Skip to main content

Alexandre E. Medina de Jesus, DSci

Academic Title:

Associate Professor

Primary Appointment:

Pediatrics

Additional Title:

D.Sci.

Location:

655 Baltimore St

Phone (Primary):

(410) 706-8135

Education and Training

Universidade Santa Ursula, Brazil B.S. 1990 Biology
Universidade Federal do Rio de Janeiro, Brazil M.Sc. 1996 Zoology
Universidade do Estado do Rio de Janeiro, Brazil D.Sci. 2000 Neuroscience
Virginia Commonwealth University Post Doc 2003 Neuroscience

Biosketch

NAME: Alexandre E. Medina

 

POSITION TITLE: Associate Professor

EDUCATION/TRAINING 

INSTITUTION AND LOCATION DEGREE (if applicable) Completion Date MM/YYYY FIELD OF STUDY
Universidade Santa Ursula, Brazil B.S. 1990 Biology
Universidade Federal do Rio de Janeiro, Brazil M.Sc. 1996 Zoology
Universidade do Estado do Rio de Janeiro, Brazil Ph.D. 2000 Neuroscience
Virginia Commonwealth University Post Doc 2003 Neuroscience
       

 

A. Positions and Honors

 

Professional positions

1999-2000, Assistant Professor, Dept. of Physiology, Universidade Federal de Juiz de Fora, Juiz de Fora, MG, Brazil.

2001-2002,  Post Doctoral Fellow, Dept. of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, VA.

2003-2005, Research Associate, Dept. of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, VA.

2005-2012- Assistant Professor, Dept. of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, VA. (promoted to Associate Professor with tenure on may 2012)

2012-current- Associate Professor, Dept of Pediatrics, University of Maryland, School of Medicine.

 

Reviewing activities- Journals (last 5 years)

Journal of Pharmacology and Experimental Therapeutics.; PNAS; Pharmacology Biochemistry and Behavior.

Journal of Neuroscience; Cerebral Cortex, Alcohol Clin Exp Ther; Alcohol; Frontiers in Pediatrics.

 

Service (last 5 years)

  • President of the Central Virginia chapter of the Society for Neuroscience, 2008-2009.
  • President of the Fetal Alcohol Spectrum Disorders Study Group (FASDsg.org): Current
  • Ad Hoc reviewer for special emphasis panels: NIH; ZRG1 IFCN-C (03) M Special emphasis panel.; NIH; ZRG1 IFCN-C (02) M Member Conflict SEP: Alcohol, Neurotoxicology and Drugs

B.        Contributions to Science

My publication list available on:  http://www.ncbi.nlm.nih.gov/sites/myncbi/alexandre.medina.1/bibliography/41140533/public/?sort=date&direction=ascending

 

Effects of early alcohol exposure on neuronal plasticity in the visual cortex

My lab has shown through in vivo electrophysiology, optical imaging of intrinsic signals and behavioral assessments that early alcohol exposure leads to a permanent reduction in neuronal plasticity.

  1. Medina, A.E., Krahe, T.E., Coppola, D.M. & Ramoa, A.S. (2003) Neonatal Alcohol Exposure Induces Long-Lasting Impairment of Visual Cortical Plasticity in Ferrets             J Neurosci 23 (31) 10002-12
  2. Medina, A.E., Krahe, T.E. & Ramoa, A.S. (2005) Early alcohol exposure induces persistent alteration of cortical columnar organization and reduced orientation selectivity in the visual cortex. J. Neurophysiol. 93: 1317-1325
  3. Lantz, C.L; Wang, W and Medina A.E. (2012) Early alcohol exposure disrupts visual cortex plasticity in mice. Int J Dev Neurosci  30(5):351-7.
  4. Lantz, C.L.;  Pulimood, N.S.;  Rodrigues Jr, W.S.;  Chen, C.K.; Kalatsky, V; Manhães, A.C . and Medina, A.E. Visual Deficits in a mouse model of Fetal Alcohol Spectrum Disorders (2014) Frontiers in Pediatrics, 2:107
  5. Lantz C.L.  &  Medina A.E., (2015)   Effects of developmental alcohol exposure on potentiation and depression of visual cortex responses Alcoholism Clin Exp Res 39(8):1434-42.

 

Mechanisms of visual cortex plasticity

During my postdoc at Ary Ramoa’s lab, I participated in a study that showed for the first time that recovery from monocular deprivation (a classic model of neuronal plasticity) can happen in hours and without the need of protein synthesis. In my own lab we showed that activation of the NMDA receptor is needed for recovery of this function. Recently we conducted experiments showing that the astrocyte secreted protein hevin is essential for ocular dominance plasticity.

 

  1. Krahe, T.E., Medina, A.E., Bittencourt-Navarrette, R.E.; Colello, R.J. & Ramoa, A.S. (2005) Protein Synthesis Independent Plasticity Mediates Rapid and Precise Recovery of Deprived Eye Responses. Neuron 48(2):329-43.
  2. Krahe, T.E. & Medina, A.E. (2010) Activation of NMDA receptors is necessary for the recovery of cortical binocularity. J Neurophysiol 103:2700-2706.
  3. Singh, S.K.; Stogsdill, J.A.; Pulimood, N.; Dingsdale, H.; Kim, Y.H.; Pilaz, L.J.; Kim, I.H.; Manhaes, A.C.; Rodrigues-Junior, W.S.; Pamukcu, A.; Enustun, E.; Ertuz, Z.; Peter Scheiffele. P; Soderling, S.; Silver, D.L.; Ji, R.R.; Medina, A.E. and Eroglu, C. (2016) Astrocytes Assemble Thalamocortical Synapses by Bridging Neurexin-1α and Neuroligin-1 via Hevin. Cell 164(1-2):183-96. doi: 10.1016/j.cell.2015.11.034.
  4. Pulimood, N.S.; Rodrigues, W.D.S. Junior; Atkinson, D.A.; Mooney, A.E. & Medina, A.E. (2017) The Role of CREB, SRF, and MEF2 in Activity-Dependent Neuronal Plasticity in the Visual Cortex. J. Neurosci. 37(28):6628-6637. doi: 10.1523/JNEUROSCI.0766-17.2017.

Effects of early alcohol exposure on SRF dependent neuronal plasticity.

We demonstrated that overexpression of SRF can restore neuronal plasticity in the ferret model of FASD. If SRF overexpression is done in astrocytes the improvement of neuronal plasticity occurs in the whole cortex, however if done in neurons the effect is restricted to the area of the injection. In these studies we described for the first time the astrocyte secretome of a gryrencephalic animal and how the profile of these proteins can be permanently affected by alcohol. Finally we showed that implantation of astrocytes in the visual cortex of ferret opens the critical period of ocular dominance plasticity and suggested a possible mechanism for this plasticity improvement.

  1. Paul A., Pohl-Guimaraes F, Krahe T.E., Filgueiras C.C., Lantz Cl, Colello R.J., Wang W., Medina, A.E. (2010) Overexpression of serum response factor restores ocular dominance plasticity in a model of fetal alcohol spectrum disorders. J. Neurosci., 30(7):2513-20
  2. Paul, A.P. and Medina A.E. (2012) Overexpression of Serum Response Factor in Astrocytes Improves Neuronal Plasticity In A Model Of Fetal Alcohol Spectrum Disorders. Neuroscience 221:193-202.
  3. Foxworthy, W.A. & Medina A.E. (2015) Overexpression of serum response factor in neurons restores ocular dominance plasticity in a model of fetal alcohol spectrum disorders Alcoholism Clin Exp Res
  4. Trindade P; Hampton B; Manhães, AC; Medina AE (2016) Developmental alcohol exposure leads to a persistent change on astrocyte secretome J. Neurochem. doi: 10.1111/jnc.13542.

 

Multisensory Processing

Currently, I am very interested on the effects of environment and teratogens (alcohol in particular) in multisensory processing. I have published one paper with Dr Alex Meredith and have one under review in collaboration with Dr Gullapali and both are related with multisensory processing.

 

  1.  Allman, B.L., Bittencourt-Navarrete, R.E., Keniston, L.P, Medina A.E., Wang, M.Y., Meredith M.A. (2008) Do cross-modal projections always result in multisensory integration? Cerebral Cortex 18, 2066-2076
  2. Sours, C. ; Raghavan, P.; Foxworthy, W.A.; Meredith, M.A.; El-Metwally, D; Zhuo, J.; Gilmore, J.; Medina, A.E.; Gullapalli, R. (2017) Cortical multisensory functional connectivity is present at birth in humans. Brain Imaging and Behavior 11(4):1207-1213. doi: 10.1007/s11682-016-9586-6.

 

Pharmacological Improvement of neuronal plasticity in models of fetal alcohol spectrum disorders

Using a pharmacologically (phosphodiesterase type 1 inhibition) we were able to restore neuronal plasticity caused by early alcohol exposure in different models

  1. Medina, A.E., Krahe, T.E. &. Ramoa, A.S. (2006) Restoration of Neuronal Plasticity by a phosphodiesterase Type 1 Inhibitor in a model of Fetal Alcohol Exposure.          J. Neurosci., 26(3):1057-1060.
  2. Krahe, T.E.; Wang, W. & Medina, A.E. (2009) Phosphodiesterase Inhibition increases CREB phosphorylation and restores Orientation Selectivity in a Model of Fetal Alcohol Spectrum Disorders PLoS ONE 4:e6643.
  3. Krahe, TE; Paul, A  & Medina, A.E. (2010) Phosphodiesterase type 4 Inhibition does not restore ocular dominance plasticity in a Ferret Model of Fetal Alcohol Spectrum Disorders. Alcohol Clin Exp Res 34:1-6.
  4. Filgueiras, C.C., Krahe, T.E., Medina A.E. (2010) Phosphodiesterase type 1 inhibition restores spatial learning in rats exposed to alcohol during the third trimester equivalent of human gestation. Neurosci Lett 473:202-207

 

C.        Research Support

Ongoing

 

 (PI: 40%)

“Improving neuronal plasticity in a mouse model of FASD”

National Institutes of Health/NIAAA, R01AA022455

 

 

(PI:40%)

 “Alcohol in Neocortex Development and Plasticity”

 National Institutes of Health/NIAAA, R01AA013023

 

 

Past

 

01/05/2006-04/30/2010           (PI: 35%)

“Alcohol in Neocortex Development and Plasticity”

National Institutes of Health/NIAAA, R01AA013023

 

 

05/01/2007-04/30/2009           (PI: 10%)

 “Restoring plasticity in a model of fetal anticonvulsant syndrome”

Thrasher Research Fund

 

 

Research/Clinical Keywords

Electrophysiology, Fetal Alcohol spectrum disorders, development, neuroscience, brain, visual cortex, vision, transcription factors, neuronal plasticity,

Highlighted Publications

Medina, A.E., Krahe, T.E., Coppola, D.M. & Ramoa, A.S. (2003) Neonatal Alcohol Exposure Induces Long-Lasting Impairment of Visual Cortical Plasticity in Ferrets

J Neurosci 23 (31) 10002-12.

Medina, A.E., Krahe, T.E. &. Ramoa, A.S. (2006) Restoration of Neuronal Plasticity by a phosphodiesterase Type 1 Inhibitor in a model of Fetal Alcohol Exposure. J. Neurosci., 26(3):1057-1060.

Paul A., Pohl-Guimaraes F, Krahe T.E., Filgueiras C.C., Lantz Cl, Colello R.J., Wang W., Medina, A.E. (2010) Overexpression of serum response factor restores ocular dominance plasticity in a model of fetal alcohol spectrum disorders. J. Neurosci., 30(7):2513-20

Lantz C.L.  &  Medina A.E., (2015)   Effects of developmental alcohol exposure on potentiation and depression of visual cortex responses Alcoholism Clin Exp Res 39(8):1434-42.

Trindade P; Hampton B; Manhães, AC; Medina AE (2016) Developmental alcohol exposure leads to a persistent change on astrocyte secretome. J. Neurochem 137(5):730-43.

Research Interests

My research is focused in elucidating how different types of external insults (such as early alcohol exposure) disrupt activity-dependent plasticity and how we can restore it. Currently we are investigating the effects of external insults on how the brain process sensory information.

Awards and Affiliations

Past President of the Fetal Alcohol Spectrum Disorders Study Group

Member of The Society for Neuroscience and Research Society on Alcoholism

Grants and Contracts

Supported by NIH/NIAAA grants R01AA13023 and R01022455

Lab Techniques and Equipment

In vivo electrophysiology in awake and anesthetized animal models, optical imaging of intrinsic signals, molecular biology techniques