Imaging of Intracellular Calcium in Hippocampal Slices: Methods, Limitations, and Achievements
Avital Schurr, Benjamin M. Rigor in BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
One of the more interesting sites of neuronal interaction is the dendritic spine. This is where synapses are made and where [Ca2+]i is assumed to rise locally to high values upon stimulation. The dendritic spine is a small organelle at the limit of optical resolution and has thus far been inaccessible to a systematic analysis in live tissue. The advent of calcium imaging methodology allows for the first time the analysis of [Ca2+]i changes in dendritic spines upon chemical and electrical stimulation. Indeed, several publications have appeared illustrating the expected properties of dendritic spines as unique calcium compartments.28,29 The presence of voltage- or specific ligand-gated calcium channels on dendritic spines is still to be demonstrated.
Acid-Sensing Ion Channels and Synaptic Plasticity: A Revisit
Tian-Le Xu, Long-Jun Wu in Nonclassical Ion Channels in the Nervous System, 2021
Synaptic plasticity is a generic term that applies to short- or long-lasting experience- or activity-dependent changes in the efficacy or connection of synaptic transmission in the brain. It can be classified into both functional and structural aspects of synaptic plasticity. For the former, except for LTP and LTD, it also includes short-term plasticity (like paired-pulse facilitation or depression), depotentiaion86, metaplasticity (plasticity of synaptic plasticity)87, and homeostatic plasticity88 (scaling up or down of the synaptic strength in response to reduction or elevation of synaptic activity). For the latter, dendritic spines may undergo activity-dependent dynamic alterations in shape, size, density, or even composition during various behavioral tasks and/or synaptic stimulations84. To date, most studies have focused on the classical LTP, with much less emphasis placed on other forms of synaptic plasticity, although the possibilities that ASICs are equally important for depotentiaion (or metaplasticity) have not been fully excluded. It would be both necessary and exciting in future studies to test these possibilities.
Synapses
Nassir H. Sabah in Neuromuscular Fundamentals, 2020
The LTP and LTD mechanisms of the preceding discussion are believed to be a prelude to activity-dependent, structural changes in synapses that can last for years. The synapses mainly affected are those on characteristic, knob-shaped, outgrowths on dendrites known as dendritic spines (Figure 6.16). As can be seen from this figure, the spine shape can vary from stubby, to mushroom-like, to spindly with a thin and relatively long neck. The spine length varies between a fraction of a µm and few µms, the neck diameter being generally less than 0.1 µm, and the head volume ranging from 0.01 µm3 to 0.8 µm3. Spines are commonly found on the dendrites of most principal neurons in the brain. Neocortical and hippocampal pyramidal cells (Section 7.1) have tens of thousands of spines that may constitute up to about 40% of the total dendritic membrane area. Cerebellar Purkinje cells are believed to have more than 100,000 spines comprising about 75% of the total membrane area. It is estimated that more than 90% of excitatory synapses in the brain terminate on spines, with generally one synapse per spine on the spine head.
Gut dysbiosis impairs hippocampal plasticity and behaviors by remodeling serum metabolome
Published in Gut Microbes, 2022
Guoqiang Liu, Quntao Yu, Bo Tan, Xiao Ke, Chen Zhang, Hao Li, Tongmei Zhang, Youming Lu
The hippocampus, a key brain region involved in various sensory, emotional, and cognitive function, is highly susceptible to various damage.16 Previous studies have shown that the absence of gut microbiota affects the structure and function of the hippocampus.17,18 Therefore, we first analyzed whether early-life dysbiosis has an effect on dendritic spine morphogenesis. Compared with the control group, antibiotic-treated mice exhibited fewer apical dendritic spines with mature-appearing morphology (mushroom spine) in the dentate gyrus (DG) of the dorsal hippocampus Figure 4a and CA1 of the ventral hippocampus (FigureS2A), suggesting that a healthy early-life gut microbiota promotes spine maturation. Dendritic spines are highly dynamic neural structures, alterations in their morphology have been recognized as critical for synaptic plasticity and long-term memory.28 Next, we determined the effect of gut dysbiosis on hippocampal neurogenesis, which has been considered as a cellular model of anxiety29 and spatial memory.30 We used antibodies against 5-ethynyl-2’-deoxyuridine (EdU) and doublecortin (DCX) to label proliferation and neuronal differentiation of adult hippocampal progenitor cells. The number of cells positive for EdU, DCX, or double-labeled DCX-EdU cells decreases significantly after antibiotic intervention, revealing an impaired adult neurogenesis in antibiotic-treated mice compared with the controls (Figure 4b, FigureS2B).
Neurophysiological symptoms and aspartame: What is the connection?
Published in Nutritional Neuroscience, 2018
Arbind Kumar Choudhary, Yeong Yeh Lee
The glutamate receptor (GluR) is critical to the formation of synaptic connections during brain development and is responsible for inducing changes in dendritic spines of adult brain.30 Changes in the shape and number of dendritic spines are correlated with synaptic plasticity and account for the persistence of memory.31 Blocking the GluRs has been associated with impaired learning and memory in humans32 and animals.33 Phenylalanine may bind to the GluR, reduce plasticity and cause impaired learning and reduced memory (Table 1). High cerebral phenylalanine concentrations can inhibit the enzyme activity of tyrosine hydroxylase and tryptophan hydroxylase and lead to depleted levels of brain serotonin (5HT).28 At high concentrations, phenylalanine may compete with cerebral tyrosine to be hydroxylated by cerebral tyrosine hydroxylase, blocking the conversion of tyrosine to dopa.34,35 Dopamine deficiency may result in prefrontal cortex deficiency which is linked to brain dysfunction and impaired cognitive function.36,37 Cerebral protein synthesis is essential for brain development and function.38 Whilst the precise mechanism behind the inhibition of brain protein synthesis is unclear, we do know that brain protein synthesis can be normalized by the administration of large neutral amino acids which compete with phenylalanine for transport into brain via the BBB.39
Dynamic alteration of dendrites and dendritic spines in the hippocampus and microglia in mouse brain tissues after kainate-induced status epilepticus
Published in International Journal of Neuroscience, 2021
Lingling Xie, Tianyi Li, Xiaojie Song, Hong Sun, Jie Liu, Jing Yang, Wenjie Zhao, Li Cheng, Hengsheng Chen, Benke Liu, Wei Han, Chen Yang, Li Jiang
As major sites of excitatory synaptic input into the CNS, dendritic spines are strongly implicated in the mechanisms of plasticity and learning [6]. Furthermore, both clinical and experimental studies have indicated that epilepsy-related loss and structural injury of dendritic spines may be associated with cognitive deficits [7–9]. Recent evidence has confirmed the existence of communication between the microglia and neurons in epilepsy [10]. Activated microglia may exert different effects on brain function depending on the phase of epileptogenesis [11], and correct timing of the modulation of microglial phenotypes can improve the outcomes in epilepsy [12]; however, this requires further exploration. In addition, reports of the dynamic alteration in microglial types, their markers and changes in dendritic spines in the hippocampus of epileptic models at different time-points after acute status epilepticus (SE) are rare.
Related Knowledge Centers
- Axon
- Dendrite
- Medium Spiny Neuron
- Neocortex
- Pyramidal Cell
- Synapse
- Electron Microscope
- Excitatory Synapse
- Neuron
- Striatum