Sociability: Comparing the Effect of Chlorpyrifos with Valproic Acid.

In recent years, exposures to organophosphate pesticide have been highlighted as a possible cause or aggravating factor of autism spectrum disorder (ASD). The present study examined if Wistar rats prenatally exposed to chlorpyrifos (CPF) at a dose of 1 mg/kg in GD 12.5-15.

Developmental Disruption of in + Neurons Impairs Serotonergic Sub-System Connectivity and Memory Formation.

The serotonergic system of mammals innervates virtually all the central nervous system and regulates a broad spectrum of behavioral and physiological functions. In mammals, serotonergic neurons located in the rostral raphe nuclei encompass diverse sub-systems characterized by specific circuitry and functional features. Substantial evidence suggest that functional diversity of serotonergic circuits has a molecular and connectivity basis.

Detecting fine and elaborate movements with piezo sensors provides non-invasive access to overlooked behavioral components.

Behavioral phenotyping devices have been successfully used to build ethograms, but many aspects of behavior remain out of reach of available phenotyping systems. We now report on a novel device, which consists in an open-field platform resting on highly sensitive piezoelectric (electromechanical) pressure-sensors, with which we could detect the slightest movements (up to individual heart beats during rest) from freely moving rats and mice. The combination with video recordings and signal analysis based on time-frequency decomposition, clustering, and machine learning algorithms provided non-invasive access to previously overlooked behavioral components.

Probing the polarity of spontaneous perisomatic GABAergic synaptic transmission in the mouse CA3 circuit in vivo.

The hypothesis that reversed, excitatory GABA may be involved in various brain pathologies, including epileptogenesis, is appealing but controversial because of the technical difficulty of probing endogenous GABAergic synaptic function in vivo. We overcome this challenge by non-invasive extracellular recording of neuronal firing responses to optogenetically evoked and spontaneously occurring inhibitory perisomatic GABAergic field potentials, generated by individual parvalbumin interneurons on their target pyramidal cells. Our direct probing of GABAergic transmission suggests a rather anecdotal participation of excitatory GABA in two specific models of epileptogenesis in the mouse CA3 circuit in vivo, even though this does not preclude its expression in other brain areas or pathological conditions.

Similarities between the Effects of Prenatal Chlorpyrifos and Valproic Acid on Ultrasonic Vocalization in Infant Wistar Rats.

Background: In recent years, ultrasonic vocalizations (USV) in pups has become established as a good tool for evaluating behaviors related to communication deficits and emotional states observed in autism spectrum disorder (ASD). Prenatal valproic acid (VPA) exposure leads to impairments and social behavior deficits associated with autism, with the effects of VPA being considered as a reliable animal model of ASD. Some studies also suggest that prenatal exposure to chlorpyrifos (CPF) could enhance autistic-like behaviors.

COUP-TFI/Nr2f1 Orchestrates Intrinsic Neuronal Activity during Development of the Somatosensory Cortex.

The formation of functional cortical maps in the cerebral cortex results from a timely regulated interaction between intrinsic genetic mechanisms and electrical activity. To understand how transcriptional regulation influences network activity and neuronal excitability within the neocortex, we used mice deficient for Nr2f1 (also known as COUP-TFI), a key determinant of primary somatosensory (S1) area specification during development. We found that the cortical loss of Nr2f1 impacts on spontaneous network activity and synchronization of S1 cortex at perinatal stages.

Potential Involvement of Impaired BK Channel Function in Sensory Defensiveness and Some Behavioral Disturbances Induced by Unfamiliar Environment in a Mouse Model of Fragile X Syndrome.

In fragile X syndrome (FXS), sensory hypersensitivity and impaired habituation is thought to result in attention overload and various behavioral abnormalities in reaction to the excessive and remanent salience of environment features that would normally be ignored. This phenomenon, termed sensory defensiveness, has been proposed as the potential cause of hyperactivity, hyperarousal, and negative reactions to changes in routine that are often deleterious for FXS patients. However, the lack of tools for manipulating sensory hypersensitivity has not allowed the experimental testing required to evaluate the relevance of this hypothesis.

The possible consequences for cognitive functions of external electric fields at power line frequency on hippocampal CA1 pyramidal neurons.

The possible effects on cognitive processes of external electric fields, such as those generated by power line pillars and household appliances are of increasing public concern. They are difficult to study experimentally, and the relatively scarce and contradictory evidence make it difficult to clearly assess these effects. In this study, we investigate how, why and to what extent external perturbations of the intrinsic neuronal activity, such as those that can be caused by generation, transmission and use of electrical energy can affect neuronal activity during cognitive processes.

Genetic deletion of the Histone Deacetylase 6 exacerbates selected behavioral deficits in the R6/1 mouse model for Huntington's disease.

Introduction: The inhibition of the Histone Deacetylase 6 (HDAC6) increases tubulin acetylation, thus stimulating intracellular vesicle trafficking and brain-derived neurotrophic factor (BDNF) release, that is, cellular processes markedly reduced in Huntington's disease (HD).

Methods: We therefore tested that reducing HDAC6 levels by genetic manipulation would attenuate early cognitive and behavioral deficits in R6/1 mice, a mouse model which develops progressive HD-related phenotypes.

Results: In contrast to our initial hypothesis, the genetic deletion of HDAC6 did not reduce the weight loss or the deficits in cognitive abilities and nest-building behavior shown by R6/1 mice, and even worsened their social impairments, hypolocomotion in the Y-maze, and reduced ultrasonic vocalizations.

Why am I lost without dopamine? Effects of 6-OHDA lesion on the encoding of reward and decision process in CA3.

There is growing evidence that Parkinson's disease, generally characterized by motor symptoms, also causes cognitive impairment such as spatial disorientation. The hippocampus is a critical structure for spatial navigation and receives sparse but comprehensive dopamine (DA) innervation. DA loss is known to be the cause of Parkinson's disease and therefore it has been hypothesized that the associated spatial disorientation could result from hippocampal dysfunction.

Recruitment of Perisomatic Inhibition during Spontaneous Hippocampal Activity In Vitro.

It was recently shown that perisomatic GABAergic inhibitory postsynaptic potentials (IPSPs) originating from basket and chandelier cells can be recorded as population IPSPs from the hippocampal pyramidal layer using extracellular electrodes (eIPSPs). Taking advantage of this approach, we have investigated the recruitment of perisomatic inhibition during spontaneous hippocampal activity in vitro. Combining intracellular and extracellular recordings from pyramidal cells and interneurons, we confirm that inhibitory signals generated by basket cells can be recorded extracellularly, but our results suggest that, during spontaneous activity, eIPSPs are mostly confined to the CA3 rather than CA1 region.

Computational modeling of the effects of amyloid-beta on release probability at hippocampal synapses.

The role of amyloid beta (Aβ) in brain function and in the pathogenesis of Alzheimer's disease (AD) remains elusive. Recent publications reported that an increase in Aβ concentration perturbs pre-synaptic release in hippocampal neurons. In particular, it was shown in vitro that Aβ is an endogenous regulator of synaptic transmission at the CA3-CA1 synapse, enhancing its release probability.

Rhythmic modulation of θ oscillations supports encoding of spatial and behavioral information in the rat hippocampus.

Oscillatory patterns of activity in various frequency ranges are ubiquitously expressed in cortical circuits. While recent studies in humans emphasized rhythmic modulations of neuronal oscillations ("second-order" rhythms), their potential involvement in information coding remains an open question. Here, we show that a rhythmic (~0.

"Ectopic" theta oscillations and interictal activity during slow-wave state in the R6/1 mouse model of Huntington's disease.

The pathophysiology of Huntington's disease (HD) is primarily associated with striatal degeneration and a number of behavioral symptoms such as involuntary movements, cognitive decline, psychiatric disorders, and in the most juvenile-onset cases with epilepsy. In addition to several changes in cellular and synaptic properties previously reported in HD, attention was recently driven towards the potential relationships between cognitive deficits and sleep disturbances in patients and animal models of Huntington's disease. In the present study, we have investigated whether the population-activity patterns normally expressed by the hippocampal and neocortical circuits during active and slow-wave states are affected in R6/1 mice, a model of Huntington's disease.

Neural circuits underlying the generation of theta oscillations.

Theta oscillations represent the neural network configuration underlying active awake behavior and paradoxical sleep. This major EEG pattern has been extensively studied, from physiological to anatomical levels, for more than half a century. Nevertheless the cellular and network mechanisms accountable for the theta generation are still not fully understood.

Early motor activity drives spindle bursts in the developing somatosensory cortex.

Sensorimotor coordination emerges early in development. The maturation period is characterized by the establishment of somatotopic cortical maps, the emergence of long-range cortical connections, heightened experience-dependent plasticity and spontaneous uncoordinated skeletal movement. How these various processes cooperate to allow the somatosensory system to form a three-dimensional representation of the body is not known.

Developmental patterns and plasticities: the hippocampal model.

Because developmental activity-dependent synaptic plasticity has been hypothesized to participate in network refinement, leading to the precise mapping of synaptic contacts constituting a functional brain, it is important to investigate the spatio-temporal structure of immature network activities. This article is briefly reviewing 15 years of studies on the immature rat hippocampus which, together with recent results obtained from awake rat pups, represent an important step toward the understanding of spontaneous patterns of activity and their potential implication in network maturation. Due to synergistic excitatory actions of GABA and glutamate receptor mediated signals during early postnatal life, spontaneous patterns of hippocampal activity that have been characterized both in vitro and in vivo are likely to provide hebbian modulation of developing glutamatergic and GABAergic synapses.

Spike train dynamics predicts theta-related phase precession in hippocampal pyramidal cells.

According to the temporal coding hypothesis, neurons encode information by the exact timing of spikes. An example of temporal coding is the hippocampal phase precession phenomenon, in which the timing of pyramidal cell spikes relative to the theta rhythm shows a unidirectional forward precession during spatial behaviour. Here we show that phase precession occurs in both spatial and non-spatial behaviours.

Correlated bursts of activity in the neonatal hippocampus in vivo.

The behavior of immature cortical networks in vivo remains largely unknown. Using multisite extracellular and patch-clamp recordings, we observed recurrent bursts of synchronized neuronal activity lasting 0.5 to 3 seconds that occurred spontaneously in the hippocampus of freely moving and anesthetized rat pups.

Hippocampal pyramidal cell-interneuron spike transmission is frequency dependent and responsible for place modulation of interneuron discharge.

The interplay between principal cells and interneurons plays an important role in timing the activity of individual cells. We investigated the influence of single hippocampal CA1 pyramidal cells on putative interneurons. The activity of CA1 pyramidal cells was controlled intracellularly by current injection, and the activity of neighboring interneurons was recorded extracellularly in the urethane-anesthetized rat.