Dr. Steve Stice to Present the Power of StemEZ Neural Cells

STEMEZ hN2 Primary Human Neurons

STEMEZ hN2 Primary Human Neurons

I have profiled Steve Stice’s research here. The focus has been the excellent research results he and his team at ArunA Biomedical have generated with STEMEZ(TM) hN2 Human Neurons and hNP1 Human Neural Progenitors.

The story continues. He will be presenting the latest at the 9th Annual World Pharmaceutical Congress in Philadelphia, June 14. Topics include: using these neural cell lines to study neurotoxicity in cell-based assays and disease modeling.  Recent work conducted in outside laboratories demonstrates that these lines are more sensitive to environmental toxicants than traditional cellular models.

Sample high throughput assay applications:

  • Cell morphology and neurite outgrowth
  • Cell signaling and transcription factor expression
  • Receptor and ion channel function
  • Cytotoxicity
  • Apoptosis, genotoxicity and DNA damage

These capabilities has been confirmed by our customers. I look for the use of the STEMEZ cell lines to continue to grow as researchers discover their value in Drug Discovery and Basic Neuroscience capabilities.

TCE and Parkinson’s

This post introduces a new twist to “News Behind the Neuroscience News”. This report was graciously submitted by Ms Pamela Brown of associatesdegree.com. I welcome her initiative in submitting this. On a side note, when I did factory work in the 1970s, trichloroethylene was a universal solvent used to clean parts. Wow. We will add more to the story as Researchers continue their studies. Thank you Pamela!

Of Chemicals and Parkinson’s Disease

Two recent studies have linked the chemical TCE, an industrial solvent, to the increased risk of Parkinson’s disease.  The first study, led by the University of Kentucky’s Don M. Gash and John T. Slevin, established a clear link between trichloroethylene and parkinsonism , which is a group of nervous disorders closely associated with Parkinson’s.

 The study investigated a group of people who had been occupationally exposed to TCE for over twenty-five years. Gash and Slevin found that of the 134 participants interviewed, 14–the group that worked closest to the TCE vat cleaning industrial parts–showed strong signs of Parkinsonism. 13 other patients who had worked further from the TCE source also showed signs of the disorder, although in milder form. The University of Kentucky study extended its investigation by exposing rats to TCE. The rats’ mitochondrial function was substantially inhibited and their dopamine-producing cells were severely damaged.

 A more recent study , revealed in January, established an even stronger link between TCE and Parkinson’s. Dr. Samuel Goldman, a researcher at the Parkinson’s Institute in Sunnyvale, California, examined 99 sets of twins in which one twin had Parkinson’s and the other didn’t. Goldman and his team gathered job histories from the group of twins and had an industrial hygienist evaluate the twins’ level of chemical exposure. The study found that those exposed to TCE had an almost six-fold increased risk of developing Parkinson’s. Occupations that often involve exposure to TCE include machinists, laundry cleaners, and electricians.

Even though the most recent findings are substantial, the idea that chemicals may be associated with increased risk of developing Parkinson’s is not very new. Earlier studies have suggested that certain pesticides and herbicides may increase risk as well.

Not all chemicals are bad news for Parkinson’s patients. A brain chemical, identified only about twenty years ago and named after the video game character, Sonic Hedgehog , has been shown to decrease the risk of developing Parkinson’s, meaning that increasing the chemical may be a viable treatment for the disease. Another study has suggested that urate, a naturally occurring chemical in the blood, may slow the progression of Parkinson’s, although the chemical has been proven to cause gout.


This guest post is contributed by Pamelia Brown, who writes on the topics of associate degree .  She welcomes your comments at her email Id: pamelia.brown@gmail.com

Consistent Human Neurons

We have featured Dr. Steve Stice here. He and his team at UGA and Aruna Biomedical are developing products that are highly desired by Neuroscience Researchers.

We are in the process of finalizing details for distributing their human neuron cultures. Here is the related press release:

ArunA Biomedical, Inc. announces alliance with Neuromics for distribution of normal human neural cells.

Athens, Georgia – - March 23, 2009 – - ArunA Biomedical, Inc., announced today an agreement with Neuromics, Inc. of Edina, MN, giving Neuromics the right to non-exclusively market and sell the ArunA hN2™ Human Neural Cells and Neural Culture Medium to support applications in neurological research.ArunA has an exclusive worldwide license to develop and commercialize neural cells derived from human embryonic stem cells (hESC), and hN2 is a second generation product from this technology. These cells offer a consistent population of normal human neural cells that the neural research and pharmaceutical market highly desires.

 “ArunA has further developed its adherent monolayer technology by creating hN2™, a normal human neural cell ideal for drug screening, toxicology studies and basic neural research, and we are pleased to have Neuromics as a distribution partner,” said David Ray, Chief Executive Officer  of ArunA Biomedical

“Neuromics growth is catalyzed by offering the unique products and expertise our customers require for research success through strategic alliances with companies like ArunA Biomedical. This relationship represents a growth opportunity for us. Their hN2™ cells fill a stated research need of the Neuroscience Community and we look forward to our customers having these cells and the related new discoveries they will help generate,” said Pete Shuster, CEO and Owner of Neuromics.

Founded in 2003, ArunA Biomedical, Inc. is a privately held biotechnology corporation dedicated to the discovery, manufacturing and commercialization of emerging new technologies in human embryonic stem cell research for use in drug discovery and neuroscience research.

Founded in 2003, Neuromics is a privately held Bio-regents Company focusing on providing research ready and proven products and methods expertise to Neuroscience, Diabetes/Obesity, Immunology and Researchers.
This press release contains forward-looking statements regarding the company’s potential impact on scientific research and collaborations with third parties.  Certain conditions could alter the outcome or progress of these statements including but not limited to unexpected manufacturing issues, product performance and quality control/assurance issues.  Forward- looking statements are based on the opinions, beliefs and expectations of the company or individuals quoted in the press release and the company does not assume any obligation to update these forward-looking statements if circumstances change. 

Featuring Dr. Evanna Gleason

 Spotlighting How Retinal Neurons Communicate

About Dr. Evanna Gleason

Dr. Evanna Gleason

Dr. Evanna Gleason


1996-Current-Associate Professor, LSU

1993-1996-Post Doc, UC San Diego

1991-1992-Post Doc, UC Davis-Wilson Lab

1990 Ph. D- UC San Diego

1984 Undergrad-ASU

How do neurons communicate across synapses? Finding answers to this is of central interest to many of our customers and colleagues. After all, it is the transmission of signals across synapses that collectively orchestrate our perceptions.

Abnormal transmission is at the root of many neuro-disorders that plague society. Research in the cell and molecular biology of synapse transmission is a piece of the puzzle in discovering cures.

This leads to why I am honored to feature Dr. Evanna Gleason and her work on how Retinal Neurons Communicate. She and her team focus on how retinal synapses are specialized to transmit visual information. Her work adds to the body of understanding of the processes that enable us to see.


Assembling the pieces of Evanna’s research begin with her graduate work in Dr. Martin Wilson’s lab at UC Davis. Here she developed the culturing techniques required to study transmission between isolated pairs of amacrine cells. These techniques enabled the lab to study the firing of individual neurons and created the platform for her current research Here are related publications:

E Gleason, S Borges and M Wilson. Synaptic transmission between pairs of retinal amacrine cells in culture. Journal of Neuroscience, Vol 13, 2359-2370, Copyright © 1993 by Society for Neuroscience.

Gleason E., Borges S., Wilson M. Control of transmitter release from retinal amacrine cells by Ca2+ influx and efflux. Neuron 1994.  Nov;13(5):1109-17.

More on Amacrine Cells-Amacrine cells operate at the inner plexiform layer (IPL), the second synaptic retinal layer where bipolar cells and retinal ganglion cells synapse. There are about 40 different types of amacrine cells, most lacking axons. Like horizontal cells, amacrine cells work laterally affecting the output from bipolar cells, however, their tasks are often more specialized. Each type of amacrine cell connects with a particular type of bipolar cell, and generally has a particular type of neurotransmitter. One such population, AII, ‘piggybacks’ rod bipolar cells onto the cone bipolar circuitry. It connects rod bipolar cell output with cone bipolar cell input, and from there the signal can travel to the respective ganglion cells.They are classified by the width of their field of connection, which layer(s) of the stratum in the IPL they are in, and by neurotransmitter type. Most are inhibitory using either GABA or glycine as neurotransmitters.

 Developmental Neurobiology 

Evanna did her post doc in Dr. Nick Spitzer’s lab at UC-San Diego. She studied the development of voltage-dependent ion channels and neurotransmitter receptors in the embryo. The focus in the lab was more on systems assembly and differentiation vs the study of synaptic transmission between individual neurons.

Although an interesting sidetrack, Evanna shared with me that her passion is the study of synaptic transmission in retinal neurons. This bring us to her current work.

From San Diego to Baton Rouge

I became acquainted with Evanna in a phone follow up concerning use of our E18 Primary Rat Hippocampal Neurons. This conversation proved enlightening as she provided specific insight on what she did with the cultures. Growing healthy an robust cultures was the easy part.

I learned that she and her team at LSU have the experience and expertise required to indentify and isolate amacrine cells. She shared how the cells were then used for studying the role of Nitric Oxide (NO) and Chloride (Cl-) in synaptic modulation and provided me with related data. This data proved to be of interest to a cross section of customers and colleagues studying synaptic transmission. Here’s the resulting publication and sample data:  

gaba_currentsFigures: Higher concentrations of NO promote a positive shift in EGABA. A and B, top traces: raw data from ruptured-patch voltage-clamp recordings of GABA-gated currents from a representative cell before and after NO application. GABA pulses (20 µM) were 300 ms in duration and are indicated by horizontal bars. A: whole cell, voltage-clamp recordings (Cs+-A internal and TEA-A external) of GABA-gated currents reveal that higher concentrations of NO induce a transient, several-fold enhancement of GABA-gated currents. *, NO-dependent current observed prior to the 2nd GABA application. B: same experiment as in A, using air-exposed NO solution. Raw data in A and B are from same cell. Scale bars are 150 pA, 1 s. C: amacrine cell is held at the predicted EGABA. GABA is applied for 300 ms during each trace. No GABA-gated currents are observed until application of NO. *, NO-dependent current. Scale bars are 25 pA, 5 s. D: voltage ramps in GABA were delivered before and after addition of NO. Leak-subtracted currents reveal a shift in EGABA after NO application (gray trace). Inset: subtraction of the NO-induced shift in reversal potential reveals an increase in the slope of the GABA-gated current-voltage relationship after NO injection (gray trace). Scale bars are 100 pA, 20 mV. E: mean EGABA values are plotted over time. F: representative GABA-gated currents from voltage ramps delivered after a 11-min treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 2 µM). Black trace, before NO injection; Gray trace, after NO injection. G: ODQ did not block the NO-induced shift in EGABA (P = 0.83, n = 5).

As I learned from from this and my interview with Evanna: she and her team are assembling a clearer picture of the relationship between NO, Cl-  and what is happing at  GABAergic synapses.

I plan to keep my eyes on how the puzzle grows and communicate the discoveries that bring the picture into clearer focus.  We will specifically be focused on the impact of Evanna’s research contributions to the overall understanding. of  how messages are communicated in the CNS and PNS.

What’s Next

Evanna indicated to me the potential of her using siRNA to do gene expression analysis.  As outlined in previous News Behind the Neuroscience News postings, this is near and dear to me. The ability to switch on and off genes involved in transmission will undoubtedly enhance the platform and drive new discoveries.