Strength Of Inputs Research Articles

Shared reality in intergroup communication: Increasing the epistemic authority of an out-group audience.

Communicators typically tune messages to their audience's attitude. Such audience tuning biases communicators' memory for the topic toward the audience's attitude to the extent that they create a shared reality with the audience. To investigate shared reality in intergroup communication, we first established that a reduced memory bias after tuning messages to an out-group (vs. in-group) audience is a subtle index of communicators' denial of shared reality to that out-group audience (Experiments 1a and 1b). We then examined whether the audience-tuning memory bias might emerge when the out-group audience's epistemic authority is enhanced, either by increasing epistemic expertise concerning the communication topic or by creating epistemic consensus among members of a multiperson out-group audience. In Experiment 2, when Germans communicated to a Turkish audience with an attitude about a Turkish (vs. German) target, the audience-tuning memory bias appeared. In Experiment 3, when the audience of German communicators consisted of 3 Turks who all held the same attitude toward the target, the memory bias again appeared. The association between message valence and memory valence was consistently higher when the audience's epistemic authority was high (vs. low). An integrative analysis across all studies also suggested that the memory bias increases with increasing strength of epistemic inputs (epistemic expertise, epistemic consensus, and audience-tuned message production). The findings suggest novel ways of overcoming intergroup biases in intergroup relations. (PsycINFO Database Record

Synchronized Beta-Band Oscillations in a Model of the Globus Pallidus-Subthalamic Nucleus Network under External Input.

Hypokinetic symptoms of Parkinson's disease are usually associated with excessively strong oscillations and synchrony in the beta frequency band. The origin of this synchronized oscillatory dynamics is being debated. Cortical circuits may be a critical source of excessive beta in Parkinson's disease. However, subthalamo-pallidal circuits were also suggested to be a substantial component in generation and/or maintenance of Parkinsonian beta activity. Here we study how the subthalamo-pallidal circuits interact with input signals in the beta frequency band, representing cortical input. We use conductance-based models of the subthalamo-pallidal network and two types of input signals: artificially-generated inputs and input signals obtained from recordings in Parkinsonian patients. The resulting model network dynamics is compared with the dynamics of the experimental recordings from patient's basal ganglia. Our results indicate that the subthalamo-pallidal model network exhibits multiple resonances in response to inputs in the beta band. For a relatively broad range of network parameters, there is always a certain input strength, which will induce patterns of synchrony similar to the experimentally observed ones. This ability of the subthalamo-pallidal network to exhibit realistic patterns of synchronous oscillatory activity under broad conditions may indicate that these basal ganglia circuits are directly involved in the expression of Parkinsonian synchronized beta oscillations. Thus, Parkinsonian synchronized beta oscillations may be promoted by the simultaneous action of both cortical (or some other) and subthalamo-pallidal network mechanisms. Hence, these mechanisms are not necessarily mutually exclusive.

Biomarkers identification in Alzheimer’s disease using effective connectivity analysis from electroencephalography recordings

Alzheimer’s disease (AD) is the most common cause of dementia, which generally affects people over 65 years old. Some genetic mutations induce early onset of AD and help to track the evolution of the symptoms and the physiological changes at different stages of the disease. In Colombia there is a large family group with the PSEN1 E280A mutation with a median age of 46,8 years old for onset of symptoms. AD has been defined as a disconnection syndrome; consequently, network approaches could help to capture different features of the disease. The aim of the current work is to identify a biomarker in AD that helps in the tracking of the neurodegenerative process. Electroencephalography (EEG) was recorded during the encoding of visual information for four groups of individuals: asymptomatic and mild cognitive impairment carriers of the PSEN1 E280A mutation, and two non-carrier control groups. For each individual, the effective connectivity was estimated using the direct Directed Transfer Function and three measurements from graph theory were extracted: input strength, output strength and total strength. A relation between the cognitive status and age of the participants with the connectivity features was calculated. For those connectivity measures in which there is a relation with the age or the clinical scale, the performance as a diagnostic feature was evaluated. We found that output strength connectivity in the right occipito-parietal region is related to age of the carrier groups (r=−0,54, p=0,0036) and has a high sensitivity and high specificity to distinguish between carriers and non-carriers (67% sensitivity and 80% specificity in asymptomatic cases, and 83% sensitivity and 67% specificity in symptomatic cases). This relationship indicates that output strength connectivity could be related to the neurodegenerative process of the disease and could help to track the conversion from the asymptomatic stage to dementia.

Experience-Dependent and Differential Regulation of Local and Long-Range Excitatory Neocortical Circuits by Postsynaptic Mef2c

Development of proper cortical circuits requires an interaction of sensory experience and genetic programs. Little is known of how experience and specific transcription factors interact to determine the development of specific neocortical circuits. Here, we demonstrate that the activity-dependent transcriptionfactor, Myocyte enhancer factor-2C (Mef2c), differentially regulates development of local versus long-range excitatory synaptic inputs onto layer 2/3 neurons in the somatosensory neocortex invivo. Postnatal, postsynaptic deletion of Mef2c in a sparse population of L2/3 neurons suppressed development of excitatory synaptic connections from all local input pathways tested. In the same cell population, Mef2c deletion promoted the strength of excitatory inputs originating from contralateral neocortex. Both the synapse promoting and synapse suppressing effects of Mef2c deletion required normal whisking experience. These results reveal a role of Mef2c in experience-dependent development of specific sensory neocortical circuits.

An Extended Normalization Model of Attention Accounts for Feature-Based Attentional Enhancement of Both Response and Coherence Gain.

Paying attention to a sensory feature improves its perception and impairs that of others. Recent work has shown that a Normalization Model of Attention (NMoA) can account for a wide range of physiological findings and the influence of different attentional manipulations on visual performance. A key prediction of the NMoA is that attention to a visual feature like an orientation or a motion direction will increase the response of neurons preferring the attended feature (response gain) rather than increase the sensory input strength of the attended stimulus (input gain). This effect of feature-based attention on neuronal responses should translate to similar patterns of improvement in behavioral performance, with psychometric functions showing response gain rather than input gain when attention is directed to the task-relevant feature. In contrast, we report here that when human subjects are cued to attend to one of two motion directions in a transparent motion display, attentional effects manifest as a combination of input and response gain. Further, the impact on input gain is greater when attention is directed towards a narrow range of motion directions than when it is directed towards a broad range. These results are captured by an extended NMoA, which either includes a stimulus-independent attentional contribution to normalization or utilizes direction-tuned normalization. The proposed extensions are consistent with the feature-similarity gain model of attention and the attentional modulation in extrastriate area MT, where neuronal responses are enhanced and suppressed by attention to preferred and non-preferred motion directions respectively.

All-optical functional synaptic connectivity mapping in acute brain slices using the calcium integrator CaMPARI.

The genetically encoded fluorescent calcium integrator calcium-modulated photoactivatable ratiobetric integrator (CaMPARI) reports calcium influx induced by synaptic and neural activity. Its fluorescence is converted from green to red in the presence of violet light and calcium. The rate of conversion - the sensitivity to activity - is tunable and depends on the intensity of violet light. Synaptic activity and action potentials can independently initiate significant CaMPARI conversion. The level of conversion by subthreshold synaptic inputs is correlated to the strength of input, enabling optical readout of relative synaptic strength. When combined with optogenetic activation of defined presynaptic neurons, CaMPARI provides an all-optical method to map synaptic connectivity. The calcium-modulated photoactivatable ratiometric integrator (CaMPARI) is a genetically encoded calcium integrator that facilitates the study of neural circuits by permanently marking cells active during user-specified temporal windows. Permanent marking enables measurement of signals from large swathes of tissue and easy correlation of activity with other structural or functional labels. One potential application of CaMPARI is labelling neurons postsynaptic to specific populations targeted for optogenetic stimulation, giving rise to all-optical functional connectivity mapping. Here, we characterized the response of CaMPARI to several common types of neuronal calcium signals in mouse acute cortical brain slices. Our experiments show that CaMPARI is effectively converted by both action potentials and subthreshold synaptic inputs, and that conversion level is correlated to synaptic strength. Importantly, we found that conversion rate can be tuned: it is linearly related to light intensity. At low photoconversion light levels CaMPARI offers a wide dynamic range due to slower conversion rate; at high light levels conversion is more rapid and more sensitive to activity. Finally, we employed CaMPARI and optogenetics for functional circuit mapping in ex vivo acute brain slices, which preserve in vivo-like connectivity of axon terminals. With a single light source, we stimulated channelrhodopsin-2-expressing long-range posteromedial (POm) thalamic axon terminals in cortex and induced CaMPARI conversion in recipient cortical neurons. We found that POm stimulation triggers robust photoconversion of layer 5 cortical neurons and weaker conversion of layer 2/3 neurons. Thus, CaMPARI enables network-wide, tunable, all-optical functional circuit mapping that captures supra- and subthreshold depolarization.

Astrocytes gate Hebbian synaptic plasticity in the striatum.

Astrocytes, via excitatory amino-acid transporter type-2 (EAAT2), are the major sink for released glutamate and contribute to set the strength and timing of synaptic inputs. The conditions required for the emergence of Hebbian plasticity from distributed neural activity remain elusive. Here, we investigate the role of EAAT2 in the expression of a major physiologically relevant form of Hebbian learning, spike timing-dependent plasticity (STDP). We find that a transient blockade of EAAT2 disrupts the temporal contingency required for Hebbian synaptic plasticity. Indeed, STDP is replaced by aberrant non-timing-dependent plasticity occurring for uncorrelated events. Conversely, EAAT2 overexpression impairs the detection of correlated activity and precludes STDP expression. Our findings demonstrate that EAAT2 sets the appropriate glutamate dynamics for the optimal temporal contingency between pre- and postsynaptic activity required for STDP emergence, and highlight the role of astrocytes as gatekeepers for Hebbian synaptic plasticity.

“SmartGlass” Obstacles for Dynamic Inducing of Light Scattering in Vision Research Experiments

We describe a technique that allows control of visual stimuli quality through the use of a setup with a polymer dispersed liquid crystal (PDLC) film positioned in the optical pathway of one or both human eyes. Nowadays, PDLC films allow alteration of the resolution and contrast limits of the transmitted light due to continuous change in the light scattering that is obtained by the application of an AC electrical field. In our experimental setup, the use of a wide-aperture up to area of 20 x 15 cm 2 PDLC sheet is combined with a flat-screen PC display or with a modified display emission block without its interference filter unit and with an installed individually controllable colored light-emitting diode (LED) backlight. In the latter case, the spatial structure of visual stimulus remains constant, but the PDLC switching-on timing for intensity, color, and contrast of visual stimuli control is done by a PC via an Arduino USB interface. Arduino applies a voltage to the backlight colored LEDs and the low voltage up to 30 – 80 V to light-scattering PDLC sheet. Modifications to this setup can improve the resolution of the timing and screen stimulus intensity and color purity, and increase the flexibility of its application in visual research tasks. A particular use of PDLC scattering sheets involves the altering of the stimuli input strength of the eye in different binocular viewing schemes. In such applications, a restricted-optical-aperture PDLC element is mounted in a goggle frame, and the element is controlled by the application of low-voltage AC field. The efficacy of the setup is demonstrated in experiments of human vision contrast sensitivity adaptation studies. Studies allow to determine the characteristic time of the contrast sensitivity altering of 4 s during adaptation phase and the same order of the characteristic time during recovery. DOI: http://dx.doi.org/10.5755/j01.ms.22.4.12907

Experimental and numerical study on local mechanical properties and failure analysis of laser welded DP980 steels

DP980 steel was welded using Nd:YAG laser with low heat input (4m/min) and high heat input (1m/min). The ultimate tensile strength (UTS) of the low heat input welded joint reached 99.7% of base metal, while the joint with high heat input reached 95.6%. The sub-critical heat affected zone (HAZ) was softened with obvious yielding platform, and higher heat input caused lower strength of local HAZs. The low heat input welded joint fractured at base metal, while the joint with high heat input failed at sub-critical HAZ with significantly lower fracture strain. The simulation results revealed that UTS of joint decreased with the increase of HAZ width and HAZ softening degree. Moreover, there were critical values of HAZ width and softening degree to predict the failure location of the joint. With the increase of fusion zone width, the UTS of joint increased gradually closing to that of base metal, and the joint tended to fail at base metal due to biaxial stress intensification effect.

Unexpected arousal modulates the influence of sensory noise on confidence.

Human perception is invariably accompanied by a graded feeling of confidence that guides metacognitive awareness and decision-making. It is often assumed that this arises solely from the feed-forward encoding of the strength or precision of sensory inputs. In contrast, interoceptive inference models suggest that confidence reflects a weighted integration of sensory precision and expectations about internal states, such as arousal. Here we test this hypothesis using a novel psychophysical paradigm, in which unseen disgust-cues induced unexpected, unconscious arousal just before participants discriminated motion signals of variable precision. Across measures of perceptual bias, uncertainty, and physiological arousal we found that arousing disgust cues modulated the encoding of sensory noise. Furthermore, the degree to which trial-by-trial pupil fluctuations encoded this nonlinear interaction correlated with trial level confidence. Our results suggest that unexpected arousal regulates perceptual precision, such that subjective confidence reflects the integration of both external sensory and internal, embodied states.

How to transform a recalcitrant Paenibacillus strain: From culture medium to restriction barrier

Paenibacillus riograndensis SBR5T is a plant growth-promoting bacterium isolated from the wheat rhizosphere. Its recalcitrance to genetic manipulation is a major bottleneck for molecular studies, as has been reported for other Paenibacillus environmental isolates. An efficient electroporation protocol was established by evaluating diverse parameters and optimizing the culture medium, culture growth phase, electroporation solution, recovery medium, DNA input, and electric field strength. Efficiencies of approximately 2.8×104transformantsμg−1 of plasmid DNA were obtained. The optimized protocol was tested with other Paenibacillus species, and the relevance of bypassing the restriction DNA defense system to transform Paenibacillus was highlighted. This protocol is the tool needed to deepen molecular studies with this strain and will aid in the manipulation of other new environmental isolates that also exhibit recalcitrant transformation difficulties.

Somatostatin-Expressing Inhibitory Interneurons in Cortical Circuits.

Cortical inhibitory neurons exhibit remarkable diversity in their morphology, connectivity, and synaptic properties. Here, we review the function of somatostatin-expressing (SOM) inhibitory interneurons, focusing largely on sensory cortex. SOM neurons also comprise a number of subpopulations that can be distinguished by their morphology, input and output connectivity, laminar location, firing properties, and expression of molecular markers. Several of these classes of SOM neurons show unique dynamics and characteristics, such as facilitating synapses, specific axonal projections, intralaminar input, and top-down modulation, which suggest possible computational roles. SOM cells can be differentially modulated by behavioral state depending on their class, sensory system, and behavioral paradigm. The functional effects of such modulation have been studied with optogenetic manipulation of SOM cells, which produces effects on learning and memory, task performance, and the integration of cortical activity. Different classes of SOM cells participate in distinct disinhibitory circuits with different inhibitory partners and in different cortical layers. Through these disinhibitory circuits, SOM cells help encode the behavioral relevance of sensory stimuli by regulating the activity of cortical neurons based on subcortical and intracortical modulatory input. Associative learning leads to long-term changes in the strength of connectivity of SOM cells with other neurons, often influencing the strength of inhibitory input they receive. Thus despite their heterogeneity and variability across cortical areas, current evidence shows that SOM neurons perform unique neural computations, forming not only distinct molecular but also functional subclasses of cortical inhibitory interneurons.

High Pressure and [Ca 2+ ] Produce an Inverse Modulation of Synaptic Input Strength and Network Excitability in the Rat Dentate Gyrus.

Hyperbaric environments induce the high pressure neurological syndrome (HPNS) characterized by hyperexcitability of the central nervous system (CNS) and memory impairment. Human divers and other animals experience the HPNS at pressures beyond 1.1 MPa. High pressure depresses synaptic transmission and alters its dynamics in various animal models. Medial perforant path (MPP) synapses connecting the medial entorhinal cortex with the hippocampal formation are suppressed by 50% at 10.1MPa. Reduction of synaptic inputs is paradoxically associated with enhanced ability of dentate gyrus (DG)’ granule cells (GCs) to generate spikes at high pressure. This mechanism allows MPP inputs to elicit standard GC outputs at 0.1–25 Hz frequencies under hyperbaric conditions. An increased postsynaptic gain of MPP inputs probably allows diving animals to perform in hyperbaric environments, but makes them vulnerable to high intensity/frequency stimuli producing hyperexcitability. Increasing extracellular Ca2+ ([Ca2+]o) partially reverted pressure-mediated depression of MPP inputs and increased MPP’s low-pass filter properties. We postulated that raising [Ca2+]o in addition to increase synaptic inputs may reduce network excitability in the DG potentially improving its function and reducing sensitivity to high intensity and pathologic stimuli. For this matter, we activated the MPP with single and 50 Hz frequency stimuli that simulated physiologic and deleterious conditions, while assessing the GC’s output under various conditions of pressure and [Ca2+]o. Our results reveal that the pressure and [Ca2+]o produce an inverse modulation on synaptic input strength and network excitability. These coincident phenomena suggest a potential general mechanism of networks that adjusts gain as an inverse function of synaptic inputs’ strength. Such mechanism may serve for adaptation to variable pressure and other physiological and pathological conditions and may explain the increased sensitivity to strong sensory stimulation suffered by human deep-divers and cetaceans under hyperbaric conditions.

Recruitment of inhibition and excitation across mouse visual cortex depends on the hierarchy of interconnecting areas.

Diverse features of sensory stimuli are selectively processed in distinct brain areas. The relative recruitment of inhibitory and excitatory neurons within an area controls the gain of neurons for appropriate stimulus coding. We examined how such a balance of inhibition and excitation is differentially recruited across multiple levels of a cortical hierarchy by mapping the locations and strengths of synaptic inputs to pyramidal and parvalbumin (PV)-expressing neurons in feedforward and feedback pathways interconnecting primary (V1) and two higher visual areas. While interareal excitation was stronger in PV than in pyramidal neurons in all layer 2/3 pathways, we observed a gradual scaling down of the inhibition/excitation ratio from the most feedforward to the most feedback pathway. Our results indicate that interareal gain control depends on the hierarchical position of the source and the target, the direction of information flow through the network, and the laminar location of target neurons.

Glucocorticoid Administration Improves Aberrant Fear-Processing Networks in Spider Phobia.

Glucocorticoids reduce phobic fear in patients with anxiety disorders. Previous studies have shown that fear-related activation of the amygdala can be mediated through the visual cortical pathway, which includes the fusiform gyrus, or through other pathways. However, it is not clear which of the pathways that activate the amygdala is responsible for the pathophysiology of a specific phobia and how glucocorticoid treatment alleviates fear processing in these neural networks. We recorded the brain activity with functional magnetic resonance imaging in patients with spider phobia, who received either 20 mg of cortisol or a placebo while viewing pictures of spiders. We also tested healthy participants who did not receive any medication during the same task. We performed dynamic causal modelling (DCM), a connectivity analysis, to examine the effects of cortisol on the networks involved in processing fear and to examine if there was an association between these networks and the symptoms of the phobia. Cortisol administration suppressed the phobic stimuli-related amygdala activity to levels comparable to the healthy participants and reduced subjective phobic fear. The DCM analysis revealed that cortisol administration suppressed the aberrant inputs into the amygdala that did not originate from the visual cortical pathway, but rather from a fast subcortical pathway mediated by the pulvinar nucleus, and suppressed the interactions between the amygdala and fusiform gyrus. This network changes were distinguishable from healthy participants and considered the residual changes under cortisol administration. We also found that the strengths of the aberrant inputs into the amygdala were positively correlated with the severity of spider phobia. This study demonstrates that patients with spider phobia show an aberrant functional connectivity of the amygdala when they are exposed to phobia-related stimuli and that cortisol administration can alleviate this fear-specific neural connectivity.

Dynamic Organization of Hierarchical Memories

In the brain, external objects are categorized in a hierarchical way. Although it is widely accepted that objects are represented as static attractors in neural state space, this view does not take account interaction between intrinsic neural dynamics and external input, which is essential to understand how neural system responds to inputs. Indeed, structured spontaneous neural activity without external inputs is known to exist, and its relationship with evoked activities is discussed. Then, how categorical representation is embedded into the spontaneous and evoked activities has to be uncovered. To address this question, we studied bifurcation process with increasing input after hierarchically clustered associative memories are learned. We found a “dynamic categorization”; neural activity without input wanders globally over the state space including all memories. Then with the increase of input strength, diffuse representation of higher category exhibits transitions to focused ones specific to each object. The hierarchy of memories is embedded in the transition probability from one memory to another during the spontaneous dynamics. With increased input strength, neural activity wanders over a narrower state space including a smaller set of memories, showing more specific category or memory corresponding to the applied input. Moreover, such coarse-to-fine transitions are also observed temporally during transient process under constant input, which agrees with experimental findings in the temporal cortex. These results suggest the hierarchy emerging through interaction with an external input underlies hierarchy during transient process, as well as in the spontaneous activity.

Spontaneous Release Regulates Synaptic Scaling in the Embryonic Spinal Network In Vivo.

Homeostatic plasticity mechanisms maintain cellular or network spiking activity within a physiologically functional range through compensatory changes in synaptic strength or intrinsic cellular excitability. Synaptic scaling is one form of homeostatic plasticity that is triggered after blockade of spiking or neurotransmission in which the strengths of all synaptic inputs to a cell are multiplicatively scaled upward or downward in a compensatory fashion. We have shown previously that synaptic upscaling could be triggered in chick embryo spinal motoneurons by complete blockade of spiking or GABAA receptor (GABAAR) activation for 2 d in vivo Here, we alter GABAAR activation in a more physiologically relevant manner by chronically adjusting presynaptic GABA release in vivo using nicotinic modulators or an mGluR2 agonist. Manipulating GABAAR activation in this way triggered scaling in a mechanistically similar manner to scaling induced by complete blockade of GABAARs. Remarkably, we find that altering action-potential (AP)-independent spontaneous release was able to fully account for the observed bidirectional scaling, whereas dramatic changes in spiking activity associated with spontaneous network activity had little effect on quantal amplitude. The reliance of scaling on an AP-independent process challenges the plasticity's relatedness to spiking in the living embryonic spinal network. Our findings have implications for the trigger and function of synaptic scaling and suggest that spontaneous release functions to regulate synaptic strength homeostatically in vivo Homeostatic synaptic scaling is thought to prevent inappropriate levels of spiking activity through compensatory adjustments in the strength of synaptic inputs. Therefore, it is thought that perturbations in spike rate trigger scaling. Here, we find that dramatic changes in spiking activity in the embryonic spinal cord have little effect on synaptic scaling; conversely, alterations in GABAA receptor activation due to action-potential-independent GABA vesicle release can trigger scaling. The findings suggest that scaling in the living embryonic spinal cord functions to maintain synaptic strength and challenge the view that scaling acts to regulate spiking activity homeostatically. Finally, the results indicate that fetal exposure to drugs that influence GABA spontaneous release, such as nicotine, could profoundly affect synaptic maturation.

Bi-directional interplay between proximal and distal inputs to CA2 pyramidal neurons

Hippocampal area CA2 is emerging as a critical region for memory formation. Excitatory Scaffer collateral (SC) inputs from CA3 do not express activity-dependent plasticity at SC-CA2 synapses, and are governed by a large feed-forward inhibition that prevents them from engaging CA2 pyramidal neurons. However, long-term depression at inhibitory synapses evoked by stimulation of SC inputs highly increases the excitatory/inhibitory balance coming from CA3 and allows the recruitment of CA2 pyramidal neurons. In contrast, distal excitatory inputs in stratum lacunosum moleculare (SLM) can drive action potential firing in CA2 pyramidal neurons and also express a long-term potentiation. However, it is unknown whether stimulation of distal inputs can also evoke plasticity at inhibitory synapses and if so, whether this plasticity can control the strength of excitatory inputs. Here we show that stimulation in SLM evokes a long-term depression at inhibitory synapses. This plasticity strongly increases the excitatory drive of both proximal and distal inputs and allows CA3 to recruit CA2 pyramidal neurons. These data reveal a bi-directional interplay between proximal and distal inputs to CA2 pyramidal neurons that is likely to play an important role in information transfer through the hippocampus.

Target-specific M1 inputs to infragranular S1 pyramidal neurons.

The functional role of input from the primary motor cortex (M1) to primary somatosensory cortex (S1) is unclear; one key to understanding this pathway may lie in elucidating the cell-type specific microcircuits that connect S1 and M1. Recently, we discovered that a subset of pyramidal neurons in the infragranular layers of S1 receive especially strong input from M1 (Kinnischtzke AK, Simons DJ, Fanselow EE. Cereb Cortex 24: 2237-2248, 2014), suggesting that M1 may affect specific classes of pyramidal neurons differently. Here, using combined optogenetic and retrograde labeling approaches in the mouse, we examined the strengths of M1 inputs to five classes of infragranular S1 neurons categorized by their projections to particular cortical and subcortical targets. We found that the magnitude of M1 synaptic input to S1 pyramidal neurons varies greatly depending on the projection target of the postsynaptic neuron. Of the populations examined, M1-projecting corticocortical neurons in L6 received the strongest M1 inputs, whereas ventral posterior medial nucleus-projecting corticothalamic neurons, also located in L6, received the weakest. Each population also possessed distinct intrinsic properties. The results suggest that M1 differentially engages specific classes of S1 projection neurons, thereby regulating the motor-related influence S1 exerts over subcortical structures.

Transcription Profile of Aging and Cognition-Related Genes in the Medial Prefrontal Cortex.

Cognitive function depends on transcription; however, there is little information linking altered gene expression to impaired prefrontal cortex function during aging. Young and aged F344 rats were characterized on attentional set shift and spatial memory tasks. Transcriptional differences associated with age and cognition were examined using RNA sequencing to construct transcriptomic profiles for the medial prefrontal cortex (mPFC), white matter, and region CA1 of the hippocampus. The results indicate regional differences in vulnerability to aging. Age-related gene expression in the mPFC was similar to, though less robust than, changes in the dorsolateral PFC of aging humans suggesting that aging processes may be similar. Importantly, the pattern of transcription associated with aging did not predict cognitive decline. Rather, increased mPFC expression of genes involved in regulation of transcription, including transcription factors that regulate the strength of excitatory and inhibitory inputs, and neural activity-related immediate-early genes was observed in aged animals that exhibit delayed set shift behavior. The specificity of impairment on a mPFC-dependent task, associated with a particular mPFC transcriptional profile indicates that impaired executive function involves altered transcriptional regulation and neural activity/plasticity processes that are distinct from that described for impaired hippocampal function.