Long-Term Potentiation ; Neuronal Plasticity ; Receptors, Metabotropic Glutamate ; Synaptic Transmission

Aquaporin-4 (AQP-4) is the predominant water channel in the central nervous system (CNS) and primarily expressed in astrocytes. Astrocytes have been generally believed to play important roles in regulating synaptic plasticity and information processing. However, the role of AQP-4 in regulating synaptic plasticity, learning and memory, cognitive function is only beginning to be investigated. It is well known that synaptic plasticity is the prime candidate for mediating of learning and memory. Long term potentiation (LTP) and long term depression (LTD) are two forms of synaptic plasticity, and they share some but not all the properties and mechanisms. Hippocampus is a part of limbic system that is particularly important in regulation of learning and memory. This article is to review some research progresses of the function of AQP-4 in synaptic plasticity, learning and memory, and propose the possible role of AQP-4 as a new target in the treatment of cognitive dysfunction.
Animals ; Aquaporin 4 ; physiology ; Hippocampus ; physiology ; Humans ; Learning ; Long-Term Potentiation ; Long-Term Synaptic Depression ; Memory ; Neuronal Plasticity

OBJECTIVETo study the roles of protein synthesis inhibitors in long-term potentiation(LTP) and depotentiation(DP) in hippocampal CA1 region of adult rats.

METHODSStandard extracellular recording technique was used to record field EPSP(fEPSP) evoked by Schaffer collateral stimulation from the CA1 subfield of adult rat hippocampal slices. Paired-pulse low-frequency stimulation(PP-LFS) or high-intensity paired-pulse low-frequency stimulation(HI-PP-LFS) was delivered to induce depotentiation 2 h after LTP induction induced by six theta-burst stimulations. Protein synthesis inhibitors were applied before and after LTP induction to study their roles in LTP and DP in hippocampal CA1 region of adult rats.

RESULTSWhen HI-PP-LFS was applied at 2 h after LTP induction, the depotentiation was induced. The mean fEPSP slopes reduced from 346.2%±26.3% to 207.1%±21.6%. This depotentiation was named as partial LTP depotentiation and maintained at least for 30 min. The percentage of depotentiation was 59.81%. Application of protein synthesis inhibitors, anisomycin and cycloheximide prior to tetanus resulted in smaller LTP compared to control group, and almost complete depotentiation was induced by HI-PP-LFS. With application of protein synthesis inhibitors anisomycin and cycloheximide 90 min after LTP induction, HI-PP-LFS still induced partial LTP depotentiation. However, there was no significant difference in the percentage of depotentiation between this group and control group.

CONCLUSIONHI-PP-LFS partially reverses late phase LTP. When protein synthesis inhibitors are applied prior to tetanus, LTP amplitude is markedly reduced, and HI-PP-LFS completely reverses late-phase LTP. Application of protein synthesis inhibitors after LTP induction does not significantly affect either the amplitude or depotentiation of LTP.

Long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission are forms of synaptic plasticity that have been studied extensively and are thought to contribute to learning and memory. The reversal of LTP, known as depotentiation (DP) has received far less attention however, and its role in behavior is also far from clear. Recently, deficits in depotentiation have been observed in models of schizophrenia, suggesting that a greater understanding of this form of synaptic plasticity may help reveal the physiological alterations that underlie symptoms experienced by patients. This review therefore seeks to summarize the current state of knowledge on DP, and then put the deficits in DP in models of disease into this context.
Depression ; Humans ; Learning ; Long-Term Potentiation ; Long-Term Synaptic Depression ; Memory ; Neuronal Plasticity ; Plastics ; Schizophrenia ; Synaptic Transmission

The neurokinin Substance P is widely distributed in the central nervous system and has been extensively studied in various functional aspects. Substance P has been reported to have memory-promoting, reinforcing, and anxiolyticlike effects when administered systemically or locally. N-terminal fragment of Substance P has memory-promoting effects, whereas the C-terminal sequence of Substance P has been shown to have a memory-reinforcing effect. These properties of Substance P are thought to be mediated through activation of the nucleus accumbensventral pallidum circuitry. Substance P facilitates long-term potentiation (LTP) in the hippocampus, and the distribution of ERK neurons seems to overlap with that of NK1 neurons. Hippocampal ERK activation is critical for the induction of LTP. In conclusion, Substance P might have a neuroprotective capacity in parallel with its recovery promoting actions.
Central Nervous System ; Hippocampus ; Learning* ; Long-Term Potentiation ; Memory* ; Neurons ; Substance P

People experience the feeling of the missing body part long after it has been removed after amputation are known as phantom limb sensations. These sensations can be painful, sometimes becoming chronic and lasting for several years (or called phantom pain). Medical treatment for these individuals is limited. Recent neurobiological investigations of brain plasticity after amputation have revealed new insights into the changes in the brain that may cause phantom limb sensations and phantom pain. In this article, I review recent progresses of the cortical plasticity in the anterior cingulate cortex (ACC), a critical cortical area for pain sensation, and explore how they are related to abnormal sensory sensations such as phantom pain. An understanding of these alterations may guide future research into medical treatment for these disorders.
Amputation ; Animals ; Brain ; Depression ; Gyrus Cinguli ; Long-Term Potentiation ; Mice ; Phantom Limb ; Sensation

At central synapses, activity-dependent synaptic plasticity has a crucial role in information processing, storage, learning, and memory under both physiological and pathological conditions. One widely accepted model of learning mechanism and information processing in the brain is Hebbian Plasticity: long-term potentiation (LTP) and long-term depression (LTD). LTP and LTD are respectively activity-dependent enhancement and reduction in the efficacy of the synapses, which are rapid and synapse-specific processes. A number of recent studies have a strong focal point on the critical importance of another distinct form of synaptic plasticity, non-Hebbian plasticity. Non-Hebbian plasticity dynamically adjusts synaptic strength to maintain stability. This process may be very slow and occur cell-widely. By putting them all together, this mini review defines an important conceptual difference between Hebbian and non-Hebbian plasticity.
Automatic Data Processing ; Brain ; Depression ; Learning ; Long-Term Potentiation ; Memory ; Plastics* ; Synapses

Vestibular compensation is a recovery process from vestibular symptoms over time after unilateral loss of peripheral vestibular end organs. The aim of the present study was to observe time-dependent changes in long-term potentiation (LTP) at Schaffer collateral-CA1 synapses in the CA1 area of the hippocampus during vestibular compensation. The input-output (I/O) relationships of fEPSP amplitudes and LTP induced by theta burst stimulation to Schaffer's collateral commissural fibers were evaluated from the CA1 area of hippocampal slices at 1 day, 1 week, and 1 month after unilateral labyrinthectomy (UL). The I/O relationships of fEPSPs in the CA1 area was significantly reduced within 1 week post-op and then showed a non-significant reduction at 1 month after UL. Compared with sham-operated animals, there was a significant reduction of LTP induction in the hippocampus at 1 day and 1 week after UL. However, LTP induction levels in the CA1 area of the hippocampus also returned to those of sham-operated animals 1 month following UL. These data suggest that unilateral injury of the peripheral vestibular end organs results in a transient deficit in synaptic plasticity in the CA1 hippocampal area at acute stages of vestibular compensation.
Animals ; Compensation and Redress* ; Hippocampus* ; Long-Term Potentiation* ; Neuronal Plasticity ; Rats* ; Synapses*

Circadian rhythms are driven by circadian oscillators, and these rhythms result in the biological phenomenon of 24-h oscillations. Previous studies suggest that learning and memory are affected by circadian rhythms. One of the genes responsible for generating the circadian rhythm is Rev-erbα. The REV-ERBα protein is a nuclear receptor that acts as a transcriptional repressor, and is a core component of the circadian clock. However, the role of REV-ERBα in neurophysiological processes in the hippocampus has not been characterized yet. In this study, we examined the time-dependent role of REV-ERBα in hippocampal synaptic plasticity using Rev-erbα KO mice. The KO mice lacking REV-ERBα displayed abnormal NMDAR-dependent synaptic potentiation (E-LTP) at CT12~CT14 (subjective night) when compared to their wild-type littermates. However, Rev-erbα KO mice exhibited normal E-LTP at CT0~CT2 (subjective day). We also found that the Rev-erbα KO mice had intact late LTP (L-LTP) at both subjective day and night. Taken together, these results provide evidence that REV-ERBα is critical for hippocampal E-LTP during the dark period.
Animals ; Biological Phenomena ; Circadian Clocks ; Circadian Rhythm ; Hippocampus ; Learning ; Long-Term Potentiation ; Memory ; Mice ; Neuronal Plasticity

Animals ; Hippocampus ; metabolism ; Long-Term Potentiation ; Male ; Neurogranin ; biosynthesis ; Rats ; Rats, Wistar ; Sleep Deprivation ; metabolism