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Excessive exposure to loud noise causes hearing loss and neural plasticity throughout the auditory pathway. [https://www.selleckchem.com/screening/inhibitor-library.html screening assay] Recent studies have identified that non-auditory regions, such as the hippocampus, are also susceptible to noise exposure; however, the electrophysiological and behavioral consequences of noise-induced hearing loss on the prefrontal cortex (PFC) are unclear. Using chronically-implanted electrodes in awake rats, we investigated neural plasticity in the auditory and prefrontal cortices in the days following noise exposure via metrics associated with spontaneous neural oscillations and the 40-Hz auditory steady-state response (ASSR). Noise exposure did not alter the profile of spontaneous oscillations in either of the cortices, yet it caused a differential plasticity in the sound-evoked activity, which was characterized by enhanced event-related potentials (ERPs) in the auditory cortex (i.e., central gain), and decreased inter-trial coherence (ITC) of the 40-Hz ASSR within the PFC. Moreover, phase synchrony between auditory and prefrontal cortices was decreased post-exposure, suggesting a reduction in functional connectivity. Cognitive-behavioral testing using the Morris water maze and a series of lever-pressing tasks revealed that noise exposure impaired spatial learning and reference memory, as well as stimulus-response habit learning, whereas cognitive flexibility tasks requiring set-shifting and reversal learning appeared unaffected. Collectively, our findings identify the complex and region-specific cortical plasticity associated with noise-induced hearing loss, and highlight the varying degrees of susceptibility of non-auditory, cognitive tasks of learning, memory and executive function to noise exposure.This study aimed at better understanding the neurochemistry underlying transcranial magnetic stimulation (TMS) and magnetic resonance spectroscopy (MRS) measurements as it pertains to GABAergic activity following administration of allosteric GABAA receptor agonist lorazepam. Seventeen healthy adults (8 females, 26.0 ± 5.4 years old) participated in a double-blind, crossover, placebo-controlled study, where participants underwent TMS and MRS two hours after drug intake (placebo or lorazepam; 2.5 mg). Neuronavigated TMS measures reflecting cortical inhibition and excitation were obtained in the left primary motor cortex. Sensorimotor cortex and occipital cortex MRS data were acquired using a 3T scanner with a MEGA-PRESS sequence, allowing water-referenced [GABA] and [Glx] (glutamate + glutamine) quantification. Lorazepam administration decreased occipital [GABA], decreased motor cortex excitability and increased GABAA-receptor mediated motor cortex inhibition (short intracortical inhibition (SICI)). Lorazepam intake did not modulate sensorimotor [GABA] and TMS measures of intra-cortical facilitation, long-interval cortical inhibition, cortical silent period, and resting motor threshold. Furthermore, higher sensorimotor [GABA] was associated with higher cortical inhibition (SICI) following lorazepam administration, suggesting that baseline sensorimotor [GABA] may be valuable in predicting pharmacological or neuromodulatory treatment response. Finally, the differential effects of lorazepam on MRS and TMS measures, with respect to GABA, support the idea that TMS measures of cortical inhibition reflect synaptic GABAergic phasic inhibitory activity while MRS reflects extrasynaptic GABA.Primates are long-lived, highly social mammals who maintain long-term social bonds and cohesive social groups through many affiliative mechanisms, foremost among them social touch. From birth through adulthood, social touch - primarily mutual grooming - creates and maintains relationships of trust and reliance, which are the basis for individual physical and emotional well-being and reproductive success. Because social touch helps to establish, maintain, and repair social alliances in primates, it contributes to the emotional stability of individuals and the cohesion of social groups. In these fundamental ways, thus, social touch supports the slow life histories of primates. The reinforcing neurochemistry of social touch insures that it is a pleasurable activity and this, in turn, makes it a behavioral commodity that can be traded between primates for desirable rewards such as protection against future aggression or opportunities to handle infants. Social touch is essential to normal primate development, and individuals deprived of social touch exhibit high levels of anxiety and lower fertility compared to those receiving regular social touch. Understanding the centrality of social touch to primate health and well-being throughout the lifespan provides the foundation for appreciating the importance of social touch in human life.Neurogenesis in the subgranular zone (SGZ) of the adult hippocampus can be stimulated by a variety of means, including via exposure of experimental animals to an enriched environment that provides additional sensory, social, and motor stimulation. Tangible health and cognitive benefits accrue in enriched animals, including the amelioration of signs modelling psychiatric, neurological and neurodegenerative conditions that affect humans, which may in part be due to enhanced production of neurons. A key factor in the neuronal response to enrichment is the release of brain-derived neurotrophic factor (BDNF) and the activation of the Mitogen-Activated Protein Kinase (MAPK) cascade, which can lead to the stimulation of neurogenesis. Mitogen- and Stress-Activated protein Kinase 1 (MSK1) is a nuclear enzyme downstream of BDNF and MAPK that regulates transcription. MSK1 has previously been implicated in both basal and stimulated neurogenesis on the basis of studies with mice lacking MSK1 protein. In the present study, using mice in which only the kinase activity of MSK1 is lacking, we show that the rate of cellular proliferation in the SGZ (Ki-67 staining) is unaffected by the MSK1 kinase-dead (KD) mutation, and no different from controls levels after five weeks of enrichment. However, compared to wild-type mice, the number of doublecortin (DCX)-positive cells was greater in both standard-housed and enriched MSK1 KD mice. These observations suggest that, while MSK1 does not influence the basal rate of proliferation of neuronal precursors, MSK1 negatively regulates the number of cells destined to become neurons, potentially as a homeostatic control on the number of new neurons integrating into the dentate gyrus.