Conditioned Place Preference Associated with Level of Palmitoylation of PSD-95 in Rat Hippocampus and Nucleus Accumbens

Abstract

Psychostimulant-mediated synaptic plasticity in the hippocampus and nucleus accumbens is one of the pathological features of addiction, a disease of learning and memory. Dynamic palmitoylation of PSD-95 modulates synaptic plasticity, but its role in addiction is not fully understood. Using a morphine-conditioned place preference (CPP) rat model and Acyl-biotin exchange (ABE) labeling we found a correlation between CPP and levels of palmitoylated PSD-95 in the hippocampus and nucleus accumbens. Rats that developed significant CPP had higher levels of palmitoylation of PSD-95 in the hippocampus and nucleus accumbens. Furthermore, palmitoylation of PSD-95 was significantly decreased in the hippocampus but increased in the nucleus accumbens during the beginning of withdrawal. With long-term withdrawal, palmitoylated PSD-95 in these regions recovered, while CPP waned and physical signs gradually disappeared. However, morphine reinjection restored strong CPP without producing any significant changes in palmitoylation of PSD-95. Our findings suggest that CPP is correlated with the dynamics of PSD-95 palmitoylation in rat hippocampus and nucleus accumbens, and could be one of the mechanisms for morphine-dependent synaptic plasticity.

H3K4 dimethylation at FosB promoter in the striatum of chronic stressed rats promotes morphine-induced conditioned place preference

“…The CPP results in our study confirm that chronic stress increases susceptibility to drugs of abusive [1–6]. The chronic stressed animals in this study established morphine-induced CPP by administrating lower dose of morphine after a shorter training period than unstressed rats reported before [37, 46]. Stress facilitates addiction has also found in animals treated with other types physical stress (e.g., forced swimming stress [47] and restraint stress [48]) or psychological stress (e.g., social defeat stress [49]).…”

“…CPP training and test were performed as described previously [37]. Briefly, animals (n = 54) were allowed to adapt to CPP apparatus 60 min per day for 2 days.…”

Maternal Exposure to Di-(2-ethylhexyl) Phthalate Impairs Hippocampal Synaptic Plasticity in Male Offspring: Involvement of Damage to Dendritic Spine Development

“…Its phosphorylation can rapidly regulate neurotransmitter release efficiency, thereby affecting synaptic plasticity . Postsynaptic density (PSD) is a protein-specific composite attached to the postsynaptic membrane that supports receptors, enzymes, and signaling molecules that are required in synaptic transmission. , A long-term increase in the synaptic strength of LTP is typically accompanied by remodeling of PSD protein content . Simultaneously, PSD thickness is also an important indicator that reflects structural synapses of hippocampal neurons plasticity …”

Differential protein expression of DARPP-32 versus Calcineurin in the prefrontal cortex and nucleus accumbens in schizophrenia and bipolar disorder

“…Dopamine- and cAMP-regulated phosphoprotein of molecular weight 32 kDa (DARPP-32), also known as phosphoprotein phosphatase-1 regulatory subunit 1B (PPP1R1B), is a key molecule that integrates dopaminergic signaling into that of several other neurotransmitters, such as a glutamate 1 . Phosphorylated DARPP-32 regulates the physiological activities of various proteins 2 . Calcineurin (CaN) is located downstream of dopaminergic and glutamatergic signaling and inactivates DARPP-32 by dephosphorylation 3 .…”