Projections from auditory cortex to midbrain cholinergic neurons that project to the inferior colliculus.
Acetylcholine/*metabolism; Amidines; Animals; Auditory Cortex/*cytology/metabolism; Auditory Perception/physiology; Brain Mapping; Choline O-Acetyltransferase/metabolism; Cholinergic Fibers/metabolism/ultrastructure; Dextrans; Female; Functional Laterality/physiology; Guinea Pigs; Immunohistochemistry; Inferior Colliculi/*cytology/metabolism; Male; Mesencephalon/*cytology/metabolism; Neural Pathways/cytology/metabolism; Neuroanatomical Tract-Tracing Techniques; Neuronal Tract-Tracers; Neurons/*cytology/metabolism; Pedunculopontine Tegmental Nucleus/*cytology/metabolism; Rhodamines; Synaptic Transmission/physiology
We have shown that auditory cortex projects to cholinergic cells in the pedunculopontine tegmental nucleus (PPT) and laterodorsal tegmental nucleus (LDT). PPT and LDT are the sources of cholinergic projections to the inferior colliculus, but it is not known if the cortical inputs contact the cholinergic cells that project to the inferior colliculus. We injected FluoroRuby into auditory cortex in pigmented guinea pigs to label cortical projections to PPT and LDT. In the same animals, we injected Fast Blue into the left or right inferior colliculus to label PPT and LDT cells that project to the inferior colliculus. We processed the brain to identify cholinergic cells with an antibody to choline acetyltransferase, which was visualized with a green fluorescent marker distinguishable from both FluoroRuby and Fast Blue. We then examined the PPT and LDT to determine whether boutons of FluoroRuby-labeled cortical axons were in close contact with cells that were double-labeled with the retrograde tracer and the immunolabel. Apparent contacts were observed ipsilateral and, less often, contralateral to the injected cortex. On both sides, the contacts were more numerous in PPT than in LDT. The results indicate that auditory cortex projects directly to brainstem cholinergic cells that innervate the ipsilateral or contralateral inferior colliculus. This suggests that cortical projections could elicit cholinergic effects on both sides of the auditory midbrain.
Schofield B R
Neuroscience
2010
2010-03
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.neuroscience.2009.12.008" target="_blank" rel="noreferrer noopener">10.1016/j.neuroscience.2009.12.008</a>
Persistence of intact retinal ganglion cell terminals after axonal transport loss in the DBA/2J mouse model of glaucoma.
*Axonal Transport/physiology; *bouton; *mitochondria; *neurodegeneration; *retinal; *RRID:IMSRJAX:000671; *RRID:IMSRJAX:007048; *RRID:SCR002716; *RRID:SCR002865; *superior colliculus; *synapse; Animal; Animals; Disease Models; Electron; Glaucoma/metabolism/*pathology; Imaging; Inbred DBA; Mice; Microscopy; Mitochondria/pathology; Neuroanatomical Tract-Tracing Techniques; Regression Analysis; Retinal Ganglion Cells/metabolism/*pathology; Scanning; Superior Colliculi/metabolism/*pathology; Synapses/metabolism/*pathology; Three-Dimensional; Visual Pathways/metabolism/pathology
Axonal transport defects are an early pathology occurring within the retinofugal projection of the DBA/2J mouse model of glaucoma. Retinal ganglion cell (RGC) axons and terminals are detectable after transport is affected, yet little is known about the condition of these structures. We examined the ultrastructure of the glaucomatous superior colliculus (SC) with three-dimensional serial block-face scanning electron microscopy to determine the distribution and morphology of retinal terminals in aged mice exhibiting varying levels of axonal transport integrity. After initial axonal transport failure, retinal terminal densities did not vary compared with either transport-intact or control tissue. Although retinal terminals lacked overt signs of neurodegeneration, transport-intact areas of glaucomatous SC exhibited larger retinal terminals and associated mitochondria. This likely indicates increased oxidative capacity and may be a compensatory response to the stressors that this projection is experiencing. Areas devoid of transported tracer label showed reduced mitochondrial volumes as well as decreased active zone number and surface area, suggesting that oxidative capacity and synapse strength are reduced as disease progresses but before degeneration of the synapse. Mitochondrial volume was a strong predictor of bouton size independent of pathology. These findings indicate that RGC axons retain connectivity after losing function early in the disease process, creating an important therapeutic opportunity for protection or restoration of vision in glaucoma. J. Comp. Neurol. 524:3503-3517, 2016. (c) 2016 Wiley Periodicals, Inc.
Smith Matthew A; Xia Christina Z; Dengler-Crish Christine M; Fening Kelly M; Inman Denise M; Schofield Brett R; Crish Samuel D
The Journal of comparative neurology
2016
2016-12
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1002/cne.24012" target="_blank" rel="noreferrer noopener">10.1002/cne.24012</a>