Rene Renteria, Ph.D.
The Retina: Neurons, synapses, and circuits
In the brain, inhibitory and excitatory circuits interact to produce coded neural output from specific brain areas. Most broadly, I am interested in how these circuits form in development and how inhibitory circuits function to modulate output.
The retina is a great place to study these issues because:
It is a central nervous tissue (i.e., is part of the brain) and has a high degree of organization.
We know, and can control in the lab, the inputs it receives.
We know, and can record from, the output neurons (the retinal ganglion cells, or RGCs).
We have detailed knowledge of what the retina is doing, what it is for.
Development and operation of ganglion cell receptive fields
Individual RGCs have a receptive field, the retinal area where light can influence its output, determined by many excitatory and inhibitory circuits. These receptive fields modulate and determine RGC spiking patterns in response to light stimulation, which means they are how the retina converts a visual image or light pattern into a neural code that the brain can understand.
I want to discover:
1) what specific contributions the inhibitory circuits and their activity make to the development of RGC receptive fields and
2) which specific inhibitory circuits, of which there are many in the retina, contribute to which receptive field properties exhibited by RGC outputs.
Getting a handle on inhibition
GABA is a major retinal inhibitory transmitter. Subunits of major GABA receptor classes are distributed with intriguing specificity in the inner synaptic layer of the retina, where much processing by lateral inhibitory circuitry occurs. This receptor distribution suggests that individual subunits may function in specific inhibitory synaptic circuits. Knockouts of individual subunits are available and viable, and these mice will be assessed for receptive field function and visual acuity to determine the role of individual circuits in retinal processing. Other circuit components can be eliminated and evaluated in a similar fashion.
Receptive fields in disease
Diabetic retinopathy is a leading cause of blindness in American adults. Diabetes leads to changes in retinal blood vessels that hurt the eye and vision. These vasculature changes were presumed to be the cause of visual deficits and certainly cause visual loss in the later stages of the disease. Recent research, however, suggests that changes in inner retinal neurons, which lead to deficits in visual function, may occur earlier than the earliest clinically detectable changes in the retinal vasculature. My lab is also pursuing receptive field deficits, and the neuronal changes that cause them, in diabetes.
The lab uses several techniques to accomplish these goals, including:
- Simultaneous extracellular recording from dozens of RGCs using multielectrode arrays.
- Whole-cell, patch-clamp recording from individual retinal neurons in the mouse retinal slice.
- Patterned visual stimulation of retinas during recording.
- Visual acuity measurements from awake, unanesthetized animals using the OptoMotry system.
- Detection of antigens in sectioned retinas (by immunofluorescent histochemistry) imaged in the UTHSCSA Physiology departmental confocal imaging facility
Akimov NP, Rentería RC.Spatial frequency threshold and contrast sensitivity of an optomotor behavior are impaired in the Ins2Akita mouse model of diabetes.Behav Brain Res. 2012 Jan 15;226(2):601-5. Epub 2011 Sep 28. PMID: 21963766 [PubMed - indexed for MEDLINE]
Barabás, P., Huang, W., Chen, H., Koehler, C., Howell, G., John, S., Tian, N., Rentería, R.C., Krizaj, D. (2011) Missing optomotor head turning reflex in the DBA/2J mouse. Investigative Ophthalmology and Visual Science. 52:6766-73. PubMed ID: 21757588
Koehler, C.L., Akimov, N.P., Rentería, R.C. (2011) Receptive field center size decreases and firing properties mature in ON and OFF retinal ganglion cells after eye opening in the mouse. Journal of Neurophysiology. 106:895-904. PubMed ID: 21613583