The spatiotemporal organization of experience dictates hippocampal involvement in primary visual cortical plasticity

AbstractThe hippocampus and neocortex are theorized to be crucial partners in the formation of long-term memories. Here, we assess hippocampal involvement in two related forms of experience-dependent plasticity in the primary visual cortex (V1) of mice. Like control animals, those with hippocampal lesions exhibit potentiation of visually evoked potentials following passive daily exposure to a phase reversing oriented grating stimulus, which is accompanied by long-term habituation of a reflexive behavioral response. Thus, low-level recognition memory is formed independently of the hippocampus. However, response potentiation resulting from daily exposure to a fixed sequence of four oriented gratings is severely impaired in mice with hippocampal damage. A feature of sequence plasticity in V1 of controls, but absent in lesioned mice, is generation of predictive responses to an anticipated stimulus element when it is withheld or delayed. Thus, hippocampus is involved in encoding temporally structured experience, even in primary sensory cortex.

Download Full-text

NMDA Receptor Antagonists Reveal Age-Dependent Differences in the Properties of Visual Cortical Plasticity

Journal of Neurophysiology ◽

10.1152/jn.90290.2008 ◽

2008 ◽

Vol 100 (4) ◽

pp. 1936-1948 ◽

Cited By ~ 26

Author(s):

Jacqueline de Marchena ◽

Adam C. Roberts ◽

Paul G. Middlebrooks ◽

Vera Valakh ◽

Koji Yashiro ◽

...

Keyword(s):

Synaptic Plasticity ◽

Nmda Receptor ◽

Cortical Plasticity ◽

Long Term Potentiation ◽

Underlying Mechanism ◽

Developmental Shift ◽

Term Potentiation ◽

Nmdar Activation ◽

Visual Cortical

The suggestion that NMDA receptor (NMDAR)-dependent plasticity is subunit specific, with NR2B-types required for long-term depression (LTD) and NR2A-types critical for the induction of long-term potentiation (LTP), has generated much attention and considerable debate. By investigating the suggested subunit-specific roles of NMDARs in the mouse primary visual cortex over development, we report several important findings that clarify the roles of NMDAR subtypes in synaptic plasticity. We observed that LTD was not attenuated by application of ifenprodil, an NR2B-type antagonist, or NVP-AAM007, a less selective NR2A-type antagonist. However, we were surprised that NVP-AAM007 completely blocked adult LTP (postnatal day (P) 45–90), while only modestly affecting juvenile LTP (P21-28). To assess whether this developmental transition reflected an increasing role for NR2A-type receptors with maturity, we characterized the specificity of NVP-AAM007. We found not only that NVP-AAM007 lacks discernable subunit specificity but also that the effects of NVP-AAM077 on LTP could be mimicked using subsaturating concentrations of APV, a global NMDAR antagonist. These results indicate that the effects of NVP-AAM077 on synaptic plasticity are largely explained by nonspecific blockade of NMDARs. Moreover our findings are the first to reveal a developmental increase in the sensitivity of LTP to NMDAR antagonism. We suggest that discrepant reports describing the effect of NVP-AAM077 on LTP may be partially explained by this developmental shift in the properties of LTP. These results indicate that the degree of NMDAR activation required for LTP increases with development, providing insight into a novel underlying mechanism governing the properties of synaptic plasticity.

Download Full-text

The critical period for long-term potentiation in primary sensory cortex

Neuron ◽

10.1016/0896-6273(95)90136-1 ◽

1995 ◽

Vol 15 (3) ◽

pp. 485-488 ◽

Cited By ~ 63

Author(s):

Kevin Fox

Keyword(s):

Critical Period ◽

Long Term Potentiation ◽

Sensory Cortex ◽

Primary Sensory Cortex ◽

Term Potentiation

Download Full-text

Evidence for reduced long-term potentiation-like visual cortical plasticity in schizophrenia and bipolar disorder

10.1101/2020.06.06.128926 ◽

2020 ◽

Author(s):

Mathias Valstad ◽

Daniël Roelfs ◽

Nora B. Slapø ◽

Clara M.F. Timpe ◽

Ahsan Rai ◽

...

Keyword(s):

Bipolar Disorder ◽

Synaptic Plasticity ◽

Symptom Severity ◽

Cortical Plasticity ◽

Long Term Potentiation ◽

Type I ◽

Term Potentiation ◽

Spectrum Disorders ◽

Visual Cortical

AbstractBackgroundSeveral lines of research suggest that impairments in long-term potentiation (LTP)-like synaptic plasticity might be a key pathophysiological mechanism in schizophrenia (SZ) and bipolar disorder type I (BDI) and II (BDII). Using modulations of visually evoked potentials (VEP) of the electroencephalogram, impaired LTP-like visual cortical plasticity has been implicated in patients with BDII, while there has been conflicting evidence in SZ, a lack of research in BDI, and mixed results regarding associations with symptom severity, mood states, and medication.MethodsWe measured the VEP of patients with SZ spectrum disorders (n=31), BDI (n=34), BDII (n=33), and other BD spectrum disorders (n=2), and age-matched healthy control participants (n=200) before and after prolonged visual stimulation.ResultsCompared to healthy controls, modulation of VEP component N1b, but not C1 or P1, was impaired both in patients within the SZ spectrum (χ2=35.1, p=3.1×10−9) and BD spectrum (χ2=7.0, p=8.2×10−3), including BDI (χ2=6.4, p=0.012), but not BDII (χ2=2.2, p=0.14). N1b modulation was also more severely impaired in SZ spectrum than BD spectrum patients (χ2=14.2, p=1.7×10−4). The reduction in N1b modulation was related to PANSS total scores (χ2=10.8, p=1.0×10−3), and nominally to number of psychotic episodes (χ2=4.9, p=0.027). Conclusions. These results suggest that LTP-like plasticity is impaired in SZ and BDI, but not BDII, and related to psychotic symptom severity. Adding to previous genetic, pharmacological, and anatomical evidence, these results implicate aberrant synaptic plasticity as a mechanism underlying SZ and BD.

Download Full-text

Distinct Laminar Requirements for NMDA Receptors in Experience-Dependent Visual Cortical Plasticity

Cerebral Cortex ◽

10.1093/cercor/bhz260 ◽

2019 ◽

Vol 30 (4) ◽

pp. 2555-2572 ◽

Cited By ~ 4

Author(s):

Ming-fai Fong ◽

Peter Sb Finnie ◽

Taekeun Kim ◽

Aurore Thomazeau ◽

Eitan S Kaplan ◽

...

Keyword(s):

Cortical Plasticity ◽

Visual Stimulation ◽

Cortical Layer ◽

Monocular Deprivation ◽

Dependent Plasticity ◽

Synaptic Modification ◽

Layer 4 ◽

Nmdar Activation ◽

Visual Cortical

Abstract Primary visual cortex (V1) is the locus of numerous forms of experience-dependent plasticity. Restricting visual stimulation to one eye at a time has revealed that many such forms of plasticity are eye-specific, indicating that synaptic modification occurs prior to binocular integration of thalamocortical inputs. A common feature of these forms of plasticity is the requirement for NMDA receptor (NMDAR) activation in V1. We therefore hypothesized that NMDARs in cortical layer 4 (L4), which receives the densest thalamocortical input, would be necessary for all forms of NMDAR-dependent and input-specific V1 plasticity. We tested this hypothesis in awake mice using a genetic approach to selectively delete NMDARs from L4 principal cells. We found, unexpectedly, that both stimulus-selective response potentiation and potentiation of open-eye responses following monocular deprivation (MD) persist in the absence of L4 NMDARs. In contrast, MD-driven depression of deprived-eye responses was impaired in mice lacking L4 NMDARs, as was L4 long-term depression in V1 slices. Our findings reveal a crucial requirement for L4 NMDARs in visual cortical synaptic depression, and a surprisingly negligible role for them in cortical response potentiation. These results demonstrate that NMDARs within distinct cellular subpopulations support different forms of experience-dependent plasticity.

Download Full-text

Plasticity in visual cortex is disrupted in a mouse model of tauopathy and neurodegeneration

10.21203/rs.3.rs-602806/v1 ◽

2021 ◽

Author(s):

Amalia Papanikolaou ◽

Fabio Rodrigues ◽

Joanna Holeniewska ◽

Keith Phillips ◽

Aman Saleem ◽

...

Keyword(s):

Visual Cortex ◽

Neural Plasticity ◽

Cortical Plasticity ◽

Brain Plasticity ◽

Early Stages ◽

Short And Long Term ◽

Intrinsic Plasticity ◽

Visual Cortical ◽

The Impact

Abstract Neurodegeneration is a hallmark of many dementias and thought to underlie a progressive impairment of neural plasticity. Previous work in mouse models of neurodegeneration shows pronounced changes in artificially-induced plasticity in hippocampus, perirhinal and prefrontal cortex. However, it is not known how neurodegeneration disrupts intrinsic forms of brain plasticity. Here we characterised the impact of tau-driven neurodegeneration on a simple form of intrinsic plasticity in the visual system, which allowed us to track plasticity at both long (days) and short (minutes) timescales. We studied rTg4510 transgenic mice at early stages of neurodegeneration (5 months) and a more advanced stage (8 months). We recorded local field potentials in the primary visual cortex while animals were repeatedly exposed to a stimulus over 9 days. We found that both short- and long-term visual plasticity were already disrupted at early stages of neurodegeneration, and further reduced in older animals, such that it was abolished in mice expressing mutant tau. Additionally, visually evoked behaviours were disrupted in both younger and older mice expressing mutant tau. Our results show that visual cortical plasticity and visually evoked behaviours are disrupted in the rTg4510 model of tauopathy.

Download Full-text