scholarly journals Sensory Activity-Dependent and Sensory Activity-Independent Properties of the Developing Rodent Trigeminal Principal Nucleus

2016 ◽  
Vol 38 (3) ◽  
pp. 163-170 ◽  
Author(s):  
Fu-Sun Lo ◽  
Reha S. Erzurumlu
Keyword(s):  
Neural Plasticity ◽  
Critical Period ◽  
Time Window ◽  
Relay Station ◽  
Sensory Inputs ◽  
Morphological Studies ◽  
Inhibitory Circuitry ◽  
Physiological Properties ◽  
Sensory Activity ◽  
Activity Dependent

The whisker-sensory trigeminal central pathway of rodents is an established model for studies of activity-dependent neural plasticity. The first relay station of the pathway is the trigeminal principal nucleus (PrV), the ventral part of which receives sensory inputs mainly from the infraorbital branch of the maxillary trigeminal nerve (ION). Whisker-sensory afferents play an important role in the development of the morphological and physiological properties of PrV neurons. In neonates, deafferentation by ION transection leads to the disruption of whisker-related neural patterns (barrelettes) and cell death within a specific time window (critical period), as revealed by morphological studies. Whisker-sensory inputs control synaptic elimination, postsynaptic AMPA receptor trafficking, astrocyte-mediated synaptogenesis, and receptive-field characteristics of PrV cells, without a postnatal critical period. Sensory activity-dependent synaptic plasticity requires the activation of NMDA receptors and involves the participation of glia. However, the basic physiological properties of PrV neurons, such as cell type-specific ion channels, presynaptic terminal function, postsynaptic NMDA receptor subunit composition, and formation of the inhibitory circuitry, are independent of sensory inputs. Therefore, the first relay station of the whisker sensation is largely mature-like and functional at birth. Delineation of activity-dependent and activity-independent features of the postnatal PrV is important for understanding the development and functional characteristics of downstream trigeminal stations in the thalamus and neocortex. This mini review focuses on such features of the developing rodent PrV.

scholarly journals Arc restores juvenile plasticity in adult mouse visual cortex

2017 ◽  
Author(s):  
Kyle R. Jenks ◽  
Taekeun Kim ◽  
Elissa D. Pastuzyn ◽  
Hiroyuki Okuno ◽  
Andrew V. Taibi ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Neural Plasticity ◽  
Critical Period ◽  
Adult Mouse ◽  
Monocular Deprivation ◽  
Protein Synthesis Inhibitor ◽  
Adult Mice ◽  
Mouse Visual Cortex ◽  
Activity Dependent

AbstractThe molecular basis for the decline in experience-dependent neural plasticity over age remains poorly understood. In visual cortex, the robust plasticity induced in juvenile mice by brief monocular deprivation (MD) during the critical period is abrogated by genetic deletion of Arc, an activity-dependent regulator of excitatory synaptic modification. Here we report that augmenting Arc expression in adult mice prolongs juvenile-like plasticity in visual cortex, as assessed by recordings of ocular dominance (OD) plasticity in vivo. A distinguishing characteristic of juvenile OD plasticity is the weakening of deprived-eye responses, believed to be accounted for by the mechanisms of homosynaptic long-term depression (LTD). Accordingly, we also found increased LTD in visual cortex of adult mice with augmented Arc expression, and impaired LTD in visual cortex of juvenile mice that lack Arc or have been treated in vivo with a protein synthesis inhibitor. Further, we found that although activity-dependent expression of Arc mRNA does not change with age, expression of Arc protein is maximal during the critical period and declines in adulthood. Finally, we show that acute augmentation of Arc expression in wild type adult mouse visual cortex is sufficient to restore juvenile-like plasticity. Together, our findings suggest a unifying molecular explanation for the age- and activity-dependent modulation of synaptic sensitivity to deprivation.Significance StatementNeuronal plasticity peaks early in life during critical periods and normally declines with age, but the molecular changes that underlie this decline are not fully understood. Using the mouse visual cortex as a model, we found that activity-dependent expression of the neuronal protein Arc peaks early in life, and that loss of activity-dependent Arc expression parallels loss of synaptic plasticity in the visual cortex. Genetic overexpression of Arc prolongs the critical period of visual cortex plasticity and acute viral expression of Arc in adult mice can restore juvenile-like plasticity. These findings provide a mechanism for the loss of excitatory plasticity with age, and suggest that Arc may be an exciting therapeutic target for modulation of the malleability of neuronal circuits.

scholarly journals An NMDA receptor-dependent mechanism for subcellular segregation of sensory inputs in the tadpole optic tectum

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Ali S Hamodi ◽  
Zhenyu Liu ◽  
Kara G Pratt
Keyword(s):  
Nmda Receptor ◽  
Ab Initio ◽  
Optic Tectum ◽  
Critical Period ◽  
Sensory Inputs ◽  
Independent Process ◽  
Circuit Development ◽  
Activity Dependent ◽  
Tectal Neuron ◽  
Dependent Mechanism

In the vertebrate CNS, afferent sensory inputs are targeted to specific depths or layers of their target neuropil. This patterning exists ab initio, from the very beginning, and therefore has been considered an activity-independent process. However, here we report that, during circuit development, the subcellular segregation of the visual and mechanosensory inputs to specific regions of tectal neuron dendrites in the tadpole optic tectum requires NMDA receptor activity. Blocking NMDARs during the formation of these sensory circuits, or removing the visual set of inputs, leads to less defined segregation, and suggests a correlation-based mechanism in which correlated inputs wire to common regions of dendrites. This can account for how two sets of inputs form synapses onto different regions of the same dendrite. Blocking NMDA receptors during later stages of circuit development did not disrupt segregation, indicating a critical period for activity-dependent shaping of patterns of innervation.

scholarly journals Arc restores juvenile plasticity in adult mouse visual cortex

2017 ◽  
Vol 114 (34) ◽  
pp. 9182-9187 ◽  
Author(s):  
Kyle R. Jenks ◽  
Taekeun Kim ◽  
Elissa D. Pastuzyn ◽  
Hiroyuki Okuno ◽  
Andrew V. Taibi ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Neural Plasticity ◽  
Critical Period ◽  
Adult Mouse ◽  
Monocular Deprivation ◽  
Protein Synthesis Inhibitor ◽  
Adult Mice ◽  
Mouse Visual Cortex ◽  
Activity Dependent

The molecular basis for the decline in experience-dependent neural plasticity over age remains poorly understood. In visual cortex, the robust plasticity induced in juvenile mice by brief monocular deprivation during the critical period is abrogated by genetic deletion of Arc, an activity-dependent regulator of excitatory synaptic modification. Here, we report that augmenting Arc expression in adult mice prolongs juvenile-like plasticity in visual cortex, as assessed by recordings of ocular dominance (OD) plasticity in vivo. A distinguishing characteristic of juvenile OD plasticity is the weakening of deprived-eye responses, believed to be accounted for by the mechanisms of homosynaptic long-term depression (LTD). Accordingly, we also found increased LTD in visual cortex of adult mice with augmented Arc expression and impaired LTD in visual cortex of juvenile mice that lack Arc or have been treated in vivo with a protein synthesis inhibitor. Further, we found that although activity-dependent expression of Arc mRNA does not change with age, expression of Arc protein is maximal during the critical period and declines in adulthood. Finally, we show that acute augmentation of Arc expression in wild-type adult mouse visual cortex is sufficient to restore juvenile-like plasticity. Together, our findings suggest a unifying molecular explanation for the age- and activity-dependent modulation of synaptic sensitivity to deprivation.

Pharmacological Manipulation of Critical Period Plasticity

2018 ◽  
Author(s):  
Ramon Guirado ◽  
Eero Castrén
Keyword(s):  
Critical Period ◽  
Adult Brain ◽  
Brain Disorders ◽  
Critical Periods ◽  
Pharmacological Treatments ◽  
New Paradigm ◽  
Early Postnatal Development ◽  
Pharmacological Manipulation ◽  
Efficient Recovery ◽  
Activity Dependent

Neuronal networks are refined through an activity-dependent competition during critical periods of early postnatal development. Recent studies have shown that critical period plasticity is influenced by a number of environmental factors, including drugs that are widely used for the treatment of brain disorders. These findings suggest a new paradigm, where pharmacological treatments can be used to open critical period–like plasticity in the adult brain. The plastic networks can then be modified through rehabilitation or psychotherapy to rewire those abnormally wired during development. This kind of combination of pharmacotherapy with physical or psychological rehabilitation may open a new opportunity for a more efficient recovery of a number of neurological and neuropsychiatric disorders.

scholarly journals Critical Period for Activity-Dependent Synapse Elimination in Developing Cerebellum

2000 ◽  
Vol 20 (13) ◽  
pp. 4954-4961 ◽  
Author(s):  
Sho Kakizawa ◽  
Miwako Yamasaki ◽  
Masahiko Watanabe ◽  
Masanobu Kano
Keyword(s):  
Critical Period ◽  
Synapse Elimination ◽  
Developing Cerebellum ◽  
Activity Dependent

Neuroplasticity and Psychiatry

1998 ◽  
Vol 32 (1) ◽  
pp. 119-128 ◽  
Author(s):  
Bruce D. Gynther ◽  
Mike B. Calford ◽  
Pankaj Sah
Keyword(s):  
Psychiatric Disorder ◽  
Psychiatric Disorders ◽  
Neural Development ◽  
Critical Period ◽  
Clinical Observation ◽  
Aggressive Treatment ◽  
Long Term Changes ◽  
Activity Dependent ◽  
The Brain

Objective: There is increasing concern that the course of psychiatric disorders may be affected by parameters such as the duration and intensity of symptoms of initial episodes of illness. As this indicates that abnormal function produces long-term changes within the brain, a review of the neuroscience literature regarding neuroplasticity is warranted. Method: This article is a selective review, focusing in particular on results obtained from physiological experiments assessing plasticity within the mammalian neocortex. The possible relevance of results to psychiatry is discussed. Results: While the most dramatic examples of neuroplasticity occur during a critical period of neural development, neuroplasticity can also occur in adult neocortex. Neuroplasticity appears to be activity-dependent: synaptic pathways that are intensively used may become strengthened, and conversely, there may be depression of transmission in infrequently used pathways. Conclusions: Results from neurophysiological experiments lend support to the clinical observation that the intensity and duration of a psychiatric disorder may adversely alter its long-term course. Rapid aggressive treatment may prevent this from occurring. While pharmacotherapy may reduce the duration and severity of symptoms, it may also have an independent, as yet unknown, effect on neuroplasticity.

Changes in TMS Measures induced by repetitive TMS

2012 ◽  
Author(s):  
Joseph Classen ◽  
Katja Stefan
Keyword(s):  
Neural Plasticity ◽  
Therapeutic Potential ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Stimulus Frequency ◽  
Physiological Properties ◽  
Stimulation Period ◽  
Ischemic Nerve Block ◽  
Cortical Regions ◽  
The Brain ◽  
Insight Into

This article reviews several protocols of repetitive transcranial magnetic stimulation (rTMS)-induced plasticity. rTMS, when applied to the motor cortex or other cortical regions of the brain, may induce effects that outlast the stimulation period. The neural plasticity, which emerges as a result of such interventions, has been studied to gain insight into plasticity mechanisms of the brain. In two protocols the structure of rTMS trains is modified, informed by the knowledge of the physiological properties of the corticospinal system. Pulse configuration, stimulus frequency, stimulus intensity, the duration of the application period, and the total number of stimuli are some variables that have to be taken into account when reviewing the physiological effects of rTMS. This article also introduces the concept of patterned rTMS pulses and rTMS with ischemic nerve block. In addition, rTMS has raised considerable interest because of its therapeutic potential; however, much needs to be done in this field.

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