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Background: Depression is a serious mental illness with symptoms such as worry, disturbed sleep and appetite, lack of interest or pleasure, and persistent sorrow. Objectives: This study aims to assess the effect of fluvoxamine (FLX) on behavioral and electrophysiological alterations of the posterior cingulate cortex (PCC) and the hippocampus in rats with depression. Materials & Methods: Thirty-two albino rats (weighing 250–300 g) were divided into four groups; control (sham), chronic mild stress (CMS), FLX, and CMS+FLX. The CMS was induced by applying different stressors for 3 weeks. Intraperitoneal injection of FLX (25 mg/Kg) was performed daily for 14 days in the treatment group. Depressive-like behaviors were assessed, and local field potentials (LFP) from the hippocampus and the PCC were recorded. Results: FLX effectively reduced depressive-like behaviors in rats with CMS (P≤0.05). Additionally, depression-induced alterations in LFP were observed in the hippocampus and the PCC. Depression reduced the power of delta and theta bands and increased the hippocampal low-gamma band power (P≤0.05). In the PCC, depression increased the power of delta and low-gamma bands and reduced the power of the alpha band (P≤0.05). Conclusion: FLX reduce depression-like behaviors in the animal model, possibly through affecting electrophysiological activity of the hippocampus and the PCC.

Background: Depression is a serious mental illness with symptoms such as worry, disturbed sleep and appetite, lack of interest or pleasure, and persistent sorrow. Objectives: This study aims to assess the effect of fluvoxamine (FLX) on behavioral and electrophysiological alterations of the posterior cingulate cortex (PCC) and the hippocampus in rats with depression. Materials & Methods: Thirty-two albino rats (weighing 250-300 g) were divided into four groups; control (sham), chronic mild stress (CMS), FLX, and CMS+FLX. The CMS was induced by applying different stressors for 3 weeks. Intraperitoneal injection of FLX (25 mg/Kg) was performed daily for 14 days in the treatment group. Depressive-like behaviors were assessed, and local field potentials (LFP) from the hippocampus and the PCC were recorded. Results: FLX effectively reduced depressive-like behaviors in rats with CMS (P=0.05). Additionally, depression-induced alterations in LFP were observed in the hippocampus and the PCC. Depression reduced the power of delta and theta bands and increased the hippocampal low-gamma band power (P=0.05). In the PCC, depression increased the power of delta and low-gamma bands and reduced the power of the alpha band (P=0.05). Conclusion: FLX reduce depression-like behaviors in the animal model, possibly through affecting electrophysiological activity of the hippocampus and the PCC. [ABSTRACT FROM AUTHOR]

• PL neurons only respond well to acoustic stimuli in the awake state. • PL neurons responded better to broadband noise than pure tone in awake state. • No obvious receptive fields found to pure tone on all the recorded neurons. • Responses of PL neurons to the CS increased after auditory fear conditioning. • Lower threshold and higher SNR relative to increased responses. Although many studies have shown that the prelimbic (PL) cortex of the mPFC is involved in the formation of conditioned freezing behavior, few have considered the acoustic response characteristics of PL cortex. Importantly, the change in auditory response characteristics of the PL cortex after conditional fear learning is largely unknown. Here we used in vivo cell-attached recordings targeting the mPFC during the waking state. We confirmed that the mPFC of adult C57 mice have neurons that respond to noise and tone in the waking state, especially in the PL cortex. Interestingly, the data also confirmed that these neurons responded well to the intensity of sound but did not have frequency topological distribution characteristics. Furthermore, we found that the number of c-fos positive neurons in the PL cortex increased significantly after auditory fear conditioning. The auditory-induced local field potential recordings and in vivo cell-attached recordings demonstrated that the PL cortex was more sensitive to the auditory conditioned stimulus after the acquisition of conditioned fear. The proportion of neurons responding to noise was significantly increased, and the signal to noise ratio of the spikes were also increased. These data reveal that PL neurons themselves responded to the main information (sound intensity), while the secondary information (frequency) response was almost negligible after auditory fear conditioning. This phenomenon may be the functional basis for handling this type of emotional memory, and this response characteristic is thought to be emotional sensitization but does not change the nature of this response. [ABSTRACT FROM AUTHOR]

Withdrawal from extended-access cocaine self-administration leads to progressive intensification ('incubation') of cocaine craving. After prolonged withdrawal (1-2 months), when craving is high, expression of incubation depends on strengthening of excitatory inputs to medium spiny neurons (MSN) of the nucleus accumbens (NAc). These excitatory inputs interact with the intra-NAc GABAergic 'microcircuit', composed of MSN axon collaterals and GABAergic interneurons. Here, we investigated whether the increased glutamatergic neurotransmission observed after prolonged withdrawal is accompanied by altered GABAergic neurotransmission, focusing on NAc core. Rats self-administered cocaine or saline (6 hours/day) and then underwent >40 days of withdrawal. First, we investigated parvalbumin positive (PV+) interneurons, GABAergic fast-spiking interneurons that regulate MSN activity. Immunohistochemical studies revealed no significant change in PV signal intensity or the number of PV+ cells in cocaine rats versus saline controls. We then screened PV and other interneuron markers using immunoblotting. We detected no changes in levels of PV, calretinin, calbindin or neuronal nitric oxide synthase. Because expression of these markers is activity dependent, our results suggest no marked changes in interneuron activity. Finally, we utilized local field potential recording, which can detect GABA-mediated alterations at the circuit level, to investigate potential changes in two circuits implicated in cocaine craving: prelimbic prefrontal cortex to NAc core and basolateral amygdala to NAc core. We detected differential adaptations in these circuits, some of which may involve GABA. Overall, our results suggest that alterations in GABA transmission may accompany incubation of cocaine craving, but they are circuit specific and less pronounced than alterations in glutamate transmission. [ABSTRACT FROM AUTHOR]

Overdose intake of ethanol can impair cerebellar cortical neurons to integrate and transfer external information, resulting in a dysfunction of cerebellar motor regulation or cerebellar ataxia. However, the mechanisms underlying ethanol-impaired transfer of sensory information from cerebellar cortical molecular layer neurons remain unclear. In the present study, we investigated the effects of ethanol on sensory stimulation-evoked responses in the cerebellar molecular layer of urethane-anesthetized mice, by electrophysiological and pharmacological methods. Our results demonstrated that air-puff stimulation (30 ms, 50-60 psi) of the ipsilateral whisker-pad evoked field potential responses in the molecular layer of the cerebellar cortex folium Crus II, which expressed a negative component (N1) followed by a gamma-aminobutyric acid receptor A (GABAA)-mediated positive component (P1). Cerebellar surface perfusion of ethanol between 2 and 5 mM did not change the latency of the evoked responses and the amplitude of N1, but enhanced the amplitude and the area under the curve of P1. Interestingly, high concentrations (>20 mM) of ethanol induced a significantly decrease in the amplitude and area under the curve of P1. Furthermore, high concentration ethanol (300 mM) significantly decreased the rise in tau and tau decay value of P1, whereas low concentration ethanol (2-5 mM) significantly increased these values of P1. Inhibition of GABAA receptor activity reversed P1 and also abolished the effects of ethanol on sensory stimulation-evoked responses. These results indicated that ethanol induced a bidirectional effect on the sensory stimulation-evoked GABAergic responses in the cerebellar cortical molecular layer, suggesting that acute alcohol intake impacted the sensory information processing of cerebellar cortex. [ABSTRACT FROM AUTHOR]

Abstract: Cluster headache is a severely debilitating disorder that can remain unrelieved by current pharmacotherapy. Alongside ablative neurosurgical procedures, neuromodulatory treatments of deep brain stimulation (DBS) and occipital nerve simulation have emerged in the last few years as effective treatments for medically refractory cluster headaches. Pioneers in the field have sought to publish guidelines for neurosurgical treatment; however, only small case series with limited long-term follow-up have been published. Controversy remains over which surgical treatments are best and in which circumstances to intervene. Here we review current data on neurosurgical interventions for chronic cluster headache focusing upon DBS and occipital nerve stimulation, and discuss the indications for and putative mechanisms of DBS including translational insights from functional neuroimaging, diffusion weighted tractography, magnetoencephalography and invasive neurophysiology. [Copyright &y& Elsevier]

Abstract: We describe a device for assessing the effects of diffusible molecules on electrophysiological recordings from multiple neurons. This device allows for the infusion of reagents through a cannula located among an array of micro-electrodes. The device can easily be customized to target specific neural structures. It is designed to be chronically implanted so that isolated neural units and local field potentials are recorded over the course of several weeks or months. Multivariate statistical and spectral analysis of electrophysiological signals acquired using this system could quantitatively identify electrical “signatures” of therapeutically useful drugs. [Copyright &y& Elsevier]

Overdose intake of ethanol can impair cerebellar cortical neurons to integrate and transfer external information, resulting in a dysfunction of cerebellar motor regulation or cerebellar ataxia. However, the mechanisms underlying ethanol-impaired transfer of sensory information from cerebellar cortical molecular layer neurons remain unclear. In the present study, we investigated the effects of ethanol on sensory stimulation-evoked responses in the cerebellar molecular layer of urethane-anesthetized mice, by electrophysiological and pharmacological methods. Our results demonstrated that air-puff stimulation (30 ms, 50-60 psi) of the ipsilateral whisker-pad evoked field potential responses in the molecular layer of the cerebellar cortex folium Crus II, which expressed a negative component (N1) followed by a gamma-aminobutyric acid receptor A (GABAA)-mediated positive component (P1). Cerebellar surface perfusion of ethanol between 2 and 5mM did not change the latency of the evoked responses and the amplitude of N1, but enhanced the amplitude and the area under the curve of P1. Interestingly, high concentrations (>20mM) of ethanol induced a significantly decrease in the amplitude and area under the curve of P1. Furthermore, high concentration ethanol (300 mM) significantly decreased the rise in tau and tau decay value of P1, whereas low concentration ethanol (2-5mM) significantly increased these values of P1. Inhibition of GABAA receptor activity reversed P1 and also abolished the effects of ethanol on sensory stimulation-evoked responses. These results indicated that ethanol induced a bidirectional effect on the sensory stimulation-evoked GABAergic responses in the cerebellar cortical molecular layer, suggesting that acute alcohol intake impacted the sensory information processing of cerebellar cortex., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)