scholarly journals Persistent Synaptic Activity Produces Long-Lasting Enhancement of Endocannabinoid Modulation and Alters Long-Term Synaptic Plasticity

2007 ◽  
Vol 97 (6) ◽  
pp. 4386-4389 ◽  
Author(s):  
Ping Jun Zhu ◽  
David M. Lovinger
Keyword(s):  
Low Frequency ◽  
Long Term Potentiation ◽  
Information Storage ◽  
Synaptic Activity ◽  
Inhibitory Synapses ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Gabaergic Synapses ◽  
Activity Dependent

Learning and memory are thought to involve activity-dependent changes in synaptic efficacy such as long-term potentiation (LTP) and long-term depression (LTD). Recent studies have indicated that endocannabinoid-dependent modulation of inhibitory transmission facilitates induction of hippocampal LTP and that endocannabinoids play a key role in certain forms of LTD. Here, we show that repetitive low-frequency synaptic stimulation (LFS) produces persistent up-regulation of endocannabinoid signaling at hippocampal CA1 GABAergic synapses. This LFS also produces LTD of inhibitory synapses and facilitates LTP at excitatory, glutamatergic synapses. These endocannabinoid-mediated plastic changes could contribute to information storage within the brain.

scholarly journals An Endogenous RNA Transcript Antisense to CNGα1 Cation Channel mRNA

2002 ◽  
Vol 13 (10) ◽  
pp. 3696-3705 ◽  
Author(s):  
Chin-Hung Cheng ◽  
David Tai-Wai Yew ◽  
Hiu-Yee Kwan ◽  
Qing Zhou ◽  
Yu Huang ◽  
...  
Keyword(s):  
Expression System ◽  
Expression Patterns ◽  
Long Term Potentiation ◽  
Information Storage ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Oocyte Expression System ◽  
Neuronal Functions ◽  
Rna Transcript

CNG channels are cyclic nucleotide-gated Ca2+-permeable channels that are suggested to be involved in the activity-dependent alterations of synaptic strength that are thought to underlie information storage in the CNS. In this study, we isolated an endogenous RNA transcript antisense to CNGα1 mRNA. This transcript was capable of down-regulating the expression of sense CNGα1 in theXenopus oocyte expression system. RT-PCR, Northern blot, and in situ hybridization analyses showed that the transcript was coexpressed with CNGα1 mRNA in many regions of human brain, notably in those regions that were involved in long-term potentiation and long-term depression, such as hippocampal CA1 and CA3, dentate gyrus, and cerebellar Purkinje layer. Comparison of expression patterns between adult and fetal cerebral cortex revealed that there were concurrent developmental changes in the expression levels of anti-CNG1 and CNGα1. Treatment of human glioma cell T98 with thyroid hormone T3 caused a significant increase in anti-CNG1 expression and a parallel decrease in sense CNGα1 expression. These data suggest that the suppression of CNGα1 expression by anti-CNG1 may play an important role in neuronal functions, especially in synaptic plasticity and cortical development. Endogenous antisense RNA-mediated regulation may represent a new mechanism through which the activity of ion channels can be regulated in the human CNS.

scholarly journals The fate of hippocampal synapses depends on the sequence of plasticity-inducing events

2018 ◽  
Author(s):  
J. Simon Wiegert ◽  
Mauro Pulin ◽  
Christine E. Gee ◽  
Thomas G. Oertner
Keyword(s):  
Hippocampal Slice ◽  
Specific Activity ◽  
Activity Patterns ◽  
Long Term Potentiation ◽  
Information Storage ◽  
Two Photon ◽  
Term Potentiation ◽  
Hippocampal Synapses ◽  
Activity Dependent

AbstractSynapses change their strength in response to specific activity patterns. This functional plasticity is assumed to be the brain’s primary mechanism for information storage. We used optogenetic stimulation of rat hippocampal slice cultures to induce long-term potentiation (LTP), long-term depression (LTD), or both forms of plasticity in sequence. Two-photon imaging of spine calcium signals allowed us to identify stimulated synapses and to follow their fate for the next 7 days. We found that plasticity-inducing protocols affected the synapse’s chance for survival: LTP increased synaptic stability, LTD destabilized synapses, and the effect of the last stimulation protocol was dominant over earlier stimulations. Interestingly, most potentiated synapses were resistant to depression-inducing protocols delivered 24 hours later. Our findings suggest that activity-dependent changes in the transmission strength of individual synapses are transient, but have long-lasting consequences for synaptic lifetime.

scholarly journals Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala

2019 ◽  
Vol 20 (17) ◽  
pp. 4310 ◽  
Author(s):  
Susanne Meis ◽  
Thomas Endres ◽  
Thomas Munsch ◽  
Volkmar Lessmann
Keyword(s):  
Synaptic Transmission ◽  
Long Term Potentiation ◽  
Fear Learning ◽  
Inhibitory Synapses ◽  
Lateral Amygdala ◽  
Term Potentiation ◽  
Gabaergic Synapses ◽  
Bdnf Signaling ◽  
The Impact

Brain-derived neurotrophic factor (BDNF) has previously been shown to play an important role in glutamatergic synaptic plasticity in the amygdala, correlating with cued fear learning. While glutamatergic neurotransmission is facilitated by BDNF signaling in the amygdala, its mechanism of action at inhibitory synapses in this nucleus is far less understood. We therefore analyzed the impact of chronic BDNF depletion on GABAA-mediated synaptic transmission in BDNF heterozygous knockout mice (BDNF+/−). Analysis of miniature and evoked inhibitory postsynaptic currents (IPSCs) in the lateral amygdala (LA) revealed neither pre- nor postsynaptic differences in BDNF+/− mice compared to wild-type littermates. In addition, long-term potentiation (LTP) of IPSCs was similar in both genotypes. In contrast, facilitation of spontaneous IPSCs (sIPSCs) by norepinephrine (NE) was significantly reduced in BDNF+/− mice. These results argue against a generally impaired efficacy and plasticity at GABAergic synapses due to a chronic BDNF deficit. Importantly, the increase in GABAergic tone mediated by NE is reduced in BDNF+/− mice. As release of NE is elevated during aversive behavioral states in the amygdala, effects of a chronic BDNF deficit on GABAergic inhibition may become evident in response to states of high arousal, leading to amygdala hyper-excitability and impaired amygdala function.

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