Anton J. Reiner, Ph.D.
Department of Anatomy and Neurobiology
The University of Tennessee Health Science Center
855 Monroe Avenue, Suite 515
Memphis, TN 38163
Tel: (901) 448-8298
Fax: (901) 448-7193
Lab: 522 Wittenborg Anatomy Building
Email: Anton J. Reiner
- Ph.D. Institution: Bryn Mawr College, Department of Psychology
- Postdoctoral: State University of New York at Stony Brook, Department of Neurobiology and Behavior
The work in our laboratory focuses on the organization, function, and diseases of the basal ganglia and eye. We have also recently begun to develop a mouse model of traumatic brain injury, to develop treatments for the adverse outcomes from traumatic brain injury. Finally, we also have a longstanding interest in the evolution and fundamental organization of the vertebrate forebrain.
With respect to basal ganglia, we are characterizing the synaptic organization of the thalamic and cortical inputs to the striatum, to better understand the neuronal functional circuitry that underlies the role of the basal ganglia in movement control. In our approach, we use neuron type selective labeling methods (immunolabeling, tracer injection, or single-cell filling, engineered mouse lines) to define the inputs to specific basal ganglia cell types from specific cortical and thalamic neuron types using high resolution LM and EM imaging. We have found that the direct pathway neurons of the striatal part of the basal ganglia, that mediate movement initiation and execution, receive their cortical input from neurons involved in pre-motor planning. By contrast, indirect pathway neurons of the striatum receive their major cortical input from corticospinal neurons that directly effect movement. In future studies, we plan to genetically disable one or the other of these cortical inputs to better understand their individual contributions to motor learning and motor function.
In our work on basal ganglia disease, we study the means by which the gene mutation in Huntington's disease (HD) leads to selective destruction of neurons in the striatal part of the basal ganglia. We use genetically engineered mice, and we have been particularly interested in the role that perturbed function of cortical neurons projecting to striatum plays in injuring their target striatal neurons. This injury process could involve excess glutamate release from corticostriatal terminals or diminished production by corticostriatal neurons of the neurotrophic factor BDNF, which is needed for survival by striatal neurons. Based on this premise, we examined and demonstrated the efficacy of an mGluR2/3 agonist in ameliorating symptoms in a mouse model of HD. This drug both diminishes corticostriatal glutamate release and enhances BDNF delivery to striatum. We plan to further test efficacy of this drug class in more genetically and phenotypically precise mouse HD models.
In our work on the visual system, we study the neural mechanisms by which blood flow in the choroid of the eye is adaptively controlled according to retinal need, and in the role disturbances in such neural control may play in age-related decline in retinal function. We are currently studying the autonomic mechanisms linking systemic and ocular blood flow that maintain the needed levels of blood flow to the retina. We are examining the possibility that disruption of such neural control of ocular blood flow predisposes it to the inflammatory injury cascade that causes outer retinal injury in age-related macular degeneration.
In our work on traumatic brain injury (TBI), we have been developing a novel closed-head air blast model in mice. We have identified a range of blast pressures that mimic human TBI in that they yield diffuse axonal injury to brain, motor impairments, and anxiety disorder resembling post-traumatic stress disorder (PTSD). We are testing treatments that improve recovery from TBI, especially the PTSD outcome, and we plan to characterize the molecular mechanisms and genetic susceptibilities underlying TBI.
Finally, we have a longstanding interest in the evolution of the cerebral cortex, basal ganglia, and thalamus, and in how these structures differ among birds, reptiles and mammals. In our studies, we use neurochemistry, hodology and the localization of developmentally regulated genes to characterize the organization of these regions, and ascertain the course evolution has taken to fashion the very different appearing brains of birds and mammals.
- Li C, Fitzgerald ME, Del Mar N, Reiner A. Stimulation of Baroresponsive Parts of the Nucleus of the Solitary Tract Produces Nitric Oxide-mediated Choroidal Vasodilation in Rat Eye. Front Neuroanat. 2016 Oct 7;10:94. PubMed PMID: 27774055; PubMed Central PMCID: PMC5053990.
- Bu W, Ren H, Deng Y, Del Mar N, Guley NM, Moore BM, Honig MG, Reiner A. Mild Traumatic Brain Injury Produces Neuron Loss That Can Be Rescued by Modulating Microglial Activation Using a CB2 Receptor Inverse Agonist. Front Neurosci. 2016 Oct 6;10:449. PubMed PMID: 27766068; PubMed Central PMCID: PMC5052277.
- Li C, Fitzgerald ME, Del Mar N, Reiner A. Disinhibition of neurons of the nucleus of solitary tract that project to the superior salivatory nucleus causes choroidal vasodilation: Implications for mechanisms underlying choroidal baroregulation. Neurosci Lett. 2016 Oct 28;633:106-111. doi: 10.1016/j.neulet.2016.09.029. PubMed PMID: 27663135; PubMed Central PMCID: PMC5117681.
- Bruce LL, Erichsen JT, Reiner A. Neurochemical compartmentalization within the pigeon basal ganglia. J Chem Neuroanat. 2016 Dec;78:65-86. doi: 10.1016/j.jchemneu.2016.08.005. PubMed PMID: 27562515; PubMed Central PMCID: PMC5135631.
- Reiner A, Wong TT, Nazor CC, Del Mar N, Fitzgerald ME. Type-specific photoreceptor loss in pigeons after disruption of parasympathetic control of choroidal blood flow by the medial subdivision of the nucleus of Edinger-Westphal. Vis Neurosci. 2016 Jan;33:E008. doi: 10.1017/S0952523816000043. PubMed PMID: 27485271.
- Deng YP, Reiner A. Cholinergic interneurons in the Q140 knockin mouse model of Huntington's disease: Reductions in dendritic branching and thalamostriatal input. J Comp Neurol. 2016 Dec 1;524(17):3518-3529. doi: 10.1002/cne.24013. PubMed PMID: 27219491; PubMed Central PMCID: PMC5050058.