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

Animals ; Brain ; physiology ; Extinction, Psychological ; physiology ; Humans ; Long-Term Potentiation ; Long-Term Synaptic Depression ; Neural Pathways ; physiology ; Neuronal Plasticity ; Neurons ; physiology ; Receptors, AMPA ; physiology

Ventral tegmental area (VTA) is an important relay station of signal transmission in the reward system. The plasticity of VTA dopaminergic neurons directly influences actions of other regions of the reward system. Studies concerning the plasticity of VTA dopaminergic neurons focus mainly on synaptic plasticity, while much less attention has been given to the plasticity of intrinsic excitability of the neurons. The aim of the present study was to investigate the effect of high-frequency stimulation (HFS) on the plasticity of excitability of VTA neuron. Whole-cell patch-clamping was performed on VTA dopaminergic neurons in midbrain slices bathed with PTX, AP-5 and CNQX, and HFS was introduced to cell soma. The result showed that, after HFS induction the pharmacologically isolated neurons showed increased input resistance and firing frequency, as well as decreased rheobase. Meanwhile, the steady-state whole-cell current decreased, and the hyperpolarization-activated current (I(h)) decreased. These results suggest that HFS on soma induces a long-term potentiation of excitability in VTA dopaminergic neurons, and the underlying mechanism involves the changes of membrane current.
Animals ; Dopaminergic Neurons ; cytology ; Long-Term Potentiation ; Patch-Clamp Techniques ; Ventral Tegmental Area ; physiology

BACKGROUNDTraumatic brain injury (TBI) often causes cognitive deficits and remote symptomatic epilepsy. Hippocampal regional excitability is associated with the cognitive function. However, little is known about injury-induced neuronal loss and subsequent alterations of hippocampal regional excitability. The present study was designed to determine whether TBI may impair the cellular circuit in the hippocampus.

METHODSForty male Wistar rats were randomized into control (n = 20) and TBI groups (n = 20). Long-term potentiation, extracellular input/output curves, and hippocampal parvalbumin-immunoreactive and cholecystokinin-immunoreactive interneurons were compared between the two groups.

RESULTSTBI resulted in a significantly increased excitability in the dentate gyrus (DG), but a significantly decreased excitability in the cornu ammonis 1 (CA1) area. Using design-based stereological injury procedures, we induced interneuronal loss in the DG and CA3 subregions in the hippocampus, but not in the CA1 area.

CONCLUSIONSTBI leads to the impairment of hippocampus synaptic plasticity due to the changing of interneuronal interaction. The injury-induced disruption of synaptic efficacy within the hippocampal circuit may underlie the observed cognitive deficits and symptomatic epilepsy.

Animals ; Brain Injuries ; physiopathology ; Hippocampus ; physiopathology ; Long-Term Potentiation ; Male ; Neuronal Plasticity ; physiology ; Rats ; Rats, Wistar

The physiological functions of endogenous amyloid-β (Aβ), which plays important role in the pathology of Alzheimer's disease (AD), have not been paid enough attention. Here, we review the multiple physiological effects of Aβ, particularly in regulating synaptic transmission, and the possible mechanisms, in order to decipher the real characters of Aβ under both physiological and pathological conditions. Some worthy studies have shown that the deprivation of endogenous Aβ gives rise to synaptic dysfunction and cognitive deficiency, while the moderate elevation of this peptide enhances long term potentiation and leads to neuronal hyperexcitability. In this review, we provide a new view for understanding the role of Aβ in AD pathophysiology from the perspective of physiological meaning.
Humans ; Alzheimer Disease/pathology* ; Amyloid beta-Peptides/metabolism* ; Long-Term Potentiation ; Synaptic Transmission/physiology* ; Hippocampus

In the present research, patch-clamp whole-cell recording was used to study the developmental changes of the internal horizontal synaptic plasticity in layer II/III of rats' primary visual cortices. Pairing stimulation was used to induce long term potentiation (LTP) of neurons in layer II/III from layer II/III and layer IV. The data indicate that: (1) Responses of layer II/III neurons can be evoked independently at II/III-II/III and IV-II/III synapses by horizontal and vertical stimulations; (2) LTP can be induced from neurons in the layer II/III by horizontal tetanic stimulation at II/III-II/III synapses till postnatal day12 (P12, before eyes open); (3) Meanwhile, only short term potentiation (STP) at IV-II/III synapses can be induced by horizontal tetanic stimulation before eyes open; (4) After P12, a robust LTP at IV-II/III synapses can be induced by horizontal tetanic stimulation; (5) At P14, when vertical and horizontal tetanic stimulations were given to the same neuron, the LTP at IV-II/III synapses was weaker than that induced by vertical stimulation alone, suggesting that vertical synaptic modification was negatively regulated by horizontal inputs when two-direction synaptic inputs were presented at the same time; (6) Spontaneous responses of AMPA receptors (AMPARs) in the layer II/III neuron of rats' primary visual cortices are regulated by the development. The frequency of AMPARs-mediated postsynaptic currents was at a low level before eyes open, increased sharply at P12-P14, and slightly decreased after P18. And the amplitude of spontaneous AMPARs currents slowly decreased after P12. The results demonstrated that both the strength of horizontal synaptic modification and the effects of horizontal inputs on the vertical synaptic connection are regulated by the development. II/III-II/III synaptic communication has dual effects on the IV-II/III synapses, which may be involved in a competitive machinery of neural circuitry maturation and the formation of visual function columns.
Animals ; Long-Term Potentiation ; Neuronal Plasticity ; Neurons ; physiology ; Patch-Clamp Techniques ; Rats ; Receptors, AMPA ; physiology ; Synapses ; physiology ; Visual Cortex ; physiology

Long-term potentiation (LTP) can be induced by various tetanic parameters in the mammalian visual cortex. However, little researches have been done on the relationship between the expression of the long-lasting LTP (late phase LTP or L-LTP) lasting more than 3 h and the tetanic parameters. In the present study, the effects of 2 Hz and 100 Hz tetanic parameters on L-LTP of the field potentials were recorded from the layer II/III of the rat visual cortical slices in response to stimulation of the layer IV. As a result, tetanic parameters that had more than 300 pulses reliably induced L-LTP in the postnatal day 15-21 rats. Obviously different L-LTP expressions were induced by 2 Hz and 100 Hz tetani. There was no difference in L-LTP expression induced by the parameters with the same frequency and different total pulses. These data suggest that L-LTPs induced by different frequency parameters may have different induction and maintenance mechanisms; L-LTPs induced by the parameters with the same frequency may have the same mechanisms.
Animals ; Electric Stimulation ; methods ; Long-Term Potentiation ; physiology ; Male ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission ; physiology ; Visual Cortex ; physiology

Animals ; Corticosterone ; pharmacology ; Hippocampus ; drug effects ; physiology ; In Vitro Techniques ; Long-Term Potentiation ; drug effects ; physiology ; Male ; Rats ; Rats, Wistar

Extracellular recordings of field excitatory postsynaptic potential (fEPSP) is one of the most common ways for studies of synaptic plasticity, such as long-term potentiation (LTP) and paired-pulse plasticity (PPP). The measurement of the changes in the different components of fEPSP waveform, such as the initial slope, initial area, peak amplitude and whole area, were commonly used as criteria for the judgement of potentiation or depression of synaptic plasticity. However, the differences in the conclusions drawn from measuring different components of fEPSP waveform at the same recording have still been largely ignored. Here we compared high-frequency stimulation (HFS)-evoked synaptic plasticity, both LTP and PPP, by measuring different components of fEPSP waveform, including the initial slope, initial area, peak amplitude, whole area and time course. The results not only indicated the acceleration of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor kinetics underlies LTP in hippocampal CA1 region of mice, but also showed that different measurements of fEPSP waveform at the same recording result in different magnitudes of LTP and different forms of PPP in hippocampal CA1 region of mice. After HFS, the paired-pulse ratio was slightly decreased by measurement of the initial area, but obviously increased by measurement of the initial slope of the pair fEPSPs. These results might draw apparently contradictory conclusions. Therefore, careful and complete analysis of the data from different parts of fEPSP waveforms is important for reflection of the faithful changes in synaptic plasticity.
Animals ; CA1 Region, Hippocampal ; physiology ; Excitatory Postsynaptic Potentials ; Long-Term Potentiation ; Mice ; Neuronal Plasticity ; Receptors, AMPA ; metabolism

Nicotine enhances the function of learning and memory, but the underlying mechanism still remains unclear. Hippocampal long-term potentiation (LTP) is assumed to be a cellular mechanism of learning and memory. Our previous experiments showed that with the single pulses evoking 80% of the maximal population spike (PS) amplitude, nicotine (10 μmol/L) induced LTP-like response in the hippocampal CA1 region. In the present study, the nicotinic acetylcholine receptor (nAChR) subtypes and relevant neurotransmitter releases involved in LTP-like response induced by nicotine were investigated by extracellularly recording the PS in the pyramidal cell layer in the hippocampal CA1 region in vitro. LTP-like response induced by nicotine was blocked by mecamylamine (1 μmol/L) or κ-bungarotoxin (0.1 μmol/L), but not by dihydro-β-erythtroidine (DHβE, 10 μmol/L). Moreover, it was inhibited by propranolol (10 μmol/L), but not by phentolamine (10 μmol/L) or atropine (10 μmol/L). The results suggest that noradrenaline release secondary to the activation of κ-bungarotoxin-sensitive nAChRs participates in LTP-like response induced by nicotine in the hippocampal CA1 region.
Animals ; Bungarotoxins ; CA1 Region, Hippocampal ; physiology ; Long-Term Potentiation ; drug effects ; Nicotine ; pharmacology ; Norepinephrine ; secretion ; Receptors, Nicotinic ; metabolism