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Jon I Arellano

Publications and source records attributed to Jon I Arellano.

5 recordsLinked to original sources

Catecholaminergic innervation of pyramidal neurons in the human temporal cortex.

In the human neocortex, catecholaminergic connections modulate the excitatory inputs of pyramidal neurons and are involved in higher cognitive functions. Catecholaminergic fibers form a dense network in which it is difficult to distinguish whether or not target specificity exists. In order to shed some light on this issue, we set out to quantify the catecholaminergic innervation of pyramidal cells in different layers of the human temporal cortex (II, IIIa, IIIb, V and VI). For this purpose, pyramidal cells were labeled in human cortical tissue by injecting them with Lucifer Yellow, and then performed immunocytochemistry for the rate limiting catecholamine synthesizing enzyme tyrosine hydroxylase (TH) to visualize catecholaminergic fibers in the same sections. Injected cells were reconstructed in three dimensions and appositions were quantified (n = 1503) in serial confocal microscopy images of each injected cell (n = 71). We found TH-immunoreactive appositions (TH-ir) in all the pyramidal cells analyzed, in both the apical and basal dendritic regions. In general, the density of TH-ir apposition was greater in layers II, V and VI than in layers IIIa and IIIb. Furthermore, TH-ir appositions showed a regular distribution in almost all dendritic compartments of the apical and basal dendritic arbors across all layers. Hence, it appears that all pyramidal neurons in the human neocortex receive catecholaminergic afferents in a rather regular pattern, independent of the layer in which they are located. Since pyramidal cells located in different layers are involved in different intrinsic and extrinsic circuits, these results suggest that catecholaminergic afferents may modify the function of a larger variety of circuits than previously thought. Thus, this aspect of human cortical organization is likely to have important implications in cortical function.

Adult↗

CA1 hippocampal neuronal loss in familial Alzheimer's disease presenilin-1 E280A mutation is related to epilepsy.

PURPOSE: Alzheimer disease (AD) and epilepsy are brain disorders frequently associated with neuronal cell loss in mesial temporal lobe structures, but presenting different patterns of damage. Recently it was proposed that a causal relation may exist between AD pathology and the appearance of epilepsy in some cases with AD. This study aimed to determine the neuronal loss in CA1 hippocampal region from patients bearing the presenilin-1 [E280A] mutation (PS1[E280A]) associated with seizures. METHODS: Coronal sections from the hippocampal formation (anterior one third) from controls (n = 5) and familial AD (FAD; n = 8) patients were stained by using thionin and thioflavine-S staining to evaluate the number of neurons in the CA1 field, beta-plaques, and neurofibrillary tangles, respectively. RESULTS: Two distinct patterns of neuronal loss in the CA1 field of FAD patients were found: (a) diffuse-patchy neuronal loss (three FAD nonepilepsy patients) characterized by both a general decrease of neurons and the presence of multiple, small regions devoid of neurons; and (b) sclerotic-like neuronal loss (five FAD epilepsy patients) similar to that found typically in the CA1 field of epilepsy patients with hippocampal sclerosis. CONCLUSIONS: This investigation shows for the first time CA1 neuronal depopulation in a subpopulation of patients (five of eight) bearing the PS1[E280A] mutation with epileptic seizures, indicating a relation between hippocampal neuronal loss and epileptic seizures in FAD patients.

Adult↗

Synaptically released acetylcholine evokes Ca2+ elevations in astrocytes in hippocampal slices.

Recent results have demonstrated the existence of bidirectional communication between glial cells and neurons. We investigated in brain slices whether rat hippocampal astrocytes respond to acetylcholine synaptically released by an extrinsic pathway. We stimulated the stratum oriens/alveus, which contains cholinergic afferents from the septum and diagonal band of Broca, and recorded whole-cell membrane currents and intracellular Ca2+ levels of astrocytes located in the hippocampal stratum oriens. Nerve-fiber stimulation evoked a long-lasting inward current and increased the Ca2+ levels in astrocytes. Both astrocytic responses were abolished by tetrodotoxin or Cd2+ and were increased by 4-aminopyridine, indicating that the responses were attributable to synaptically released neurotransmitter. The inward current was inhibited by glutamate transporter antagonists, indicating that it was attributable to the electrogenic glutamate transporter activity. The synaptically evoked intracellular Ca2+ elevations were not affected by glutamate receptor antagonists but were abolished by atropine, indicating that they were mediated by muscarinic cholinergic receptors. Thapsigargin prevented the Ca2+ elevation but did not modify the inward current, indicating that the Ca2+ signal was attributable to intracellular Ca2+ mobilization. These results indicate that hippocampal astrocytes respond to acetylcholine released by synaptic terminals. The synaptically released acetylcholine acts on muscarinic receptors, mobilizing Ca2+ from the intracellular stores. Different regions in the recorded astrocytes showed independent stimulus-induced Ca2+ variations, suggesting the existence of subcellular domains in the astrocytic responses evoked by the synaptic cholinergic activity. Therefore, our results show the existence of cholinergic neuron-astrocyte signaling and suggest that astrocytes are a target of axonal inputs from different brain areas.

Acetylcholine↗

PSA-NCAM immunoreactivity in chandelier cell axon terminals of the human temporal cortex.

In the adult central nervous system, the expression of polysialylated forms of the cell-surface glycoprotein NCAM (PSA-NCAM) is thought to be confined to areas particularly susceptible to plastic changes. In the present study, PSA-NCAM was found to be expressed in the somata, dendrites and axonal processes of some neurons, including cartridge-like elements, which according to our criteria, were identified as chandelier cell axon terminals (chandelier terminals), in the adult human entorhinal cortex and neocortex. These chandelier terminals were very numerous in layers II and III, whereas in deeper layers they were found only occasionally. Double immunocytochemical staining for PSA-NCAM with parvalbumin (PV), with GABA transporter (GAT-1) or with the 5-HT(1A) serotonin receptor allowed us to verify them as true chandelier terminals. Nearly all (92-95%) PV-immunoreactive (-ir) and GAT-1-ir chandelier terminals in layers II and III coexpressed PSA-NCAM. Most of the PSA-NCAM-ir chandelier terminals (89-98%) were also labeled for PV and GAT-1. The results suggest that chandelier terminals in layers II and III of the human entorhinal cortex and temporal neocortex might be particularly susceptible to plastic changes.

Adult↗

Microstructure of the neocortex: comparative aspects.

The appearance of the neocortex, its expansion, and its differentiation in mammals, represents one of the principal episodes in the evolution of the vertebrate brain. One of the fundamental questions in neuroscience is what is special about the neocortex of humans and how does it differ from that of other species? It is clear that distinct cortical areas show important differences within both the same and different species, and this has led to some researchers emphasizing the similarities whereas others focus on the differences. In general, despite of the large number of different elements that contribute to neocortical circuits, it is thought that neocortical neurons are organized into multiple, small repeating microcircuits, based around pyramidal cells and their input-output connections. These inputs originate from extrinsic afferent systems, excitatory glutamatergic spiny cells (which include other pyramidal cells and spiny stellate cells), and inhibitory GABAergic interneurons. The problem is that the neuronal elements that make up the basic microcircuit are differentiated into subtypes, some of which are lacking or highly modified in different cortical areas or species. Furthermore, the number of neurons contained in a discrete vertical cylinder of cortical tissue varies across species. Additionally, it has been shown that the neuropil in different cortical areas of the human, rat and mouse has a characteristic layer specific synaptology. These variations most likely reflect functional differences in the specific cortical circuits. The laminar specific similarities between cortical areas and between species, with respect to the percentage, length and density of excitatory and inhibitory synapses, and to the number of synapses per neuron, might be considered as the basic cortical building bricks. In turn, the differences probably indicate the evolutionary adaptation of excitatory and inhibitory circuits to particular functions.

Animals↗