Object-Place Recognition Learning Triggers Rapid Induction of Plasticity-Related Immediate Early Genes and Synaptic Proteins in the Rat Dentate Gyrus

Abstract

Long-term recognition memory requires protein synthesis, but little is known about the coordinate regulation of specific genes. Here, we examined expression of the plasticity-associated immediate early genes (Arc, Zif268, and Narp) in the dentate gyrus following long-term object-place recognition learning in rats. RT-PCR analysis from dentate gyrus tissue collected shortly after training did not reveal learning-specific changes in Arc mRNA expression. In situ hybridization and immunohistochemistry were therefore used to assess possible sparse effects on gene expression. Learning about objects increased the density of granule cells expressing Arc, and to a lesser extent Narp, specifically in the dorsal blade of the dentate gyrus, while Zif268 expression was elevated across both blades. Thus, object-place recognition triggers rapid, blade-specific upregulation of plasticity-associated immediate early genes. Furthermore, Western blot analysis of dentate gyrus homogenates demonstrated concomitant upregulation of three postsynaptic density proteins (Arc, PSD-95, and α-CaMKII) with key roles in long-term synaptic plasticity and long-term memory.

Early growth response gene 1 (Egr-1) is required for new and reactivated fear memories in the lateral amygdala

“…One widely studied candidate gene is the early growth response gene-1 (EGR-1; also known as zif-268, NGFI-1, Krox-24), a member of a family of zinc finger inducible transcription factors that is believed to be critical for regulating the transcription of late-response genes that promote functional and/or structural changes underlying long-term synaptic plasticity and memory formation (Davis et al 2003;Knapska and Kaczmarek 2004). In other memory systems, EGR-1 has been implicated in long-term forms of experience-dependent synaptic plasticity (Cole et al 1989;Richardson et al 1992;Abraham et al 1993;Bramham et al 1996;Davis et al 2000;Jones et al 2001;Håvik et al 2003;Renaudineau et al 2009) and in memory formation, including song learning in songbirds, in vitro eye-blink conditioning in turtles, and in object recognition memory and spatial learning in rats (Mello and Clayton 1994;Jones et al 2001;Bozon et al 2003a;Mokin and Keifer 2005;Soulé et al 2008). Recent studies have also implicated EGR-1 in memory reconsolidation processes, including those associated with contextual fear conditioning in the hippocampus (Lee et al 2004;Lee 2008) and cue-induced drug seeking in the amygdala (Lee et al 2006).…”

Activity-dependent expression of miR-132 regulates immediate-early gene induction during olfactory learning in the greater short-nosed fruit bat, Cynopterus sphinx

“…In fact, it has been demonstrated that the inhibition of miR-132 attenuates spine formation and dendritic plasticity through a down regulation of P250 GAP Miller et al, 2012;Vo et al, 2005;Wayman et al, 2008). Synaptic proteins, including PSD-95, in the synaptic region critically regulate synaptic plasticity (Soulě et al, 2008). It has been stated that PSD-95 expression is epigenetically regulated by CREB and is critically involved in synaptic plasticity (Ehrlich et al, 2007;Meyer, Bonhoeffer, & Scheuss, 2014;Pollak et al, 2005;Wang, Yan, Hui, & Zhang, 2014).…”

Involvement of Neurotransmitter and Nrf2 in Nicotine- and Cigarette Smoke-Induced Testicular Toxicity in Adult Rats

“…7 Further, like DA, brain-derived neurotrophic factor (BDNF) is another major neurochemical that promotes cell survival, neural outgrowth, differentiation, plasticity and regeneration of damaged neurons sprouting through Trkβ R activation, and modulation of chemical synapses. 8,9 Evidences suggest that nicotine induces BDNF and upregulates BDNF R (Trkβ) in rat brain. 10 Acute Trkβ activation potentiates presynaptic DA release and transport in different brain regions.…”