scholarly journals Brief environmental enrichment elicits metaplasticity of hippocampal synaptic potentiation in vivo

2012 ◽  
Vol 6 ◽  
Author(s):  
Arne Buschler ◽  
Denise Manahan-Vaughan
Keyword(s):  
Environmental Enrichment ◽  
Synaptic Potentiation

Temporal constraints in associative synaptic plasticity in hippocampus and neocortex

1995 ◽  
Vol 73 (9) ◽  
pp. 1295-1311 ◽  
Author(s):  
Dominique Debanne ◽  
Daniel E. Shulz ◽  
Yves Frégnac
Keyword(s):  
Visual Cortex ◽  
Membrane Potential ◽  
Temporal Frequency ◽  
Postsynaptic Membrane ◽  
Synaptic Potentiation ◽  
Test Input ◽  
Homosynaptic Depression ◽  
Postsynaptic Cell

We present comparative experimental evidence for the induction of synaptic potentiation and depression in organotypic cultures of hippocampus and in visual cortex in vitro and in vivo. The effects of associative pairings on the efficacy of synaptic transmission are analyzed as a function of the temporal delay between presynaptic activity and post-synaptic changes imposed in membrane potential. Synchronous association at a low temporal frequency (<0.5 Hz) between presynaptic input and postsynaptic depolarization resulted in homosynaptic potentiation of functionally identified postsynaptic potentials in the three types of preparation. Synchronous pairing of afferent activity with hyperpolarization of the postsynaptic cell resulted in homosynaptic depression in visual cortex in vivo and in vitro. An associative form of depression was induced in hippocampus when the test input was followed repeatedly with a fixed-delay postsynaptic depolarization imposed either by intracellular current injection or synaptically. The latter process might play a significant role in heterosynaptic plasticity in visual cortex in vivo and in vitro, if it is assumed that associative depression still operates in visual cortex a few seconds after the initial surge of calcium in the postsynaptic cell. We conclude that the precise timing between presynaptic activity and polarization changes in postsynaptic membrane potential up- and down-regulates the efficacy of active pathways.Key words: synaptic potentiation, synaptic depression, asynchrony, covariance, supervised learning.

Duration of NMDA-Dependent Synaptic Potentiation in Piriform Cortex In Vivo Is Increased After Epileptiform Bursting

1998 ◽  
Vol 80 (4) ◽  
pp. 1623-1629 ◽  
Author(s):  
A. Kapur ◽  
L. B. Haberly
Keyword(s):  
Seizure Activity ◽  
Piriform Cortex ◽  
Long Term Potentiation ◽  
Excitatory Postsynaptic Potential ◽  
Synaptic Potentiation ◽  
Lateral Olfactory Tract ◽  
Afferent Fibers ◽  
Stimulation Of

Kapur, A. and L. B. Haberly. Duration of NMDA-dependent synaptic potentiation in piriform cortex in vivo is increased after epileptiform bursting. J. Neurophysiol. 80: 1623–1629, 1998. Stimulation of afferent fibers with current pulse trains has been reported to induce long-term potentiation (LTP) in piriform cortex in vitro but not in vivo. LTP has been observed in vivo only when trains are paired with behavioral reinforcement and as a consequence of kindled epileptogenesis. This study was undertaken in the urethan-anesthetized rat to determine if the reported failures to observe pulse-train evoked LTP in vivo may be related to a lesser persistence rather than lack of occurrence, if disinhibition might facilitate induction, and to examine the nature of the relationship between seizure activity and LTP. Stimulation of afferent fibers in the lateral olfactory tract with θ-burst trains under control conditions potentiated the monosynaptic field excitatory postsynaptic potential (EPSP) by approximately the same extent (20.3 ± 2%; n = 12) as reported for the slice. However, in contrast to the slice, potentiation in vivo decayed to a low level within 1–2 h after induction (70% loss in 1.5 h, on average). The N-methyl-d-aspartate (NMDA)-receptor antagonists d-APV and MK-801 blocked the induction of this decremental potentiation. Pharmacological reduction of γ-aminobutyric acid–mediated inhibition at the recording site did not increase the duration of potentiation. In contrast, θ-burst stimulation applied after recovery from a period of epileptiform bursting induced stable NMDA-dependent potentiation. Mean increase in the population EPSP was approximately the same as under control conditions (21 ± 2%; n = 6), but in five of six experiments there was little or no decay in potentiation for the duration of the monitoring period (≤6 h). It is concluded that seizure activity has an enabling action on the induction of persistent synaptic potentiation by stimulus trains that bypasses the need for behavioral reinforcement.

scholarly journals Re-silencing of silent synapses unmasks anti-relapse effects of environmental enrichment

2016 ◽  
Vol 113 (18) ◽  
pp. 5089-5094 ◽  
Author(s):  
Yao-Ying Ma ◽  
Xiusong Wang ◽  
Yanhua Huang ◽  
Helene Marie ◽  
Eric J. Nestler ◽  
...  
Keyword(s):  
Environmental Enrichment ◽  
Behavioral Treatment ◽  
Basolateral Amygdala ◽  
Drug Exposure ◽  
Therapeutic Effects ◽  
Self Administration ◽  
Cocaine Withdrawal ◽  
Silent Synapses ◽  
Cocaine Craving

Environmental enrichment (EE) has long been postulated as a behavioral treatment for drug addiction based on its preventive effects in animal models: rodents experiencing prior EE exhibit increased resistance to establishing drug taking and seeking. However, the therapeutic effects of EE, namely, the effects of EE when applied after drug exposure, are often marginal and transient. Using incubation of cue-induced cocaine craving, a rat relapse model depicting progressive intensification of cocaine seeking after withdrawal from cocaine self-administration, our present study reveals that after cocaine withdrawal, in vivo circuit-specific long-term depression (LTD) unmasks the therapeutic power of EE to achieve long-lasting anti-relapse effects. Specifically, our previous results show that cocaine self-administration generates AMPA receptor (AMPAR)-silent excitatory synapses within the basolateral amygdala (BLA) to nucleus accumbens (NAc) projection, and maturation of these silent synapses via recruiting calcium-permeable (CP) AMPARs contributes to incubation of cocaine craving. Here, we show that after cocaine withdrawal and maturation of silent synapses, the BLA-to-NAc projection became highly resistant to EE. However, optogenetic LTD applied to this projection in vivo transiently re-silenced these silent synapses by removing CP-AMPARs. During this transient window, application of EE resulted in the insertion of nonCP-AMPARs, thereby remodeling the “incubated” BLA-to-NAc projection. Consequently, incubation of cocaine craving was decreased persistently. These results reveal a mechanistic basis through which the persistent anti-relapse effects of EE can be unleashed after drug withdrawal.

Environmental enrichment increases the in vivo extracellular concentration of dopamine in the nucleus accumbens: a microdialysis study

2010 ◽  
Vol 117 (10) ◽  
pp. 1123-1130 ◽  
Author(s):  
Gregorio Segovia ◽  
Alberto Del Arco ◽  
Marta De Blas ◽  
Pedro Garrido ◽  
Francisco Mora
Keyword(s):  
Nucleus Accumbens ◽  
Environmental Enrichment ◽  
Extracellular Concentration ◽  
Microdialysis Study

scholarly journals Addictive Nicotine Alters Local Circuit Inhibition during the Induction of In Vivo Hippocampal Synaptic Potentiation

2010 ◽  
Vol 30 (18) ◽  
pp. 6443-6453 ◽  
Author(s):  
T. A. Zhang ◽  
J. Tang ◽  
V. I. Pidoplichko ◽  
J. A. Dani
Keyword(s):  
Synaptic Potentiation ◽  
Local Circuit

Beyond clinical changes: Rehabilitation-induced neuroplasticity in MS

2019 ◽  
Vol 25 (10) ◽  
pp. 1348-1362 ◽  
Author(s):  
Luca Prosperini ◽  
Massimiliano Di Filippo
Keyword(s):  
Animal Models ◽  
Neural Plasticity ◽  
Immune Modulation ◽  
Environmental Enrichment ◽  
Small Sample ◽  
Laboratory Research ◽  
Tissue Destruction ◽  
Beneficial Effects ◽  
Network Function

Background: Neural plasticity represents the substrate by which the damaged central nervous system (CNS) re-learns lost behaviors in response to rehabilitation. In persons with multiple sclerosis (MS), rehabilitation can therefore exploit the potential of neural plasticity to restore CNS functions beyond the spontaneous mechanisms of recovery from MS-related damage. Methods: Here, we reviewed the currently available evidence on the occurrence of mechanisms of structural and functional plasticity following rehabilitation, motor, and/or cognitive training. We presented both data gained from basic laboratory research on animal models and data on persons with MS obtained by advanced magnetic resonance imaging (MRI) techniques. Results: Studies on physical and environmental enrichment in experimental MS models showed beneficial effects mediated by both immune modulation and activity-dependent plasticity, lowering tissue destruction and restoring of CNS network function. Translational researches in MS people demonstrated structural and/or functional MRI changes after various interventions, but their heterogeneity and small sample sizes (5–42 patients) raise concerns about the interpretation and generalization of the obtained results. Discussion: We highlighted the limitations of published studies, focusing on the knowledge gaps to be filled in terms of neuropathological correlations between changes detected in animal models and changes detected in vivo by neuroimaging.

scholarly journals Sleep slow-wave oscillations trigger seizures in a genetic epilepsy model of Dravet syndrome

2022 ◽  
Author(s):  
Mackenzie A. Catron ◽  
Rachel K. Howe ◽  
Gai-Linn K. Besing ◽  
Emily K. St. John ◽  
Cobie Victoria Potesta ◽  
...  
Keyword(s):  
Slow Wave ◽  
Epileptic Seizures ◽  
Nrem Sleep ◽  
Dravet Syndrome ◽  
Brain State ◽  
Synaptic Potentiation ◽  
Sleep Period ◽  
State Dependent ◽  
Slow Wave Oscillations

Sleep is the brain state when cortical activity decreases and memory consolidates. However, in human epileptic patients, including genetic epileptic seizures such as Dravet syndrome, sleep is the preferential period when epileptic spike-wave discharges (SWDs) appear, with more severe epileptic symptoms in female patients than male patients, which influencing patient sleep quality and memory. Currently, seizure onset mechanisms during sleep period still remain unknown. Our previous work has shown that the sleep-like state-dependent synaptic potentiation mechanism can trigger epileptic SWDs (Zhang et al., 2021). In this study, using one heterozygous (het) knock-in (KI) transgenic mice (GABAA receptor γ2 subunit Gabrg2Q390X mutation) and an optogenetic method, we hypothesized that slow-wave oscillations (SWOs) themselves in vivo could trigger epileptic seizures. We found that epileptic SWDs in het Gabrg2+/Q390X KI mice exhibited preferential incidence during NREM sleep period, accompanied by motor immobility/ facial myoclonus/vibrissal twitching, with more frequent incidence in female het KI mice than male het KI mice. Optogenetic induced SWOs in vivo significantly increased epileptic seizure incidence in het Gabrg2+/Q390X KI mice with increased duration of NREM sleep or quiet-wakeful states. Furthermore, suppression of SWO-related homeostatic synaptic potentiation by 4-(diethylamino)-benzaldehyde (DEAB) injection (i.p.) greatly decreased seizure incidence in het KI mice, suggesting that SWOs did trigger seizure activity in het KI mice. In addition, EEG delta-frequency (0.1-4 Hz) power spectral density during NREM sleep was significantly larger in female het Gabrg2+/Q390X KI mice than male het Gabrg2+/Q390X KI mice, which likely contributes to the gender difference in seizure incidence during NREM sleep/quiet-wake as that in human patients.

scholarly journals Miglustat Reverts the Impairment of Synaptic Plasticity in a Mouse Model of NPC Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
G. D’Arcangelo ◽  
D. Grossi ◽  
M. Racaniello ◽  
A. Cardinale ◽  
A. Zaratti ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Autosomal Recessive ◽  
Neurological Deficits ◽  
Synaptic Potentiation ◽  
Unesterified Cholesterol ◽  
Severe Dementia ◽  
Type C ◽  
Niemann Pick

Niemann-Pick type C disease is an autosomal recessive storage disorder, characterized by abnormal sequestration of unesterified cholesterol within the late endolysosomal compartment of cells and accumulation of gangliosides and other sphingolipids. Progressive neurological deterioration and insurgence of symptoms like ataxia, seizure, and cognitive decline until severe dementia are pathognomonic features of the disease. Here, we studied synaptic plasticity phenomena and evaluated ERKs activation in the hippocampus of BALB/c NPC1−/− mice, a well described animal model of the disease. Our results demonstrated an impairment of both induction and maintenance of long term synaptic potentiation in NPC1−/− mouse slices, associated with the lack of ERKs phosphorylation. We then investigated the effects of Miglustat, a recent approved drug for the treatment of NPCD. We found thatin vivoMiglustat administration in NPC1−/− mice was able to rescue synaptic plasticity deficits, to restore ERKs activation and to counteract hyperexcitability. Overall, these data indicate that Miglustat may be effective for treating the neurological deficits associated with NPCD, such as seizures and dementia.

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