Stress Affects Synaptic Plasticity and Basal Synaptic Transmission in the Rat Hippocampus In Vivo

2008 ◽  
pp. 37-41
Author(s):  
Amer Kamal ◽  
Ivan Urban ◽  
Willem Hendrik Gispen
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Rat Hippocampus ◽  
Basal Synaptic Transmission

Corticotropin-Releasing Factor Produces a Protein Synthesis–Dependent Long-Lasting Potentiation in Dentate Gyrus Neurons

2000 ◽  
Vol 83 (1) ◽  
pp. 343-349 ◽  
Author(s):  
Hai L. Wang ◽  
Li Y. Tsai ◽  
Eminy H. Y. Lee
Keyword(s):  
Protein Synthesis ◽  
Synaptic Transmission ◽  
Dentate Gyrus ◽  
Late Phase ◽  
Long Term Potentiation ◽  
Corticotropin Releasing Factor ◽  
Rat Hippocampus ◽  
Protein Synthesis Inhibitor ◽  
Synthesis Inhibitor

Corticotropin-releasing factor (CRF) was shown to produce a long-lasting potentiation of synaptic efficacy in dentate gyrus neurons of the rat hippocampus in vivo. This potentiation was shown to share some similarities with tetanization-induced long-term potentiation (LTP). In the present study, we further examined the mechanism underlying CRF-induced long-lasting potentiation in rat hippocampus in vivo. Results indicated that the RNA synthesis inhibitor actinomycin-D, at a concentration that did not change basal synaptic transmission alone (5 μg), significantly decreased CRF-induced potentiation. Similarly, the protein synthesis inhibitor emetine, at a concentration that did not affect hippocampal synaptic transmission alone (5 μg), also markedly inhibited CRF-induced potentiation. These results suggest that like the late phase of LTP, CRF-induced long-lasting potentiation also critically depend on protein synthesis. Further, prior maximum excitation of dentate gyrus neurons with tetanization occluded further potentiation of these neurons produced by CRF and vise versa. Moreover, quantitative reverse transcription-polymerase chain reaction analysis revealed that CRF mRNA level in the dentate gyrus was significantly increased 1 h after LTP recording. Together with our previous findings that CRF antagonist dose-dependently diminishes tetanization-induced LTP, these results suggest that both CRF-induced long-lasting potentiation and tetanization-induced LTP require protein synthesis and that CRF neurons are possibly involved in the neural circuits underlying LTP.

scholarly journals The effects of hyperbilirubinaemia on synaptic plasticity in the dentate gyrus region of the rat hippocampus in vivo

2020 ◽  
Vol 16 (1) ◽  
pp. 200-204
Author(s):  
Li Yang ◽  
De Wu ◽  
Baotian Wang ◽  
Xiaosong Bu ◽  
Jing Zhu ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Dentate Gyrus ◽  
Rat Hippocampus ◽  
Dentate Gyrus Region

Cholesterol depletion inhibits synaptic transmission and synaptic plasticity in rat hippocampus

2008 ◽  
Vol 212 (2) ◽  
pp. 407-414 ◽  
Author(s):  
C. Frank ◽  
S. Rufini ◽  
V. Tancredi ◽  
R. Forcina ◽  
D. Grossi ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Rat Hippocampus ◽  
Cholesterol Depletion

scholarly journals Lrfn2-mutant mice display suppressed synaptic plasticity and inhibitory synapse development and abnormal social communication and startle response

2018 ◽  
Author(s):  
Yan Li ◽  
Ryunhee Kim ◽  
Yi Sul Cho ◽  
Doyoun Kim ◽  
Kyungdeok Kim ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Nmda Receptor ◽  
Synaptic Transmission ◽  
Social Communication ◽  
Acoustic Startle ◽  
Ultrasonic Vocalization ◽  
Inhibitory Synapse ◽  
Excitatory Synapse ◽  
Synapse Development

AbstractSALM1, also known as LRFN2, is a PSD-95-interacting synaptic adhesion molecule implicated in the regulation of NMDA receptor (NMDAR) clustering largely based on in vitro data, although its in vivo functions remain unclear. Here, we found that mice lacking SALM1/LRFN2 (Lrfn2-/- mice) show a normal density of excitatory synapses but altered excitatory synaptic function, including enhanced NMDAR-dependent synaptic transmission but suppressed NMDAR-dependent synaptic plasticity in the hippocampal CA1 region. Unexpectedly, SALM1 expression is detected in both glutamatergic and GABAergic neurons, and Lrfn2-/- CA1 pyramidal neurons show decreases in the density of inhibitory synapses and frequency of spontaneous inhibitory synaptic transmission. Behaviorally, ultrasonic vocalization was suppressed in Lrfn2-/- pups separated from their mothers, and acoustic startle was enhanced, but locomotion, anxiety-like behavior, social interaction, repetitive behaviors, and learning and memory were largely normal in adult Lrfn2-/- mice. These results suggest that SALM1/LRFN2 regulates excitatory synapse function, inhibitory synapse development, and social communication and startle behaviors in mice.Significance StatementSynaptic adhesion molecules regulate synapse development and function, which govern neural circuit and brain functions. The SALM/LRFN family of synaptic adhesion proteins consists of five known members whose in vivo functions are largely unknown. Here we characterized mice lacking SALM1/LRFN2 (SALM1 knockout) known to associate with NMDA receptors and found that these mice showed altered NMDA receptor-dependent synaptic transmission and plasticity, as expected, but unexpectedly also exhibited suppressed inhibitory synapse development and synaptic transmission. Behaviorally, SALM1 knockout pups showed suppressed ultrasonic vocalization upon separation from their mothers, and SALM1 knockout adults showed enhanced responses to loud acoustic stimuli. These results suggest that SALM1/LRFN2 regulates excitatory synapse function, inhibitory synapse development, social communication, and acoustic startle behavior.

scholarly journals In vivo assessment of mechanisms underlying the neurovascular basis of postictal amnesia

2020 ◽  
Author(s):  
Jordan S. Farrell ◽  
Roberto Colangeli ◽  
Barna Dudok ◽  
Marshal D. Wolff ◽  
Sarah L. Nguyen ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Neural Activity ◽  
Long Term Potentiation ◽  
Activity Network ◽  
Network Oscillations ◽  
Short Period ◽  
Cox 2

AbstractLong-lasting confusion and memory difficulties during the postictal state remain a major unmet problem in epilepsy that lacks pathophysiological explanation and treatment. We previously identified that long-lasting periods of severe postictal hypoperfusion/hypoxia, not seizures per se, are associated with memory impairment after temporal lobe seizures. While this observation suggests a key pathophysiological role for insufficient energy delivery, it is unclear how the networks that underlie episodic memory respond to vascular constraints that ultimately give rise to amnesia. Here, we focused on cellular/network level analyses in the CA1 of hippocampus in vivo to determine if neural activity, network oscillations, synaptic transmission, and/or synaptic plasticity are impaired following kindled seizures. Importantly, the induction of severe postictal hypoperfusion/hypoxia was prevented in animals treated by a COX-2 inhibitor, which experimentally separated seizures from their vascular consequences. We observed complete activation of CA1 pyramidal neurons during brief seizures, followed by a short period of reduced activity and flattening of the local field potential that resolved within minutes. During the postictal state, constituting tens of minutes to hours, we observed no changes in neural activity, network oscillations, and synaptic transmission. However, long-term potentiation of the temporoammonic pathway to CA1 was impaired in the postictal period, but only when severe local hypoxia occurred. Lastly, we tested the ability of rats to perform object-context discrimination, which has been proposed to require temporoammonic input to differentiate between sensory experience and the stored representation of the expected object-context pairing. Deficits in this task following seizures were reversed by COX-2 inhibition, which prevented severe postictal hypoxia. These results support a key role for hypoperfusion/hypoxia in postictal memory impairments and identify that many aspects of hippocampal network function are resilient during severe hypoxia except for long-term synaptic plasticity.

scholarly journals Altered short-term synaptic plasticity and reduced muscle strength in mice with impaired regulation of presynaptic CaV2.1 Ca2+ channels

2016 ◽  
Vol 113 (4) ◽  
pp. 1068-1073 ◽  
Author(s):  
Evanthia Nanou ◽  
Jin Yan ◽  
Nicholas P. Whitehead ◽  
Min Jeong Kim ◽  
Stanley C. Froehner ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Muscle Strength ◽  
Neuromuscular Junction ◽  
Synaptic Transmission ◽  
Motor Coordination ◽  
Tibialis Anterior Muscle ◽  
Short Term ◽  
Synaptic Facilitation ◽  
Cas Proteins

Facilitation and inactivation of P/Q-type calcium (Ca2+) currents through the regulation of voltage-gated Ca2+ (CaV) 2.1 channels by Ca2+ sensor (CaS) proteins contributes to the facilitation and rapid depression of synaptic transmission in cultured neurons that transiently express CaV2.1 channels. To examine the modulation of endogenous CaV2.1 channels by CaS proteins in native synapses, we introduced a mutation (IM-AA) into the CaS protein-binding site in the C-terminal domain of CaV2.1 channels in mice, and tested synaptic facilitation and depression in neuromuscular junction synapses that use exclusively CaV2.1 channels for Ca2+ entry that triggers synaptic transmission. Even though basal synaptic transmission was unaltered in the neuromuscular synapses in IM-AA mice, we found reduced short-term facilitation in response to paired stimuli at short interstimulus intervals in IM-AA synapses. In response to trains of action potentials, we found increased facilitation at lower frequencies (10–30 Hz) in IM-AA synapses accompanied by slowed synaptic depression, whereas synaptic facilitation was reduced at high stimulus frequencies (50–100 Hz) that would induce strong muscle contraction. As a consequence of altered regulation of CaV2.1 channels, the hindlimb tibialis anterior muscle in IM-AA mice exhibited reduced peak force in response to 50 Hz stimulation and increased muscle fatigue. The IM-AA mice also had impaired motor control, exercise capacity, and grip strength. Taken together, our results indicate that regulation of CaV2.1 channels by CaS proteins is essential for normal synaptic plasticity at the neuromuscular junction and for muscle strength, endurance, and motor coordination in mice in vivo.

Adenosine induces initial hypoxic-ischemic depression of synaptic transmission in the rat hippocampus in vivo

2001 ◽  
Vol 280 (3) ◽  
pp. R639-R645 ◽  
Author(s):  
L. M. Gervitz ◽  
L. O. Lutherer ◽  
D. G. Davies ◽  
J. H. Pirch ◽  
J. C. Fowler
Keyword(s):  
Carotid Artery ◽  
Synaptic Transmission ◽  
Rat Hippocampus ◽  
In Vivo Model ◽  
Hippocampal Field ◽  
The Common ◽  
Initial Depression ◽  
Inspired Oxygen

The present study was designed to investigate the role of adenosine in the hypoxic depression of synaptic transmission in rat hippocampus. An in vivo model of hypoxic synaptic depression was developed in which the common carotid artery was occluded on one side in the urethane-anesthetized rat. Inspired oxygen levels were controlled through a tracheal cannula. Rats were placed in a stereotaxic apparatus for stimulation and recording of bilateral hippocampal field excitatory postsynaptic potentials. The percent inspired oxygen could be reduced to levels that produced a reversible and repeatable depression of evoked synaptic transmission restricted to the hippocampus ipsilateral to the occlusion. Further reduction in the level of inspired oxygen depressed synaptic transmission recorded from both hippocampi. The adenosine nonselective antagonist caffeine and the A1selective antagonist 8-cyclopentyltheophylline prevented the initial depression in synaptic transmission. We conclude that the initial depression of synaptic transmission observed in the rat hippocampus in vivo is due to endogenous adenosine acting at neuronal adenosine A1 receptors.

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