsible for the encoding of memories in the nervous system. A number of transcription factors have been involved in this process. We are investigating the details of the participation of activity-regulated transcription factors, such as members of the CREB family, in plasticity and memory.
2. Chromatin remodeling and neuronal plasticity.
The post-translational modification of histone proteins is thought to participate in the regulation of gene expression. Specifically, the acetylation and methylation of nucleosomes may provide a mechanism for epigenetic regulation of the activity of loci that are relevant in neuronal plasticity and behaviour. We are interested in exploring the contribution of histone modifications to learning, memory and other long-lasting modification of the animal’s behavior. We also investigate on different mouse model for neurological conditions, such as Huntington disease and some intellectual disability syndromes, in which these epigenetic mechanisms seem to be affected.