Synaptic proliferation in the motor cortex of adult cats after long-term thalamic stimulation

1. One of the hypotheses for information storage in the CNS postulates the induction of structural changes in synaptic circuits. This postulate predicts that behavioral experiences produce changes in neural activity that subsequently induce synaptogenesis in the mature CNS. Available data indicate that the establishment of engrams for novel motor acts may involve alterations of synaptic interactions within the primary motor cortex. The present study examines the hypothesis that patterns of synaptic circuitry and of synaptic activation are rearranged after enhanced neural activity in pathways projecting to the motor cortex. 2. Electrodes implanted in the ventroposterolateral (VPL) nucleus of the thalamus were used for long-term stimulation (20 microA, 4 days) of afferents to the motor cortex in freely behaving, adult cats. This stimulation primarily affected corticocortical inputs from the somatosensory cortex (area 2) to area 4 gamma of the motor cortex. Electron microscopy and stereological procedures were used to compare the numerical density (Nv) of various types of synapses in layers II/III of the stimulated (experimental) motor cortex with the Nv of the corresponding synapses in the contralateral (control) hemisphere. 3. Long-term stimulation produced a significant increase (25.6%) in synaptic Nv in experimental motor cortex. This increase was due primarily to an increase in the Nv of asymmetrical synapses with dendritic spines. The numbers of symmetrical synapses, and of asymmetrical synapses with dendritic shafts, were not affected by long-term stimulation. 4. Synaptic active zones [calculated by measuring the lengths of postsynaptic densities (PSDs)] were significantly longer in experimental motor cortex. Lengthening of PSDs occurred selectively in asymmetrical synapses with dendritic shafts (28% increase). 5. The Nv of synapses having perforations in their PSDs (perforated synapses) was significantly higher in experimental hemispheres. Also increased was the incidence of synapse-associated polyribosomes, which are most commonly found at the base of dendritic spines. An increase in the number of perforated synapses and of polyribosomes are both morphological hallmarks of synaptogenesis. 6. The percentages of synapses having different curvatures (i.e., presynaptically concave, convex, or flat) were similar in experimental and in control motor cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

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Long-term depression and associativity in rat primary motor cortex following thalamic stimulation

European Journal of Neuroscience ◽

10.1111/j.1460-9568.2006.05220.x ◽

2006 ◽

Vol 24 (12) ◽

pp. 3553-3560 ◽

Cited By ~ 1

Author(s):

M. J. Eckert ◽

R. J. Racine

Keyword(s):

Motor Cortex ◽

Primary Motor Cortex ◽

Long Term Depression ◽

Thalamic Stimulation

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One Week of Motor Adaptation Induces Structural Changes in Primary Motor Cortex That Predict Long-Term Memory One Year Later

Journal of Neuroscience ◽

10.1523/jneurosci.2253-11.2011 ◽

2011 ◽

Vol 31 (33) ◽

pp. 11808-11813 ◽

Cited By ~ 82

Author(s):

S. M. Landi ◽

F. Baguear ◽

V. Della-Maggiore

Keyword(s):

Motor Cortex ◽

Structural Changes ◽

Primary Motor Cortex ◽

Motor Adaptation ◽

Long Term Memory ◽

Term Memory ◽

One Year

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Brain stimulation for arm recovery after stroke (B-STARS): protocol for a randomised controlled trial in subacute stroke patients

BMJ Open ◽

10.1136/bmjopen-2017-016566 ◽

2017 ◽

Vol 7 (8) ◽

pp. e016566

Author(s):

Eline C C van Lieshout ◽

Johanna M A Visser-Meily ◽

Sebastiaan F W Neggers ◽

H Bart van der Worp ◽

Rick M Dijkhuizen

Keyword(s):

Motor Cortex ◽

Upper Limb ◽

Brain Stimulation ◽

Primary Outcome ◽

Primary Motor Cortex ◽

Repetitive Transcranial Magnetic Stimulation ◽

Stroke Patients ◽

Post Stroke ◽

Subacute Stroke

IntroductionMany patients with stroke have moderate to severe long-term sensorimotor impairments, often including inability to execute movements of the affected arm or hand. Limited recovery from stroke may be partly caused by imbalanced interaction between the cerebral hemispheres, with reduced excitability of the ipsilesional motor cortex while excitability of the contralesional motor cortex is increased. Non-invasive brain stimulation with inhibitory repetitive transcranial magnetic stimulation (rTMS) of the contralesional hemisphere may aid in relieving a post-stroke interhemispheric excitability imbalance, which could improve functional recovery. There are encouraging effects of theta burst stimulation (TBS), a form of TMS, in patients with chronic stroke, but evidence on efficacy and long-term effects on arm function of contralesional TBS in patients with subacute hemiparetic stroke is lacking.Methods and analysisIn a randomised clinical trial, we will assign 60 patients with a first-ever ischaemic stroke in the previous 7–14 days and a persistent paresis of one arm to 10 sessions of real stimulation with TBS of the contralesional primary motor cortex or to sham stimulation over a period of 2 weeks. Both types of stimulation will be followed by upper limb training. A subset of patients will undergo five MRI sessions to assess post-stroke brain reorganisation. The primary outcome measure will be the upper limb function score, assessed from grasp, grip, pinch and gross movements in the action research arm test, measured at 3 months after stroke. Patients will be blinded to treatment allocation. The primary outcome at 3 months will also be assessed in a blinded fashion.Ethics and disseminationThe study has been approved by the Medical Research Ethics Committee of the University Medical Center Utrecht, The Netherlands. The results will be disseminated through (open access) peer-reviewed publications, networks of scientists, professionals and the public, and presented at conferences.Trial registration numberNTR6133

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Non-ionotropic NMDA receptor signaling gates bidirectional structural plasticity of dendritic spines

10.1101/2020.08.19.258269 ◽

2020 ◽

Author(s):

Ivar S. Stein ◽

Deborah K. Park ◽

Nicole Claiborne ◽

Karen Zito

Keyword(s):

Dendritic Spines ◽

Structural Changes ◽

Brain Plasticity ◽

Structural Plasticity ◽

Ion Flow ◽

Neuronal Connections ◽

Vital Component ◽

Brain Circuit ◽

Signaling Components

SUMMARYExperience-dependent refinement of neuronal connections is critically important for brain development and learning. Here we show that ion flow-independent NMDAR signaling is required for the long-term dendritic spine growth that is a vital component of brain circuit plasticity. We found that inhibition of p38 MAPK, shown to be downstream of non-ionotropic NMDAR signaling in LTD and spine shrinkage, blocked LTP-induced spine growth but not LTP. We hypothesized that non-ionotropic NMDAR signaling drives the cytoskeletal changes that support bidirectional spine structural plasticity. Indeed, we found that key signaling components downstream of non-ionotropic NMDAR function in LTD-induced spine shrinkage also are necessary for LTP-induced spine growth. Furthermore, NMDAR conformational signaling with coincident Ca2+ influx is sufficient to drive CaMKII-dependent long-term spine growth, even when Ca2+ is artificially driven through voltage-gated Ca2+ channels. Our results support a model in which non-ionotropic NMDAR signaling gates the bidirectional spine structural changes vital for brain plasticity.

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