Publications by authors named "Zhi-ru Zhu"

Memory consolidation refers to a process by which labile newly formed memory traces are progressively strengthened into long term memories and become more resistant to interference. Recent work has revealed that spontaneous hippocampal activity during rest, commonly referred to as "offline" activity, plays a critical role in the process of memory consolidation. Hippocampal reactivation occurs during sharp-wave ripples (SWRs), which are events associated with highly synchronous neural firing in the hippocampus and modulation of neural activity in distributed brain regions.

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Article Synopsis
  • The study investigates how blocking adenosine A receptors (AR) might help protect against memory problems in Alzheimer's disease (AD), especially in a specific type of mouse with AD.
  • Researchers looked at whether blocking AR could improve spatial memory deficits and found that these mice had problems with certain brain functions early on.
  • After treating the mice with a special drug that blocks AR, they showed improvements in memory and brain connections, suggesting that AR blockade could be a possible treatment for early cognitive issues in AD.
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Background: The incidence of sleep disorders in children with autism spectrum disorder (ASD) is very high. Sleep disorders can exacerbate the development of ASD and impose a heavy burden on families and society. The pathological mechanism of sleep disorders in autism is complex, but gene mutations and neural abnormalities may be involved.

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Soluble amyloid beta (Aβ) is believed to contribute to cognitive deficits in the early stages of Alzheimer's disease (AD). Increased soluble Aβ in the hippocampus is closely correlated with spatial learning and memory deficits in AD. Riluzole (RLZ), an FDA-approved drug for amyotrophic lateral sclerosis (ALS), has beneficial effects for AD.

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Rhynchophylline (RIN) is a significant active component isolated from the Chinese herbal medicine Uncaria rhynchophylla. The overproduction of soluble amyloid β protein (Aβ) oligomers in the hippocampus is closely involved in impairments in cognitive function at the early stage of Alzheimer's disease (AD). Growing evidences show that RIN possesses neuroprotective effects against Aβ-induced neurotoxicity.

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Hypobaric hypoxia (HH) at high altitudes leads to a wide range of cognitive impairments which can handicap human normal activities and performances. However, the underlying mechanism is still unclear. Adenosine A receptors (ARs) of the brain are pivotal to synaptic plasticity and cognition.

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Rhynchophylline (RIN) is a significant active component isolated from the Chinese herbal medicine Uncaria rhynchophylla. Several studies have demonstrated that RIN has a significant anticonvulsant effect in many types of epilepsy models in vivo. However, the mechanisms of the anticonvulsant effect remain elusive.

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Temporal lobe epilepsy (TLE) is one of the most refractory types of adult epilepsy, and treatment options remain unsatisfactory. Gastrodin (GAS), a phenolic glucoside used in Chinese herbal medicine and derived from Gastrodia elata Blume, has been shown to have remarkable anticonvulsant effects on various models of epilepsy in vivo. However, the mechanisms of GAS as an anticonvulsant drug remain to be established.

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Accumulated soluble amyloid β (Aβ)-induced aberrant neuronal network activity has been recognized as a key causative factor leading to cognitive deficits which are the most outstanding characteristic of Alzheimer's disease (AD). As an important structure associated with learning and memory, the hippocampus is one of the brain regions that are impaired very early in AD, and the hippocampal CA1 region is selectively vulnerable to soluble Aβ oligomers. Our recent study showed that soluble Aβ1-42 oligomers induced hyperactivity and perturbed the firing patterns in hippocampal neurons.

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Accumulated soluble amyloid beta- (Aβ-) induced aberrant neuronal network activity may directly contribute to cognitive deficits, which are the most outstanding characteristics of Alzheimer's disease (AD). The entorhinal cortex (EC) is one of the earliest affected brain regions in AD. Impairments of EC neurons are responsible for the cognitive deficits in AD.

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Abnormal accumulation of soluble amyloid beta (Aβ) is believed to cause malfunction of neurons in Alzheimer's disease (AD). The hippocampus is one of the earliest affected brain regions in AD. However, little effort has been made to investigate the effects of soluble Aβ1-42 oligomers on discharge properties of hippocampal neurons in vivo.

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Patients with Alzheimer's disease (AD) have elevated incidence of epilepsy. Moreover, neuronal hyperexcitation occurs in transgenic mouse models overexpressing amyloid precursor protein and its pathogenic product, amyloid β protein (Aβ). However, the cellular mechanisms of how Aβ causes neuronal hyperexcitation are largely unknown.

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Electrical stimulation of ventral division of medial geniculate body (MGBv) neurons evokes a shift of the frequency-tuning curves of auditory cortical (AC) neurons toward the best frequency (BF) of the stimulated MGBv neurons (frequency-specific plasticity). The shift of BF is induced by inhibition of responses at the BF of the recorded AC neuron, with coincident facilitation of responses at the BF of the stimulated MGBv neuron. However, the synaptic mechanisms are not yet understood.

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In a process known as frequency-specific plasticity, electrical stimulation of the ventral division of the medial geniculate body (MGBv) in the thalamus evokes a shift in the frequency-tuning curves of auditory cortical (AC) neurons toward the best frequency (BF) of stimulated MGBv neurons. However, the underlying synaptic mechanisms of this process are uncharacterized. To investigate whether this dynamic change depends on thalamocortical (TC) synaptic plasticity, we studied frequency-specific changes in synaptic transmission efficacy in TC pathways evoked by thalamic stimulation.

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Behavioral studies have demonstrated that both medial prefrontal cortex (mPFC) and cerebellum play critical roles in trace eyeblink conditioning. However, little is known regarding the mechanism by which the two brain regions interact. By use of electrical stimulation of the caudal mPFC as a conditioned stimulus, we show evidence that persistent outputs from the mPFC to cerebellum are necessary and sufficient for the acquisition and expression of a trace conditioned response (CR)-like response.

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The cerebellum plays an essential role in motor learning. Recently, orexins, the newfound lateral hypothalamic neuropeptides, have been found to excite Purkinje cells in the cerebellar cortex and neurons in the deep cerebellar nuclei (DCN). However, little is known about their roles in cerebellum-dependent motor learning.

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Usually, the main axon is assumed to faithfully conduct action potentials (APs). Recent data have indicated that neural processing can occur along the axonal path. However, the patterns and mechanisms of temporal coding are not clear.

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Learning-induced changes of synaptic ultrastructure have long been proposed as a mechanism that may contribute to support memory formation. Although recent studies have demonstrated that the interpositus nuclei (IN) play critical role in acquisition and retention of trace conditioned eyeblink responses (CRs), there is now limited evidence associating trace eyeblink conditioning with changes of synaptic ultrastructure in the IN. Here, we investigated this issue using a transmission electron microscope.

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Recent experimental and theoretical data indicate that the functional capabilities of axons with specialized structures are much more diverse than traditionally thought. However, few observations were concerned with the main axons without arborization. In the present study, electrical stimulation of the saphenous nerve at different frequencies (2, 5, 10, 20 Hz) was used to test the role of activity-dependent effects on the pattern of action potentials that propagate along individual unmyelinated fibers (C fibers) within the trunk of the saphenous nerve in rabbits.

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To determine the characteristics of spontaneous discharges of hippocampal pyramidal cells (PCs), extracellular neuronal firing in CA1 and CA3 regions of dorsal hippocampus was recorded, the firing modes and interspike interval (ISI) were analyzed with the conventional and nonlinear methods. PCs were discriminated from interneurons using the measurement of action-potential duration and firing rate in this study. There was no significant difference in duration, mean firing frequency, complexity and firing mode between the neurons in CA1 and CA3 regions both in anesthetized and awake animals.

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