Medication impact on oral health in schizophrenia.

Background: Patients with schizophrenia constitute a particularly vulnerable group for oral diseases. Among the different factors involved, we aimed to examine the evidence of how drugs could contribute to the poorer oral health of this population.

Material And Methods: An overview of the potential impact of medication on dental/oral health among people with schizophrenia was proposed focusing on selected literature.

Chemogenetic activation of the ventral subiculum-BNST pathway reduces context fear expression.

An inability to reduce fear in nonthreatening environments characterizes many anxiety disorders. The pathway from the ventral subiculum (vSUB) to the bed nucleus of the stria terminalis (BNST) is more active in safe contexts than in aversive ones, as indexed by FOS expression. Here, we used chemogenetic techniques to specifically activate the vSUB-BNST pathway during both context and cued fear expression by expressing a Cre-dependent hM3D(Gq) receptor in BNST-projecting vSUB neurons.

Aversive Contexts Reduce Activity in the Ventral Subiculum- BNST Pathway.

Many anxiety disorders can be characterized by abnormalities in detecting and learning about threats, and the inability to reduce fear responses in non-threatening environments. PTSD may be the most representative of context processing pathology, as intrusive memories are experienced in "safe" contexts. The ventral subiculum (vSUB), the main output of the ventral hippocampus, encodes environmental cues and is critical for context processing.

Sex Differences in BNST and Amygdala Activation by Contextual, Cued, and Unpredictable Threats.

Fear and anxiety can be described as emotional and physical responses to predictable and unpredictable threats. While the amygdala is necessary for context and cued fear conditioning, the bed nucleus of the stria terminalis (BNST) is important for anxiety-like behavior and conditioned responses to diffuse and/or unpredictable threats. However, we still lack knowledge about how the BNST and amygdala nuclei act in coordination.

Extended amygdala circuits are differentially activated by context fear conditioning in male and female rats.

As the incidence of anxiety disorders is more prevalent in females, comparing the neural underpinnings of anxiety in males and females is imperative. The bed nucleus of the stria terminalis (BNST) contributes to long-lasting, anxiety-like states including the expression of context fear conditioning. Currently, there is conflicting evidence as to which nuclei of the BNST contribute to these behaviors.

Top-Down Cortical Control of Acute and Chronic Pain.

Acute pain has an evolutionary role in the detection of physical harm and the response to it. In some cases, however, acute pain can impair function and lead to other morbidities. Chronic pain, meanwhile, can present as a psychopathological condition that significantly interferes with daily living.

Rate and Temporal Coding Mechanisms in the Anterior Cingulate Cortex for Pain Anticipation.

Pain is a complex sensory and affective experience. Through its anticipation, animals can learn to avoid pain. Much is known about passive avoidance during a painful event; however, less is known about active pain avoidance.

Scaling Up Cortical Control Inhibits Pain.

Acute pain evokes protective neural and behavioral responses. Chronic pain, however, disrupts normal nociceptive processing. The prefrontal cortex (PFC) is known to exert top-down regulation of sensory inputs; unfortunately, how individual PFC neurons respond to an acute pain signal is not well characterized.

Assessment of Aversion of Acute Pain Stimulus through Conditioned Place Aversion.

Pain is a complex experience. The aversive component of pain has been assessed through conditioned place aversion in rodents. However, this behavioral test does not allow the evaluation of the aversion of an acute pain stimulus.

Chronic pain induces generalized enhancement of aversion.

A hallmark feature of chronic pain is its ability to impact other sensory and affective experiences. It is notably associated with hypersensitivity at the site of tissue injury. It is less clear, however, if chronic pain can also induce a generalized site-nonspecific enhancement in the aversive response to nociceptive inputs.

Genetic ablation of GINIP-expressing primary sensory neurons strongly impairs Formalin-evoked pain.

Primary sensory neurons are heterogeneous by myriad of molecular criteria. However, the functional significance of this remarkable heterogeneity is just emerging. We precedently described the GINIP neurons as a new subpopulation of non peptidergic C-fibers encompassing the free nerve ending cutaneous MRGPRD neurons and C-LTMRs.

GINIP, a Gαi-interacting protein, functions as a key modulator of peripheral GABAB receptor-mediated analgesia.

One feature of neuropathic pain is a reduced GABAergic inhibitory function. Nociceptors have been suggested to play a key role in this process. However, the mechanisms behind nociceptor-mediated modulation of GABA signaling remain to be elucidated.

Uncoupling of molecular maturation from peripheral target innervation in nociceptors expressing a chimeric TrkA/TrkC receptor.

Neurotrophins and their receptors control a number of cellular processes, such as survival, gene expression and axonal growth, by activating multiple signalling pathways in peripheral neurons. Whether each of these pathways controls a distinct developmental process remains unknown. Here we describe a novel knock-in mouse model expressing a chimeric TrkA/TrkC (TrkAC) receptor from TrkA locus.