The effect of maternal deprivation to GABA A receptors in the prefrontal cortex of adult rats.

Abstract Background Methamphetamine (METH) is one of the most widely abused illicit substances worldwide; unfortunately, its addiction mechanism remains unclear. Based on accumulating evidence, changes in gene expression and chromatin modifications might be related to the persistent effects of METH on the brain. In the present study, we took advantage of METH-induced behavioral sensitization as an animal model that reflects some aspects of drug addiction and examined the changes in gene expression and histone acetylation in the prefrontal cortex (PFC) of adult rats. Methods We conducted mRNA microarray and chromatin immunoprecipitation (ChIP) coupled to DNA microarray (ChIP-chip) analyses to screen and identify changes in transcript levels and histone acetylation patterns. Functional enrichment analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, were performed to analyze the differentially expressed genes. We then further identified alterations in ANP32A (acidic leucine-rich nuclear phosphoprotein-32A) and POU3F2 (POU domain, class 3, transcription factor 2) using qPCR and ChIP-PCR assays. Results In the rat model of METH-induced behavioral sensitization, METH challenge caused 275 differentially expressed genes and a number of hyperacetylated genes (821 genes with H3 acetylation and 10 genes with H4 acetylation). Based on mRNA microarray and GO and KEGG enrichment analyses, 24 genes may be involved in METH-induced behavioral sensitization, and 7 genes were confirmed using qPCR. We further examined the alterations in the levels of the ANP32A and POU3F2 transcripts and histone acetylation at different periods of METH-induced behavioral sensitization. H4 hyperacetylation contributed to the increased levels of ANP32A mRNA and H3/H4 hyperacetylation contributed to the increased levels of POU3F2 mRNA induced by METH challenge-induced behavioral sensitization, but not by acute METH exposure. Conclusions The present results revealed alterations in transcription and histone acetylation in the rat PFC by METH exposure and provided evidence that modifications of histone acetylation contributed to the alterations in gene expression caused by METH-induced behavioral sensitization.

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Differential Methylation of Genes in the Medial Prefrontal Cortex of Developing and Adult Rats Following Exposure to Maltreatment or Nurturing Care During Infancy

Developmental Neuroscience ◽

10.1159/000350716 ◽

2013 ◽

Vol 35 (4) ◽

pp. 306-316 ◽

Cited By ~ 69

Author(s):

Jennifer Blaze ◽

Lisa Scheuing ◽

Tania L. Roth

Keyword(s):

Prefrontal Cortex ◽

Medial Prefrontal Cortex ◽

Differential Methylation ◽

Adult Rats

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Prenatal stress modifies the insulin-like growth factor-1 levels in the hippocampus and prefrontal cortex of adult rats

Pharmacological Reports ◽

10.1016/s1734-1140(11)70568-0 ◽

2011 ◽

Vol 63 (2) ◽

pp. 593-594

Author(s):

Ewa Szczęsny ◽

Agnieszka Basta-Kaim ◽

Aneta Dardzińska ◽

Monika Leśkiewicz ◽

Magdalena Regulska ◽

...

Keyword(s):

Prefrontal Cortex ◽

Growth Factor ◽

Prenatal Stress ◽

Insulin Like Growth Factor ◽

Adult Rats

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Impairment of cognitive performance after reelin knockdown in the medial prefrontal cortex of pubertal or adult rats

Neurobiology of Disease ◽

10.1016/j.nbd.2011.07.008 ◽

2011 ◽

Vol 44 (2) ◽

pp. 239-247 ◽

Cited By ~ 27

Author(s):

Jan Brosda ◽

Frank Dietz ◽

Michael Koch

Keyword(s):

Prefrontal Cortex ◽

Cognitive Performance ◽

Medial Prefrontal Cortex ◽

Adult Rats

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Early social isolation disrupts latent inhibition and increases dopamine D2 receptor expression in the medial prefrontal cortex and nucleus accumbens of adult rats

Brain Research ◽

10.1016/j.brainres.2012.01.058 ◽

2012 ◽

Vol 1447 ◽

pp. 38-43 ◽

Cited By ~ 25

Author(s):

Xiao Han ◽

Nanxin Li ◽

Xiaofang Xue ◽

Feng Shao ◽

Weiwen Wang

Keyword(s):

Prefrontal Cortex ◽

Nucleus Accumbens ◽

Social Isolation ◽

Medial Prefrontal Cortex ◽

Latent Inhibition ◽

Dopamine D2 Receptor ◽

D2 Receptor ◽

Receptor Expression ◽

Adult Rats ◽

Dopamine D2

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Intranasal oxytocin administration improves depression-like behaviors in adult rats that experienced neonatal maternal deprivation

Behavioural Pharmacology ◽

10.1097/fbp.0000000000000248 ◽

2016 ◽

Vol 27 (8) ◽

pp. 689-696 ◽

Cited By ~ 16

Author(s):

Haoyi Ji ◽

Wenlong Su ◽

Ruchen Zhou ◽

Jing Feng ◽

Yue Lin ◽

...

Keyword(s):

Maternal Deprivation ◽

Adult Rats

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Amygdala inputs drive feedforward inhibition in the medial prefrontal cortex

Journal of Neurophysiology ◽

10.1152/jn.00531.2012 ◽

2013 ◽

Vol 110 (1) ◽

pp. 221-229 ◽

Cited By ~ 47

Author(s):

Jonathan Dilgen ◽

Hugo A. Tejeda ◽

Patricio O'Donnell

Keyword(s):

Prefrontal Cortex ◽

Basolateral Amygdala ◽

Pyramidal Neurons ◽

Reversal Potential ◽

Intracellular Recordings ◽

Action Potential Firing ◽

Gaba A ◽

Potential Firing ◽

Feedforward Inhibition

Although interactions between the amygdala and prefrontal cortex (PFC) are critical for emotional guidance of behavior, the manner in which amygdala affects PFC function is not clear. Whereas basolateral amygdala (BLA) output neurons exhibit many characteristics associated with excitatory neurotransmission, BLA stimulation typically inhibits PFC cell firing. This apparent discrepancy could be explained if local PFC inhibitory interneurons were activated by BLA inputs. Here, we used in vivo juxtacellular and intracellular recordings in anesthetized rats to investigate whether BLA inputs evoke feedforward inhibition in the PFC. Juxtacellular recordings revealed that BLA stimulation evoked action potentials in PFC interneurons and silenced most pyramidal neurons. Intracellular recordings from PFC pyramidal neurons showed depolarizing postsynaptic potentials, with multiple components evoked by BLA stimulation. These responses exhibited a relatively negative reversal potential (Erev), suggesting the contribution of a chloride component. Intracellular administration or pressure ejection of the GABA-A antagonist picrotoxin resulted in action-potential firing during the BLA-evoked response, which had a more depolarized Erev. These results suggest that BLA stimulation engages a powerful inhibitory mechanism within the PFC mediated by local circuit interneurons.

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