In my laboratory, we are interested in the molecular mechanisms underlying memory storage, the remarkable capability that allows the adaptation of animals to their ever-changing environment.
To investigate these processes we use a multidisciplinary approach that combines mouse genetics, molecular biology, physiology and behavioral studies.
Our long-term goal is to decipher the genetic programs activated by neuronal activity and required to maintain long-lasting changes in synaptic plasticity and memory.
This knowledge may reveal how dysfunction of these molecular processes leads to neurological disorders and open new therapeutics avenues for restoring normal brain function.

More about our lab.

Viosca J, Lopez de Armentia M, Jancic D and Barco A (2009). Enhanced CREB-dependent gene expression increases the excitability of neurons in the basal amygdala and primes the consolidation of contextual and cued fear memory. Learn Mem 16(3): 193-197.

Viosca J, Malleret G, Bourtchouladze R, Benito E, Vronskava S, Kandel ER and Barco A (2009). Chronic enhancement of CREB activity in the hippocampus interferes with the retrieval of spatial information. Learn Mem 16(3): 198-209.

Jancic D, Lopez de Armentia M, Valor LM, Olivares R and Barco A (2009). Inhibition of cAMP-response element binding protein reduces neuronal excitability and plasticity, and triggers neurodegeneration. Cerebral Cortex 2009 Feb 12 [Epub ahead of print].

Lopez de Armentia M, Jancic D, Olivares R, Alarcon ER, Kandel ER and Barco A (2007). CREB-mediated gene expression increases the intrinsic excitability of CA1 pyramidal neurons. J. Neurosci. 27(50): 13909-13918.

Barco A, Patterson S, Alarcon JM, Gromova P, Mata-Roig M, Morozov A and Kandel ER (2005). Gene expression profiling of facilitated L-LTP in VP16-CREB mice reveals that BDNF is critical for both the maintenance of LTP and for synaptic capture. Neuron, 48(1): 123-137.

Alarcon JM, Malleret G, Touzani K, Vronskaya S, Ishii S, Kandel ER and Barco A (2004). Chromatin acetylation, memory, and LTP are impaired in CBP+/- mice: a model for the cognitive deficit in Rubinstein-Taybi syndrome and its amelioration. Neuron 42(6):947-959. 

Barco A, Alarcon JM and Kandel ER (2002) Expression of constitutively active CREB protein facilitates the late phase of long-term potentiation by enhancing synaptic capture. Cell 108(5):689-703. 

See all publications by Angel Barco

My laboratory utilizes a bottom-up approach based on the generation of genetically modified mice and their parallel analysis at the biochemical, molecular, electrophysiological and behavioral levels. We are currently using the following methodologies:

•    Mouse genetics (brain restricted and inducible mutant strains) and use of recombinant lentiviruses

•    Molecular and cell biology techniques with focus on the analysis of gene expression

•    Electrophysiological studies in brain slices

•    Behavioral studies in mice

More information about our expertise can be found here:

http://in.umh.es/paginas_particulares/barco/what%20methods.html