Conditioned morphine tolerance promotes neurogenesis, dendritic remodelling and pro-plasticity molecules in the adult rat hippocampus.

Structural neuroplasticity of the hippocampus in the form of neurogenesis and dendritic remodelling underlying morphine tolerance is still less known. Therefore, in this study, we aimed to assess whether unconditioned- and conditioned-morphine tolerance can trigger structural neuroplasticity in the dorsal and ventral parts of the adult male rat hippocampus. Evaluation of the levels of neurogenesis markers (Ki67 and DCX) by immunohistochemistry shows that conditioned morphine tolerance is sufficient to increase the baseline topographic level of hippocampal neurogenesis in adult rats.

Avoidance and escape conditioning adjust adult neurogenesis to conserve a fit hippocampus in adult male rodents.

In this study, the connection between cognitive behaviors and the adult rodent hippocampus was investigated. Recording field potentials at performant pathway (PP)-hippocampal dentate gyrus (DG) synapses in transverse slices from the dorsal (d), intermediate (i), and ventral (v) hippocampus showed differences in paired-pulse responses and long-term potentiation in rats. The Barnes maze (BM) and passive avoidance (PA) tests indicated a decrease in escape latency and step-through latency in both rats and mice over training days.

Maladaptive plasticity induced by morphine is mediated by hippocampal astrocytic Connexin-43.

Aims: Drug addiction is an aberrant learning process that involves the recruitment of memory systems. We have previously demonstrated that morphine exposure causes maladaptive synaptic plasticity which involved hippocampal glial cells, especially astrocytes. Morphine addiction has been associated with astrocytic connexin 43 (Cx43), which plays a role in synaptic homeostasis.

Electrical impulses evoked activity patterns in ventral tegmental area and locus coeruleus modulate endogenous and learning-dependent disparity of cell proliferation along the mouse dentate gyrus.

This study aimed to examine the effects of the ventral tegmental area (VTA) and the locus coeruleus (LC) patterned electrical stimulation on hippocampal-dependent learning and hippocampal neurogenesis in adult mouse. For this, mice were given unilateral electrical stimulation of VTA or LC using phasic or tonic stimulation protocols. Behavior acquisition rates were evaluated using the Barnes maze (BM) and a passive avoidance (PA) task.

Glial cells inhibition affects the incidence of metaplasticity in the hippocampus of Pentylentetrazole-induced kindled rats.

Epilepsy is characterized by the unpredictability but recurrence of seizures caused by the synchronized aberrant firing of neuronal populations. It has been shown that astrocytes (one of the most prominent glial cells) are ideally positioned to induce or contribute to neural network synchronization. Although astrocytes cannot generate action potentials, they have the capacity to sense and respond to neuronal activity, which allows them to function as homeostatic regulators of synaptic interactions.

The role of hippocampal glial glutamate transporter (GLT-1) in morphine-induced behavioral responses.

Opioid abuse modifies synaptic plasticity, which leads to behavioral changes, such as morphine dependence, but the mechanism remains poorly understood. Glial cells play an important role in the modulation of synaptic plasticity and are involved in addictive-like behaviors. The indisputable role of glutamate in opiate addiction has been shown.

5-HT7 receptor activation rescues impaired synaptic plasticity in an autistic-like rat model induced by prenatal VPA exposure.

Autism spectrum disorder (ASD) is a severe life-long neuropsychiatric disorder. Alterations and imbalance of several neurochemical systems may be involved in ASD pathophysiology, of them, serotonergic neurotransmission dysfunction and deficiency may underlie behavioral abnormalities associated with ASD. However, the functional importance of serotonergic receptors, particularly 5HT7 receptors in ASD pathology remains poorly defined.