Plasticity of synaptopodin and the spine apparatus organelle in the rat fascia dentata following entorhinal cortex lesion

Abstract

Synaptopodin is an actin-associated molecule essential for the formation of a spine apparatus in telencephalic spines. To study whether synaptopodin and the spine apparatus organelle are regulated under conditions of lesion-induced plasticity, synaptopodin and the spine apparatus were analyzed in granule cells of the rat fascia dentata following entorhinal denervation. Confocal microscopy was employed to quantify layer-specific changes in synaptopodin-immunoreactive puncta densities. Electron microscopy was used to quantify layer-specific changes in spine apparatus organelles. Within the denervated middle and outer molecular layers, the layers of deafferentation-induced spine loss, synaptogenesis, and spinogenesis, the density of synaptopodin puncta and the number of spine apparatuses decreased by 4 days postlesion and slowly recovered in parallel with spinogenesis by 180 days postlesion. Within the nondenervated inner molecular layer, the zone without deafferentation-induced spine loss, a rapid loss of synaptopodin puncta and spine apparatuses was also observed. In this layer, spine apparatus densities recovered by 14 days postlesion, in parallel with plastic remodeling at the synaptic level and the postlesional recovery of granule cell activity. These data demonstrate layer-specific changes in the distribution of synaptopodin and the spine apparatus organelle following partial denervation of granule cells: in the layer of spine loss, spine apparatus densities follow spine densities; in the layer of spine maintenance, however, spine apparatus densities appear to be regulated by other signals.

Synaptopodin Regulates Plasticity of Dendritic Spines in Hippocampal Neurons

“…These observations indicate that SP is associated with mature spines and that synaptic innervations may contribute to the targeting and maintenance of SP in dendritic spines. The results are consistent with studies which show lamina-specific alterations in the distribution of SP in the hippocampus after denervation (Deller et al, 2006) and after synaptic stimulation (Roth et al, 2001;Yamazaki et al, 2001;Fukazawa et al, 2003).…”

Morphological changes of cortical pyramidal neurons in hepatic encephalopathy

“…Unlike dendritic arbors, dendritic spines are highly motile structures that have been shown to be swiftly and dynamically modulated by many factors such as changes in environment [29], gonadal hormones [27,28,30], physical compression and decompression [21,22], fatigue [20], insults such as axonal injury [31], deafferentation [32], and aging [33]. Here, we have shown that hyperammonemia significantly decreased the spine density in layer V sensorimotor cortical neurons (23-46%) and in hippocampal CA1 pyramidal neurons (24-47%).…”

Synaptic plasticity at the interface of health and disease: New insights on the role of endoplasmic reticulum intracellular calcium stores

“…1B). Considering that SP expression is altered under numerous pathological conditions (e.g., Reddy et al, 2005;Deller et al, 2006;Vlachos et al, 2008Vlachos et al, , 2013aStrehl et al, 2014), it is plausible that the ability of the ER to form these highly organized (SP-dependent) organelles might be of relevance in pathology.…”