Ana FrancoUniversity of Alcalá | UAH · Department of Medicine and Medical Specialties
Ana Franco
PhD
SimpSoCoS grant (REA-European Commission)
https://cordis.europa.eu/project/id/101030864/results/de
About
27
Publications
3,913
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299
Citations
Citations since 2017
Introduction
During my postdoctoral stay in the Herman lab I gained a strong background on the physiological basis of stress responses, the effects of acute stress in the medial prefrontal cortex neurophysiology and the role of infralimbic PFC activation in stress responding and fear behavior. Furthermore, I acquired a general perspective in neuroanatomy, neurocircuitry, integrative biology and study designs accounting for sex-differences.
My long-term goal is to contribute to bridge the gap between basic neuroscience research and mental health services. Psychosocial stressors impact on circuit based brain activity, integrative physiology and behavior, from early life to adulthood. Knowledge on stress neurobiology is key to inform psychosocial, neurophysiological and pharmacological interventions.
Additional affiliations
January 2015 - February 2019
Position
- PostDoc Position
Description
- mPFC role in emotional regulation in response to acute stress: DREADDs, HPA axis, fear behavior and physiology of L5 pyramidal neurons of the infralimbic cortex
January 2012 - January 2013
September 2007 - December 2011
Publications
Publications (27)
The purpose of the current study was to determine how biological sex shapes behavioral coping and metabolic health across the lifespan after chronic stress. We hypothesized that examining chronic stress-induced behavioral and endocrine outcomes would reveal sex differences in the biological basis of susceptibility. During late adolescence, male and...
Exposure to prolonged stress during adolescence taxes adaptive and homeostatic processes leading to deleterious behavioral and metabolic outcomes. Although previous pre-clinical studies found effects of early life stress on cognition and stress hormone reactivity, these studies largely focused on males. The purpose of the current study was to deter...
Hypofunction of the prefrontal cortex (PFC) contributes to stress-related neuropsychiatric illnesses. Mechanisms leading to prefrontal hypoactivity remain to be determined. Prior evidence suggests that chronic stress leads to an increase in activity of parvalbumin (PV) expressing GABAergic interneurons (INs) in the PFC. The purpose of the study was...
Stress confers risk for the development and progression of Alzheimer's disease (AD). Relative to men, women are disproportionately more likely to be diagnosed with this neurodegenerative disease. We hypothesized that sex differences in endocrine stress responsiveness may be a factor in this statistic. To test this hypothesis, we assessed basal and...
DEK is a chromatin-remodeling phosphoprotein found in most human tissues, but its expression and function in the human brain is largely unknown. DEK depletion in vitro induces cellular and molecular anomalies associated with cognitive impairment, including down-regulation of the canonical Wnt/β-catenin signaling pathway. ToppGene analyses link DEK...
Clinical data suggest that the neuroendocrine stress response is chronically dysregulated in a subset of patients with temporal lobe epilepsy (TLE), potentially contributing to both disease progression and the development of psychiatric comorbidities such as anxiety and depression. Whether neuroendocrine dysregulation and psychiatric comorbidities...
DEK, a chromatin-remodeling gene expressed in most human tissues, is known for its role in cancer biology and autoimmune diseases. DEK depletion in vitro reduces cellular proliferation, induces DNA damage subsequently leading to apoptosis, and down-regulates canonical Wnt/β-catenin signaling, a molecular pathway essential for learning and memory. D...
In response to stress, defined as a real or perceived threat to homeostasis or well-being, brain systems initiate divergent physiological and behavioral processes that mobilize energy and promote adaptation. The brainstem contains multiple nuclei that engage in autonomic control and reflexive responses to systemic stressors. However, brainstem nucl...
IntroductionNeuronal morphogenesis is governed mainly by two interconnected processes, cytoskeletal reorganization, and signal transduction. The actin-binding molecule WIP (Wiskott-Aldrich syndrome protein [WASP]-interacting protein) was identified as a negative regulator of neuritogenesis. Although WIP controls activity of the actin-nucleation-pro...
Tumor expression of certain chemokine receptors is associated with resistance to apoptosis, migration, invasiveness and metastasis. Because CCR9 chemokine receptor expression is very restricted in healthy tissue, whereas it is present in tumors of distinct origins including leukemias, melanomas, prostate and ovary carcinomas, it can be considered a...
We identify Wiskott–Aldrich syndrome protein (WASP)-interacting protein (WIP) as a novel component of neuronal synapses whose
absence increases dendritic spine size and filamentous actin levels in an N-WASP/Arp2/3-independent, RhoA/ROCK/profilinIIa-dependent
manner. These effects depend on the reduction of membrane sphingomyelin (SM) due to transcr...
Effects of FGL on passive membrane properties of CA1 hippocampal neurons. (A–B) Application of FGL to cultured hippocampal slices did not alter input resistance (a) or holding current (b) when compared with untreated control neurons. N, number of cells.
(TIF)
FGL alters NMDAR decay kinetics in a PKC-independent manner. Organotypic slice cultures were treated with FGL (with or without chelerythrine) for 24 h and then transferred to fresh culture medium for an additional 24 h prior to recordings. Control slices were kept in regular culture medium until the recordings. NMDAR-mediated synaptic responses wer...
FGL does not alter structural plasticity of dendritic spines. (A) Representative confocal fluorescence image of dendritic spines expressing actin-GFP before (0′) or at different times after induction of LTP (5′, 20′) from untreated or FGL-treated organotypic slices. Spine heads undergoing plasticity are marked with arrows. LTP was induced using a s...
Chelerythrine inhibition of PKC activity on MARCKS (Myristoylated Alanine-Rich C-Kinase Substrate). (A) Left panels. Representative confocal images of BHK cells transfected with GFP-MARCKS under basal conditions (“no treatment”) or 20 s after application of the PKC activator 12-O-tetradecanoylphorbol-13-acetate (“TPA,” 0.1 µM). Right panels. Simila...
FGL does not alter long-term synaptic depression. Organotypic slice cultures were treated with FGL for 24 h and then transferred to fresh culture medium (without FGL) for an additional 24 h prior to recordings. Control slices were kept in regular culture medium until the recordings. LTD was induced by pairing presynaptic 1 Hz stimulation (300 pulse...
Unaltered spine neck length after FGL treatment. (A) Representative confocal projection image of CA1 pyramidal neurons. Bar = 150 µm. (B) Representative high magnification confocal projection image of apical dendrites to illustrate dendritic spines. Bar = 1.5 µm. (C) Quantification of spine neck length measured three-dimensionally. N, number of rat...
Spatial learning in the Morris water maze is altered by MEK and PI3K inhibitors. Mean distances traveled to find the hidden platform in the Morris water maze over the 2 training days (four trials each). N, number of animals. Rats injected with vehicle, FGL (20 µg), PD98059 (MEK inhibitor, 20 nmol), or LY294002 (PI3K inhibitor, 4.5 nmol), as indicat...
Additional experimental procedures are described in this supplementary text.
(DOCX)
FGL facilitates LTP in CA1 neurons. Cumulative frequency distribution of EPSC fold potentiation from the individual LTP experiments plotted in Figure 6D–E. Data are presented for control slices or slices treated with FGL, chelerythrine, or FGL plus chelerythrine, as indicated.
(TIF)
PKC inhibition does not alter spatial learning. Mean distances swam to find the hidden platform in the Morris water maze from vehicle- (white column) and PKC inhibitor-treated rats (gray columns; A, chelerythrine; B, GF109203X), over the eight training trials (four trials per day). N, the number of animals.
(TIF)
Author Summary
The human brain contains trillions of neuronal connections, called synapses, whose pattern of activity controls all our cognitive functions. These synaptic connections are dynamic and constantly changing in their strength and properties, and this process of synaptic plasticity is essential for learning and memory. Alterations in syna...
Wiskott-Aldrich syndrome protein (WASP) -interacting protein (WIP) is an actin-binding protein involved in the regulation of actin polymerization in cells, such as fibroblasts and lymphocytes. Despite its recognized function in non-neuronal cells, the role of WIP in the central nervous system has not been examined previously. We used WIP-deficient...
In immature dendritic cells (DCs) podosomes form and turn over behind the leading edge of migrating cells. The Arp2/3 complex activator Wiskott-Aldrich Syndrome Protein (WASP) localises to the actin core of forming podosomes together with WASP-Interacting Protein (WIP). A second weaker Arp2/3 activator, cortactin, is also found at podosomes where i...
Inflammation refers to a physiological process aimed at preventing or repairing the damage induced by infection, injury or intoxication. This process requires the coordinated activation and migration of leukocytes to the damaged area and therefore it is associated with changes in cell morphology and actin cytoskeleton reorganization. Actin cytoskel...
Questions
Questions (2)
Hi all,
I am trying to implement the perforated patch-clamp method to assess intrinsic excitability in mPFC slices from adult rats (PND 70-90).
Maintaining enough positive pressure in my electrode holder has always been a limiting factor in my rig, while working with the regular whole-cell patch clamp. My first attempts to work with perforated patch clamp using the regular Amphotericin B solubilization in DMSO (followed by tip filling the electrode with antibiotic free internal solution and back-filling with the internal containing Amphotericin B), are being especially frustrating given the requirement to keep positive air pressure to a minimum, due to the limitation I always have in my rig.
In the references below, I saw this alternative method to solubilize the antibiotics.
"An alternative method used the bipolar molecule N-methyl-d-glucamine (NMDG) to help disperse and solubilize nystatin or amphotericin B. A stock solution is made from a 0.1 M solution of NMDG dissolved in methanol (pH adjusted to about 7 with methanesulfonic acid in the presence of 0.01 M phenol red) to which nystatin (5 mg/ml) was added. Immediately before use, 50 ml of the stock solution is placed in a polyethylene test tube and dried completely with a stream of N2 gas. Pipette solution is added to the tube and briefly vortexed. The pipette solution can be filtered through a 0.22-um syringe filter; tip filling is not required (hence perforation is achieved more rapidly). Positive pressure can be applied during the approach to the cell, which makes this particularly useful for blind patch-clamping in tissues slices."
Endo K and Yawo H. J Physiol. 200
Ishibashi, Moorhouse and Nabekura. Patch Clamp Techniques: From Beginning to Advanced Protocols, 2012
Since it is compatible with applying positive pressure while approaching the cell, I am really tempted to give it a try. However, I haven't found any other citation of the method in the bibliography and I wonder if there is any reason for that.
Does anyone have experience with this alternative method? Any feedback and advice would be greatly appreciated!
Please, let me know if there is any further information that you need
Thank you so much in advance.
Best,
Ana
Hi All. I need to prepare dissociated primary neuronal cultures enriched in parvalbumin (PV) positive neurons. I have experience culturing hippocampal and cortical neurons up to 21 DIV using the Banker’s protocol. However, for my current aims, I would need to prepare mouse cell cultures enriched in PV expressing neurons. It seems that most of protocols based on cortical dissociated neurons yield between 10-20% of GABAergic neurons, half of which could become PV positive, at most. Does any of you could recommend a protocol to get further enrichment in interneurons, specifically in PV positive ones? Should I prepare cultures from Striatum or MGE better than from cortex? Which brain area do you think is the best to work with as a source for this purpose?
Thank you very much in advance for all the help and advice.
