Experience-Enabled Enhancement of Adult Visual Cortex Function
Departments of Physiology and Biophysics and Ophthalmology, Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, New York, 10605, and Department of Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, British Columbia, Canada V5Z 3N9. The Journal of Neuroscience : The Official Journal of the Society for Neuroscience
(Impact Factor: 6.34).
03/2013; 33(12):5362-6. DOI: 10.1523/JNEUROSCI.5229-12.2013
We previously reported in adult mice that visuomotor experience during monocular deprivation (MD) augmented enhancement of visual-cortex-dependent behavior through the non-deprived eye (NDE) during deprivation, and enabled enhanced function to persist after MD. We investigated the physiological substrates of this experience-enabled form of adult cortical plasticity by measuring visual behavior and visually evoked potentials (VEPs) in binocular visual cortex of the same mice before, during, and after MD. MD on its own potentiated VEPs contralateral to the NDE during MD and shifted ocular dominance (OD) in favor of the NDE in both hemispheres. Whereas we expected visuomotor experience during MD to augment these effects, instead enhanced responses contralateral to the NDE, and the OD shift ipsilateral to the NDE were attenuated. However, in the same animals, we measured NMDA receptor-dependent VEP potentiation ipsilateral to the NDE during MD, which persisted after MD. The results indicate that visuomotor experience during adult MD leads to enduring enhancement of behavioral function, not simply by amplifying MD-induced changes in cortical OD, but through an independent process of increasing NDE drive in ipsilateral visual cortex. Because the plasticity is resident in the mature visual cortex and selectively effects gain of visual behavior through experiential means, it may have the therapeutic potential to target and non-invasively treat eye- or visual-field-specific cortical impairment.
Available from: Henrique Rocha Mendonça
- "The precise connectivity patterns of CNS are tuned during development through several mechanisms that rely on genetic fate counterbalanced by experience    . The ability to undergo neural reorganization based on experience is termed neuroplasticity. "
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ABSTRACT: Adenosine is an important modulator of the central nervous system (CNS) that acts mainly by A1 (A1AR) and A2a (A2aAR) receptors, which are found in neurons and glial cells, and are coupled to different intracellular signaling pathways. These receptors modulate neurotransmitter release and regulate different aspects of neuroplasticity, an important process to ensure circuit development and remodeling after lesion. Neural plasticity involves pre-and postsynaptic changes in circuit strength. In this context, adenosine maintains the relation of neuronal excitability within the network, allowing plasticity to occur. Adenosine receptors are expressed throughout lifespan, but their expression and function varies accordingly to the stage of development in different structures, suggesting that they can contribute differently to the formation, maintenance and modification of circuits. Usually, A1AR activation has been associated with decrease in neurotransmitter release or excitatory postsynaptic current and long-term depression (LTD), whereas A2aAR activation has opposite effects. Therefore, A1AR activation is important to synaptic elimination of weaker connections, while A2aAR activity is related to the establishment of appropriated stronger contacts, indicating that adenosine produces a dynamic adjustment in the synaptic strength. This adjustment is also necessary during disorder-induced plasticity, such as observed in different kinds of injury and in neurodegenerative and neuropsychiatric disorders. In Parkinson´s disease (PD),
Adenosine Signaling Mechanisms: Pharmacology, Functions and Therapeutic Aspects, 1 edited by Vickram Ramkumar and Roberto Paes de Carvalho, 01/2015: chapter EMERGING ROLES FOR ADENOSINE IN NERVOUS SYSTEM PLASTICITY: pages 295-332; Nova Science Publishers., ISBN: 978-1-63483-186-4
Available from: Roberto Paes-de-Carvalho
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ABSTRACT: Nitric oxide (NO) is a very reactive molecule, and its short half-life would make it virtually invisible until its discovery. NO activates soluble guanylyl cyclase (sGC), increasing 3',5'-cyclic guanosine monophosphate levels to activate PKGs. Although NO triggers several phosphorylation cascades due to its ability to react with Fe II in heme-containing proteins such as sGC, it also promotes a selective posttranslational modification in cysteine residues by S-nitrosylation, impacting on protein function, stability, and allocation. In the central nervous system (CNS), NO synthesis usually requires a functional coupling of nitric oxide synthase I (NOS I) and proteins such as NMDA receptors or carboxyl-terminal PDZ ligand of NOS (CAPON), which is critical for specificity and triggering of selected pathways. NO also modulates CREB (cAMP-responsive element-binding protein), ERK, AKT, and Src, with important implications for nerve cell survival and differentiation. Differences in the regulation of neuronal death or survival by NO may be explained by several mechanisms involving localization of NOS isoforms, amount of NO being produced or protein sets being modulated. A number of studies show that NO regulates neurotransmitter release and different aspects of synaptic dynamics, such as differentiation of synaptic specializations, microtubule dynamics, architecture of synaptic protein organization, and modulation of synaptic efficacy. NO has also been associated with synaptogenesis or synapse elimination, and it is required for long-term synaptic modifications taking place in axons or dendrites. In spite of tremendous advances in the knowledge of NO biological effects, a full description of its role in the CNS is far from being completely elucidated.
Vitamins and Hormones, Vol. 96, Burlington: Academic Press, 2014, Edited by Gerald Litwack, 08/2014: pages 75-125; Elsevier., ISBN: 978-0-12-800254-4
Available from: Michael P Stryker
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ABSTRACT: The adult brain continues to learn and can recover from injury, but the elements and operation of the neural circuits responsible for this plasticity are not known. In previous work, we have shown that locomotion dramatically enhances neural activity in the visual cortex (V1) of the mouse (Niell and Stryker, 2010), identified the cortical circuit responsible for this enhancement (Fu et al., 2014), and shown that locomotion also dramatically enhances adult plasticity (Kaneko and Stryker, 2014). The circuit that is responsible for enhancing neural activity in the visual cortex contains both vasoactive intestinal peptide (VIP) and somatostatin (SST) neurons (Fu et al., 2014). Here, we ask whether this VIP-SST circuit enhances plasticity directly, independent of locomotion and aerobic activity. Optogenetic activation or genetic blockade of this circuit reveals that it is both necessary and sufficient for rapidly increasing V1 cortical responses following manipulation of visual experience in adult mice. These findings reveal a disinhibitory circuit that regulates adult cortical plasticity.
eLife Sciences 01/2015; 4(4). DOI:10.7554/eLife.05558 · 9.32 Impact Factor
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