Network vs Individual Bursting Neurons

Motor Neurons and MEA
Dysregulated bursting is at the root of many motor neuron/neuromuscular junction disease. ArunA Biomedical teaming with Axion Biosystems have generated relevant bursting data from our Mouse Motor Neurons cultured on Axion-Bioystem’s Maestro MEA.

Figure: Mouse Motor Neuron Network Modulation by Bicuculline-ckeck out the entire presentation to learn more: GFP+ Motor Neurons: Development and in-vitro Functional Assessment on Microelectrode Arrays

Protocol User’s Guide for Culturing Motor Neuron on MEA(pdf – 679Kb)

Name Catalog # Type Species Applications Size Price
Motor Neurons-GFP+ Quick Start Kit mMN7205.QS Primary Neurons M Cell Assays 750,000 $349
Motor Neurons-GFP+ HTS Kit mMN7205-HTS Primary Neurons M Cell Assays 4 X 750,000 $989
GDNF (Human, Mouse) PR27022-2 Protein H; M 2 ug 10 ug $108 $205
AB2™ Basal Neural Medium AB27011.3 Cell Growth Media H; M Cell Assays 500 ml $69

We will continue providing you content we believe important. Should you have questions, do not hesitate to contact us. Thank you and we stand ready to serve you and your team.

Pete Shuster-CEO and Owner, Neuromics, 612-801-1007,

On Deck-Dr. Richard Rogers

I am exciting to be profiling Dr. Richard Rogers in my upcoming Neuroscience Backstory feature. This is an important feature because it focuses on the timely topic of modulation of the brain-gut axis by cytokines, hormones and CNS pathways involved in the control of feeding behavior and energy utilization. Given the acceleration in the growth of obesity in the US and related pathologies, his research is becoming increasingly important.  We will also be featuring related research on what drives lack of appetite in cancer patients. This is a key intersection as the signaling pathways involved in insatiable and cessation of appetite are related.

I also wanted to share a recent article on yet another intersection which focuses on thermogensis which occures in brown adipose tissue (BAT): Maria J. Barnes, Richard C. Rogers, Montina J. Van Meter and Gerlinda E. Hermann. Co-localization of TRHR1 and LepRb receptors on neurons in the hindbrain of the rat. doi:10.1016/j.brainres.2010.07.094.


Example images: Distribution of LepRb+ fibers in hindbrain. LepRb-ir (red) fibers and varicosities are seen among TRHR1-ir (green) cells and fibers. These red and green fibers are adjacent and co-mingle but do not show co-localization of receptors. This pattern is seen in (A) fascicles of the solitary tract (ST); (B) raphe pallidus (RP), and (C) raphe obscurrus (RO). (D) Border between the medial solitary nucleus (NST) and the area postrema (AP; white dashed line) showing an abundance of LepRb-ir (red) fibers and
 neurons (white arrows for selected neurons) in the NST but not the AP. (E) LepRb-ir staining is suppressed by pretreatment of tissue with LepRb epitope blocking peptide. (F) TRHR1-ir staining is suppressed by treatment with excess TRHR1. Scale bar A–D=100 microns; E, F=300 microns. cc=central canal. Note: this pus references use of our LepRb (OB-Rb) and GAD1 antibodies.

Featuring Dr. Pat Carr

Amyotrophic Lateral Sclerosis (ALS)-New Twists on Root Causes

Teacher, Mentor and Friend    Dr. Pat Carr has been a key figure in helping shape the direction of my company. He has a gift for communicating the nuances of his research and coaching me on how to best serve labs like his. Based on these interactions, it came as no surprise to learn of his being Recognized for Excellence in Teaching, Research and Service at University of North Dakota.

“Dr. Carr has a magic way of teaching,” said second-year medical student, Tyson Bolinske. “He is able to take the most difficult topics and, through detailed notes, logically break down the material.

From a recent dialog, I learned of his growing work on the Ventral Horn and search for root causes of Amyotrophic Lateral Sclerosis (ALS).   I wanted to learn more! I would like to thank Pat for agreeing to share his story and giving me the opportunity to feature highlights in  “News Behind the Neuroscience News”.

 Information on ALS

ALS is an insidious disease.  It is a progressive neurodenerative disease that is always fatal. Approximately 5600 new cases are diagnosed each year. Average survival is typically 3-5 years from onset. The most common form of ALS in the United States is “sporadic” ALS. It can happen to anyone at anytime.  The other is the inherited form named “Familial” ALS (FALS). Only about 5 to 10% of all ALS patients appear to have FALS. As the disease progresses the symptons become more acute. Paralysis spreads through the body affecting  speech, swallowing, chewing and breathing. Ventilator support is need in late stages

 Pat’s Journey

Pat took the “road less traveled”.  He was a passionate hockey player in Canada. He  concluded in his late teens that he was not at a level to take this road to wealth and fame.

Pat Carr

Pat Carr

06/04–present Associate Professor, Department of Anatomy & Cell Biology, School of Medicine and Health Sciences, University of North Dakota 

1996–98 Research Associate/Adjunct Assistant Professor/Auxilliary Assistant Professor, Department of Anatomy;Wright State University

 07/98–06/04 Assistant Professor, Department of Anatomy & Cell Biology, School of Medicine and Health Sciences, University of North Dakota

Postdoc, National Institutes of Health, Neuroscience, 1994-96

Postdoc, University of Manitoba, Neuroscience, 1992-1994    

Ph.D., University of Manitoba, Physiology, 1992

Next was a stint as an automechanic in Brandon, Canada. The discipline and logic involved in fixing cars catalyzed an interest in Science which led to him going to Brandon University to study Geology. When the oil market collapsed in 1983, he decided to change his studies to Zoology and earned a BS in 1984.

A passion was sparked when he did field research in the Canadien Rockies studying parasites in Columbian Ground  Squirrels. He loved it, but recognized the limited value of continuing thsese studies. This lead to the wide open field of Neuroscience and the opportunity to study and solve problems that could benefit mankind. His graduate work at University of Manitoba and focusing on Neuropathic Pain and the Dorsal Horn. He then moved on to studying Ventral Horn and Motor Control Function for his Post Doc at Wright State.

From Pain to ALS

It was Pat’s work in Pain at the University of North Dakota that brought me into initial contact with him. He generously put some of our key Pain/Inflammation and  Neurotransmission Research Antibodies through their paces. These included some of our Neuropeptide and Neuropeptide Receptors , P2X Receptors and TRPV1s (Vanilloids).

His previous work in studying the Ventral Horn combined with a colleagues mouse model of ALS combined to create a prefect opportunity to advance the understanding of ALS.  Pat cautioned me with this insight:  “sometimes it is  not what you want to study; it is what you can study.  The model is  SOD1 (superoxide dismutase 1) which is core to FALS.(occurs in only about 10% of the ALS cases).

Pat is broadening the play field by looking at what else is happening in sporadic ALS vs FALS. Specifically, he is looking at modulation of alpha Motor Neurons and how the activity of adjacent Renshaw Cells impact signaling and modulation.  Renshaw Cells act as a “governor” on the activity of these alpha Motor Neurons. 

He is drilling down by studying the signaling of ChAT (Choline Acetyltransferase), VAChT (Vesicular acetylcholine transporter) and related molecules. By gaining a deeper understanding of how Renshaw Cells signaling changes the activity of alpha Motor Neurons in ALS,  Pat and his team are taking steps towards discovering roots causes.

As these root causes are further illuminated, I will be reporting specifics in my blog.

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.