Short-term Depression Research Articles

Effects as a function of implementation fidelity of a transdiagnostic prevention program in young school-aged children

Super Skills for Life (SSL) is a transdiagnostic prevention program for school-aged children with internalizing problems. The current study aimed to examine the short- and long-term (12-month follow-up) effectiveness of SSL, depending on implementation fidelity. Participants were 123 Spanish-speaking children aged 6–8 years with internalizing symptoms and their parents. High (n = 41) and low fidelity (n = 26) groups were established and compared with a control group (CG) (n = 56). Compared to CG, the high-fidelity group (HFG) achieved better outcomes than the low-fidelity group (LFG) at short and long term, including symptoms of anxiety, depression, and internalizing problems, and also externalizing problems at long-term. The LFG improved key symptoms at short term (depression) and long term (anxiety and depression). Findings suggest that SSL is beneficial even if not delivered at maximum fidelity, although considering the influence of implementation fidelity is critical because the high-fidelity implementation yielded the greatest effects when compared to the CG. This research provides valuable data, analyzing for the first time the influence of fidelity on SSL outcomes in young school-aged children exhibiting internalizing symptoms, while there is still a lack of studies of these characteristics concerning transdiagnostic prevention programs targeting childhood anxiety and depression.

A robust model of Stimulus-Specific Adaptation validated on neuromorphic hardware

Stimulus-Specific Adaptation (SSA) to repetitive stimulation is a phenomenon that has been observed across many different species and in several brain sensory areas. It has been proposed as a computational mechanism, responsible for separating behaviorally relevant information from the continuous stream of sensory information. Although SSA can be induced and measured reliably in a wide variety of conditions, the network details and intracellular mechanisms giving rise to SSA still remain unclear. Recent computational studies proposed that SSA could be associated with a fast and synchronous neuronal firing phenomenon called Population Spikes (PS). Here, we test this hypothesis using a mean-field rate model and corroborate it using a neuromorphic hardware. As the neuromorphic circuits used in this study operate in real-time with biologically realistic time constants, they can reproduce the same dynamics observed in biological systems, together with the exploration of different connectivity schemes, with complete control of the system parameter settings. Besides, the hardware permits the iteration of multiple experiments over many trials, for extended amounts of time and without losing the networks and individual neural processes being studied. Following this “neuromorphic engineering” approach, we therefore study the PS hypothesis in a biophysically inspired recurrent networks of spiking neurons and evaluate the role of different linear and non-linear dynamic computational primitives such as spike-frequency adaptation or short-term depression (STD). We compare both the theoretical mean-field model of SSA and PS to previously obtained experimental results in the area of novelty detection and observe its behavior on its neuromorphic physical equivalent model. We show how the approach proposed can be extended to other computational neuroscience modelling efforts for understanding high-level phenomena in mechanistic models.

Mental Health Interventions to Improve Psychological Outcomes in Informal Caregivers of Critically Ill Patients: A Systematic Review and Meta-Analysis.

Determine effect of mental health interventions on psychologic outcomes in informal caregivers of critically ill patients. Searches conducted in MEDLINE, Embase, and other databases from inception to October 31, 2019. Interventions for informal caregivers of critically ill patients in adult ICU, PICU, or neonatal ICU. Two independent, blinded reviewers screened citations and extracted data. Random-effects models with inverse variance weighting pooled outcome data when suitable. Psychologic outcomes categorized: 1) negative (anxiety, depression, post-traumatic stress disorder, distress, and burden) or 2) positive (courage, humanity, justice, transcendence, temperance, and wisdom and knowledge). Stratification according to intervention type and patient population was performed. Of 11,201 studies, 102 interventional trials were included (n = 12,676 informal caregivers). Interventions targeted caregiver experience (n = 58), role (n = 6), or support (n = 38). Meta-analysis (56 randomized controlled trials; n = 22 [39%] in adult ICUs; n = 34 [61%] in neonatal ICU or PICU) demonstrated reduced anxiety (ratio of means = 0.92; 95% CI, 0.87-0.97) and depression (ratio of means = 0.83; 95% CI, 0.69-0.99), but not post-traumatic stress disorder (ratio of means = 0.91; 95% CI, 0.80-1.04) or distress (ratio of means = 1.01; 95% CI, 0.95-1.07) among informal caregivers randomized to mental health interventions compared with controls within 3 months post-ICU discharge. Increased humanity (ratio of means = 1.11; 95% CI, 1.07-1.15), transcendence (ratio of means = 1.11; 95% CI, 1.07-1.15), and caregiver burden (ratio of means = 1.08; 95% CI, 1.05-1.12) were observed. No significant effects of mental health interventions observed after 3 months postdischarge. Mental health interventions for caregivers of critically ill patients improved short-term anxiety, depression, humanity, and transcendence while increasing burden. Clinicians should consider short-term prescriptions of mental health interventions to informal caregivers of critically ill patients with capacity to manage interventions.

Role of AMPA receptor desensitization in short term depression - lessons from retinogeniculate synapses.

Repetitive synapse activity induces various forms of short-term plasticity. The role of presynaptic mechanisms such as residual Ca2+ and vesicle depletion in short-term facilitation and short-term depression is well established. On the other hand, the contribution of postsynaptic mechanisms such as receptor desensitization and saturation to short-term plasticity is less well known and often ignored. In this review, I will describe short-term plasticity in retinogeniculate synapses of relay neurons of the dorsal lateral geniculate nucleus (dLGN) to exemplify the synaptic properties that facilitate the contribution of AMPA receptor desensitization to short-term plasticity. These include high vesicle release probability, glutamate spillover and, importantly, slow recovery from desensitization of AMPA receptors. The latter is strongly regulated by the interaction of AMPA receptors with auxiliary proteins such as CKAMP44. Finally, I discuss the relevance of short-term plasticity in retinogeniculate synapses for the processing of visual information by LGN relay neurons.

Action potential-coupled Rho GTPase signaling drives presynaptic plasticity

In contrast to their postsynaptic counterparts, the contributions of activity-dependent cytoskeletal signaling to presynaptic plasticity remain controversial and poorly understood. To identify and evaluate these signaling pathways, we conducted a proteomic analysis of the presynaptic cytomatrix using in vivo biotin identification (iBioID). The resultant proteome was heavily enriched for actin cytoskeleton regulators, including Rac1, a Rho GTPase that activates the Arp2/3 complex to nucleate branched actin filaments. Strikingly, we find Rac1 and Arp2/3 are closely associated with synaptic vesicle membranes in adult mice. Using three independent approaches to alter presynaptic Rac1 activity (genetic knockout, spatially restricted inhibition, and temporal optogenetic manipulation), we discover that this pathway negatively regulates synaptic vesicle replenishment at both excitatory and inhibitory synapses, bidirectionally sculpting short-term synaptic depression. Finally, we use two-photon fluorescence lifetime imaging to show that presynaptic Rac1 activation is coupled to action potentials by voltage-gated calcium influx. Thus, this study uncovers a previously unrecognized mechanism of actin-regulated short-term presynaptic plasticity that is conserved across excitatory and inhibitory terminals. It also provides a new proteomic framework for better understanding presynaptic physiology, along with a blueprint of experimental strategies to isolate the presynaptic effects of ubiquitously expressed proteins.

THE EFFECTIVENESS OF SHORT-TERM PSYCHODYNAMIC PSYCHOTHERAPY IN DEPRESSION AND ANXIETY DISORDERS

ABSTRACT Short-term psychodynamic psychotherapy (STPP) is a treatment modality for depressive disorder, anxiety disorder, and personality disorders. In this study, we aimed to assess the effectiveness of the STPP programme in patients with depression and anxiety who were partially responsive to previous treatments. Participants were consisted of 36 patients, 27 of whom were female and 9 were male. A total of 12 sessions of STPP were applied to the patients included in the study, sessions lasting 45 minutes, every 2 weeks, for 6 months. During the STPP procedure, the nature of unconscious conflicts was tried to be understood. The quality of object relations and defence mechanisms were evaluated. The elements of resistance, transference, and counter-transference were examined. Psychodynamic formulation was formed. Treatment goals were determined together with the patient. In this direction, psychotherapeutic strategies have been developed. We evaluated pre- and post-treatment effectiveness according to clinical variables and also the change in self-destructive behaviours. Scales measuring their psychiatric status were administered at base-line, pre-and post-treatment. The primary outcome measures were depression and anxiety scores. At the end of STPP, depression, and anxiety scores were all significantly decreased. A significant improvement was observed in 94% of our patients who could not achieve adequate improvement with previous treatment interventions. During the psychotherapy process, none of the patients attempted suicide and there was a significant decrease in self-destructive behaviours. These findings suggest that STPP is an effective treatment in patients with anxiety disorders and depression, who have not achieved adequate response to previous standard psychiatric treatments.

Remote and adjacent psychological predictors of early-adulthood resilience: Role of early-life trauma, extraversion, life-events, depression, and social-support.

Resilience is important for people to maintain mental health after negative life-events. However, its longitudinal psychological and social predictors are poorly revealed. Based on the ecological system theory model, the current study aimed to determine the longitudinal temporal mechanism underlying the development of early-adulthood resilience using long-term (early-life trauma and personality), medium-term and short-term (life-events, social support, and depression) psychosocial predictors. A total of 505 university students were recruited at baseline (T1), 433 of whom took part in a three-year longitudinal investigation (T2). The results showed that at T1 and T2, the resilience scores of individuals were identically high (72.98 and 73.21, respectively). Pearson correlation analysis showed that early-adulthood resilience was negatively correlated with early-life trauma, psychoticism and neuroticism, depression, ad life-events, and positively correlated with extraversion, social-support, and resilience. Regression and structural equation models showed that extraversion had a direct positive effect on T1 resilience through the mediation of T1 life-events, depression, and social-support, while childhood emotional neglect (EN) had indirect negative effect and extraversion had direct positive effect on T2 resilience through the mediation of T1 resilience, and T2 depression and social-support. In conclusion, this study is among the first to reveal the longitudinal temporal process of the development of early-adulthood resilience using remote and adjacent psychosocial predictors. The findings confirm that childhood EN and extraversion have a remote impact on early-adulthood resilience through recent and current depression and social-support. Our results imply that early-life trauma does not hinder the development of early-adulthood resilience in a linear trend.

Light stimulation during postnatal development is not determinant for glutamatergic neurotransmission from the retinohypothalamic tract to the suprachiasmatic nucleus in rats.

The hypothalamic suprachiasmatic nucleus (SCN) is the leading circadian pacemaker in mammals, which synchronizes with environmental light through the retinohypothalamic tract (RHT). Although the SCN regulates circadian rhythms before birth, postnatal synaptic changes are needed for the RHT-SCN pathway to achieve total functional development. However, it is unknown whether visual experience affects developmental maturation. Here, we studied the effects of constant darkness (DD) rearing on the physiology (at pre- and postsynaptic levels) of glutamatergic neurotransmission between RHT and SCN during postnatal development in rats. Upon recording spontaneous and evoked excitatory postsynaptic currents (EPSCs) by electrical stimulation of RHT fibers, we found that DD animals at early postnatal ages (P3-19) exhibited different frequencies of spontaneous EPSCs and lower synaptic performance (short-term depression, release sites, and recruitment of RHT fibers) when compared with their normal light/dark (LD) counterparts. At the oldest age evaluated (P30-35), there was a synaptic response strengthening (probability of release, vesicular re-filling rate, and reduced synaptic depression) in DD rats, which functionally equaled (or surmounted) that of LD animals. Control experiments evaluating EPSCs in ventral SCN neurons of LD rats during day and night revealed no significant differences in spontaneous or evoked EPSCs by high-frequency trains in the RHT at any postnatal age. Our results suggest that DD conditions induce a compensatory mechanism in the glutamatergic signaling of the circadian system to increase the chances of synchronization to light at adult ages, and that the synaptic properties of RHT terminals during postnatal development are not critically influenced by environmental light.

RNA editing-mediated regulation of calcium-dependent activator protein for secretion (CAPS1) localization and its impact on synaptic transmission.

Calcium-dependent activator protein for secretion 1 (CAPS1) is a SNARE accessory protein that facilitates formation of the SNARE complex to enable neurotransmitter release. Messenger RNAs encoding CAPS1 are subject to a site-specific adenosine-to-inosine (A-to-I) editing event resulting in a glutamate-to-glycine (E-to-G) substitution in the C-terminal domain of the encoded protein product. The C-terminal domain of CAPS1 is necessary for its synaptic enrichment and Cadps RNA editing has been shown previously to enhance the release of neuromodulatory transmitters. Using mutant mouse lines engineered to solely express CAPS1 protein isoforms encoded by either the non-edited or edited Cadps transcript, primary neuronal cultures from mouse hippocampus were used to explore the effect of Cadps editing on neurotransmission and CAPS1 synaptic localization at both glutamatergic and GABAergic synapses. While the editing of Cadps does not alter baseline evoked neurotransmission, it enhances short-term synaptic plasticity, specifically short-term depression, at inhibitory synapses. Cadps editing also alters spontaneous inhibitory neurotransmission. Neurons that solely express edited Cadps have a greater proportion of synapses that contain CAPS1 than neurons that solely express non-edited Cadps for both glutamatergic and GABAergic synapses. Editing of Cadps transcripts is regulated by neuronal activity, as global network stimulation increases the extent of transcripts edited in wild-type hippocampal neurons, whereas chronic network silencing decreases the level of Cadps editing. Taken together, these results provide key insights into the importance of Cadps editing in modulating its own synaptic localization, as well as the modulation of neurotransmission at inhibitory synapses in hippocampal neurons.

5-HT7 receptor activation rescues impaired synaptic plasticity in an autistic-like rat model induced by prenatal VPA exposure

Autism spectrum disorder (ASD) is a severe life-long neuropsychiatric disorder. Alterations and imbalance of several neurochemical systems may be involved in ASD pathophysiology, of them, serotonergic neurotransmission dysfunction and deficiency may underlie behavioral abnormalities associated with ASD. However, the functional importance of serotonergic receptors, particularly 5HT7 receptors in ASD pathology remains poorly defined. Serotonin receptor subtype 7 (5-HT7R) plays a direct regulatory role in the development and also for the mature function of the brain, therefore, further studies are necessary to elucidate the role of these receptors in the etiology of autism. To address this issue, we combined here behavioral, electrophysiological methods to further characterize the contribution of 5-HT7Rs in the prenatal valproic acid (VPA) exposure-induced impairment in synaptic plasticity and their impact on the associated behavioral changes. This may help to unravel the underlying cellular mechanisms involved in ASD and can lead to new treatment and/or prevention therapies based on the role of the serotonergic system for autism.Findings revealed that compared to control, autistic-like offspring showed increased anxiety-like behavior, reduced social interaction, decreased locomotor activity, and impaired identification of the novel object. However, administration of 5-HT7Rs agonist, LP-211, for 7 consecutive days before testing from postnatal day 21 to 27 reversed all behavioral deficits induced by prenatal exposure to VPA in offspring. Also, both short-term depression and long-term potentiation were impaired in the autistic-like pups, but activation of 5-HT7Rs rescued the LTP impairment in the autistic-like group so that there was no significant difference between the two groups. Blockade of 5-HT7Rs caused LTP impairment following HFS in the autistic-like group. Besides, there was a significant difference in LTD induction following SB-269970 application between the control and the autistic-like groups measured at first 10 min following TPS. Moreover, both the number and the size of retrograde fast blue-labelled neurons in the raphe nuclei were reduced.Overall, these results provide for the first time, as far as we know, functional evidence for the restorative role of 5-HT7Rs activation against prenatal VPA exposure induced behavioral deficits and hippocampal synaptic plasticity impairment. Therefore, these receptors could be a potential and promising pharmacotherapy target for the treatment of autism.

A theoretical framework for the site-specific and frequency-dependent neuronal effects of deep brain stimulation

BackgroundDeep brain stimulation is an established therapy for several neurological disorders; however, its effects on neuronal activity vary across brain regions and depend on stimulation settings. Understanding these variable responses can aid in the development of physiologically-informed stimulation paradigms in existing or prospective indications. ObjectiveProvide experimental and computational insights into the brain-region-specific and frequency-dependent effects of extracellular stimulation on neuronal activity. MethodsIn patients with movement disorders, single-neuron recordings were acquired from the subthalamic nucleus, substantia nigra pars reticulata, ventral intermediate nucleus, or reticular thalamus during microstimulation across various frequencies (1–100 Hz) to assess single-pulse and frequency-response functions. Moreover, a biophysically-realistic computational framework was developed which generated postsynaptic responses under the assumption that electrical stimuli simultaneously activated all convergent presynaptic inputs to stimulation target neurons. The framework took into consideration the relative distributions of excitatory/inhibitory afferent inputs to model site-specific responses, which were in turn embedded within a model of short-term synaptic plasticity to account for stimulation frequency-dependence. ResultsWe demonstrated microstimulation-evoked excitatory neuronal responses in thalamic structures (which have predominantly excitatory inputs) and inhibitory responses in basal ganglia structures (predominantly inhibitory inputs); however, higher stimulation frequencies led to a loss of site-specificity and convergence towards neuronal suppression. The model confirmed that site-specific responses could be simulated by accounting for local neuroanatomical/microcircuit properties, while suppression of neuronal activity during high-frequency stimulation was mediated by short-term synaptic depression. ConclusionsBrain-region-specific and frequency-dependant neuronal responses could be simulated by considering neuroanatomical (local microcircuitry) and neurophysiological (short-term plasticity) properties.

Ca2+ sensor proteins in spontaneous release and synaptic plasticity: Limited contribution of Doc2c, rabphilin-3a and synaptotagmin 7 in hippocampal glutamatergic neurons

Presynaptic neurotransmitter release is strictly regulated by SNARE proteins, Ca2+ and a number of Ca2+ sensors including synaptotagmins (Syts) and Double C2 domain proteins (Doc2s). More than seventy years after the original description of spontaneous release, the mechanism that regulates this process is still poorly understood. Syt-1, Syt7 and Doc2 proteins contribute predominantly, but not exclusively, to synchronous, asynchronous and spontaneous phases of release. The proteins share a conserved tandem C2 domain architecture, but are functionally diverse in their subcellular location, Ca2+-binding properties and protein interactions. In absence of Syt-1, Doc2a and -b, neurons still exhibit spontaneous vesicle fusion which remains Ca2+-sensitive, suggesting the existence of additional sensors. Here, we selected Doc2c, rabphilin-3a and Syt-7 as three potential Ca2+ sensors for their sequence homology with Syt-1 and Doc2b. We genetically ablated each candidate gene in absence of Doc2a and -b and investigated spontaneous and evoked release in glutamatergic hippocampal neurons, cultured either in networks or on microglial islands (autapses). The removal of Doc2c had no effect on spontaneous or evoked release. Syt-7 removal also did not affect spontaneous release, although it altered short-term plasticity by accentuating short-term depression. The removal of rabphilin caused an increased spontaneous release frequency in network cultures, an effect that was not observed in autapses. Taken together, we conclude that Doc2c and Syt-7 do not affect spontaneous release of glutamate in hippocampal neurons, while our results suggest a possible regulatory role of rabphilin-3a in neuronal networks. These findings importantly narrow down the repertoire of synaptic Ca2+ sensors that may be implicated in the spontaneous release of glutamate.

Association between short-term ambient air pollution exposure and depression outpatient visits in cold seasons: a time-series analysis in northwestern China

ABSTRACT Depression is known to be one of the most common mental disorders raising global concerns. However, evidence regarding the association between short-term air pollution exposure and risk of development of depression is limited. The aim of this was to assess the relationship between short-term ambient air pollution exposure and depression in outpatient visits in Xi’an, a northwestern Chinese metropolis. Data for air pollutants including particulate matter (PM10), sulfur dioxide (SO2), and nitrogen dioxide (NO2) levels from October 1, 2010 to December 31, 2013 and number of daily depression outpatient visits (92,387 in total) were collected. A time-series quasi-Poisson regression model was adopted to determine the association between short-term air pollutant concentrations and frequency of outpatient visits for depression with different lag models. Consequently, 10 μg/m3 increase of SO2 and NO2 levels corresponded to significant elevation in number of outpatient-visits for depression on concurrent days (lag 0), and this relationship appeared stronger in cool seasons (October to March). However, the association of PM10 was only significant in males aged 30–50 at lag 0. Evidence indicated that short-term exposure to ambient air pollutants especially in cool seasons might be associated with increased risk of outpatient visits for depression.

An artifical synapse based on graphene field-effect transistor with silver gel/polarized-aptamer gate

Abstract In this work, we present an artificial synapse based on side-gate graphene-field-effect-transistor (GFET) using biocompatible silver gel/polarized-aptamer as gate dielectric. The gate functions as the presynaptic membrane, while the drain works as postsynaptic membrane. Various synaptic plasticities, including short-term enhancement (STE), short-term depression (STD), long-term potentiation (LTP), long-term depression (LTD) and the transformation from short-term plasticity to long-term plasticity have been emulated by the GFET artificial synapse. A model based on the function of a difference of two exponentials that is widely used to model the biological synapses is proposed, well fitting the behavior of the fabricated artificial synapses under different presynaptic spikes. With a fixed current of −1 μA applied to postsynaptic membrane, the excitatory-postsynaptic-potential-like spikes can be generated at postsynaptic membrane under the positive spikes applied to presynaptic membrane, suggesting the similarities between the artificial and biological synapses.

Synaptotagmin 7 switches short-term synaptic plasticity from depression to facilitation by suppressing synaptic transmission

Short-term synaptic plasticity is a fast and robust modification in neuronal presynaptic output that can enhance release strength to drive facilitation or diminish it to promote depression. The mechanisms that determine whether neurons display short-term facilitation or depression are still unclear. Here we show that the Ca2+-binding protein Synaptotagmin 7 (Syt7) determines the sign of short-term synaptic plasticity by controlling the initial probability of synaptic vesicle (SV) fusion. Electrophysiological analysis of Syt7 null mutants at Drosophila embryonic neuromuscular junctions demonstrate loss of the protein converts the normally observed synaptic facilitation response during repetitive stimulation into synaptic depression. In contrast, overexpression of Syt7 dramatically enhanced the magnitude of short-term facilitation. These changes in short-term plasticity were mirrored by corresponding alterations in the initial evoked response, with SV release probability enhanced in Syt7 mutants and suppressed following Syt7 overexpression. Indeed, Syt7 mutants were able to display facilitation in lower [Ca2+] where release was reduced. These data suggest Syt7 does not act by directly sensing residual Ca2+ and argues for the existence of a distinct Ca2+ sensor beyond Syt7 that mediates facilitation. Instead, Syt7 normally suppresses synaptic transmission to maintain an output range where facilitation is available to the neuron.

Short-Term Plasticity in Cortical GABAergic Synapses on Olfactory Bulb Granule Cells Is Modulated by Endocannabinoids

Olfactory bulb and higher processing areas are synaptically interconnected, providing rapid regulation of olfactory bulb circuit dynamics and sensory processing. Short-term plasticity changes at any of these synapses could modulate sensory processing and potentially short-term sensory memory. A key olfactory bulb circuit for mediating cortical feedback modulation is granule cells, which are targeted by multiple cortical regions including both glutamatergic excitatory inputs and GABAergic inhibitory inputs. There is robust endocannabinoid modulation of excitatory inputs to granule cells and here we explored whether there was also endocannabinoid modulation of the inhibitory cortical inputs to granule cells. We expressed light-gated cation channel channelrhodopsin-2 (ChR2) in GABAergic neurons in the horizontal limb of the diagonal band of Broca (HDB) and their projections to granule cells in olfactory bulb. Selective optical activation of ChR2 positive axons/terminals generated strong, frequency-dependent short-term depression of GABAA-mediated-IPSC in granule cells. As cannabinoid type 1 (CB1) receptor is heavily expressed in olfactory bulb granule cell layer (GCL) and there is endogenous endocannabinoid release in GCL, we investigated whether activation of CB1 receptor modulated the HDB IPSC and short-term depression at the HDB→granule cell synapse. Activation of the CB1 receptor by the exogenous agonist Win 55,212-2 significantly decreased the peak amplitude of individual IPSC and decreased short-term depression, while blockade of the CB1 receptor by AM 251 slightly increased individual IPSCs and increased short-term depression. Thus, we conclude that there is tonic endocannabinoid activation of the GABAergic projections of the HDB to granule cells, similar to the modulation observed with glutamatergic projections to granule cells. Modulation of inhibitory synaptic currents and frequency-dependent short-term depression could regulate the precise balance of cortical feedback excitation and inhibition of granule cells leading to changes in granule cell mediated inhibition of olfactory bulb output to higher processing areas.

Septohippocampal transmission from parvalbumin-positive neurons features rapid recovery from synaptic depression

Parvalbumin-containing projection neurons of the medial-septum-diagonal band of Broca (hbox {PV}_{text{MS-DBB}}) are essential for hippocampal rhythms and learning operations yet are poorly understood at cellular and synaptic levels. We combined electrophysiological, optogenetic, and modeling approaches to investigate hbox {PV}_{text{MS-DBB}} neuronal properties. hbox {PV}_{text{MS-DBB}} neurons had intrinsic membrane properties distinct from acetylcholine- and somatostatin-containing MS-DBB subtypes. Viral expression of the fast-kinetic channelrhodopsin ChETA-YFP elicited action potentials to brief (1–2 ms) 470 nm light pulses. To investigate hbox {PV}_{text{MS-DBB}} transmission, light pulses at 5–50 Hz frequencies generated trains of inhibitory postsynaptic currents (IPSCs) in CA1 stratum oriens interneurons. Using a similar approach, optogenetic activation of local hippocampal PV (hbox {PV}_{text{HC}}) neurons generated trains of hbox {PV}_{text{HC}}-mediated IPSCs in CA1 pyramidal neurons. Both synapse types exhibited short-term depression (STD) of IPSCs. However, relative to hbox {PV}_{text{HC}} synapses, hbox {PV}_{text{MS-DBB}} synapses possessed lower initial release probability, transiently resisted STD at gamma (20–50 Hz) frequencies, and recovered more rapidly from synaptic depression. Experimentally-constrained mathematical synapse models explored mechanistic differences. Relative to the hbox {PV}_{text{HC}} model, the hbox {PV}_{text{MS-DBB}} model exhibited higher sensitivity to calcium accumulation, permitting a faster rate of calcium-dependent recovery from STD. In conclusion, resistance of hbox {PV}_{text{MS-DBB}} synapses to STD during short gamma bursts enables robust long-range GABAergic transmission from MS-DBB to hippocampus.

Implementation of Neuro-Memristive Synapse for Long-and Short-Term Bio-Synaptic Plasticity.

In this paper, we propose a complex neuro-memristive synapse that exhibits the physiological acts of synaptic potentiation and depression of the human-brain. Specifically, the proposed neuromorphic synapse efficiently imitates the synaptic plasticity, especially long-term potentiation (LTP) and depression (LTD), and short-term facilitation (STF) and depression (STD), phenomena of a biological synapse. Similar to biological synapse, the short- or long-term potentiation (STF and LTP) or depression (STD or LTD) of the memristive synapse are distinguished on the basis of time or repetition of input cycles. The proposed synapse is also designed to exhibit the effect of reuptake and neurotransmitters diffusion processes of a bio-synapse. In addition, it exhibits the distinct bio-realistic attributes, i.e., strong stimulation, exponentially decaying conductance trace of synapse, and voltage dependent synaptic responses, of a neuron. The neuro-memristive synapse is designed in SPICE and its bio-realistic functionalities are demonstrated via various simulations.

Ebola: A review and focus on neurologic manifestations

Ebolavirus disease (EVD) is a severe, highly contagious, and often fatal systemic disease in human and non-human primates. Zoonotic and human-to-human transmission have been well documented. Ebolaviruses are endemic to Equatorial and West Africa and there have been over 20 outbreaks in sub-Saharan Africa since 1976. The largest known outbreak of EVD occurred between 2013 and 2016 across several West African countries. It resulted in 28,646 suspected and confirmed cases and 11,323 deaths. There are 5 species within the genus Ebolavirus with 4 of them being clinically significant. In patients with EVD, neurologic manifestations range from mild symptoms such as confusion to severe neurologic diseases such as meningitis and encephalitis. Altered mental status, from mild confusion to delirium with hallucinations, may also occur. Rare neuropsychiatric manifestations of EVD include psychological or cognitive symptoms, including short-term memory loss, insomnia, and depression or anxiety. Although Ebolavirus RNA has been detected in cerebrospinal fluid, the body of knowledge around the pathogenic mechanisms of neurological disease is not yet fully understood. Studies are needed to understand the acute and chronic neuronal pathologic as well as biochemical cerebrospinal fluid changes in Ebolavirus infection.

Anticipative Tracking with the Short-Term Synaptic Plasticity of Spintronic Devices

Real-time tracking of high-speed objects in cognitive tasks is challenging in the present artificial intelligence techniques because the data processing and computation are time-consuming resulting in impeditive time delays. A brain-inspired continuous attractor neural network (CANN) can be used to track quickly moving targets, where the time delays are intrinsically compensated if the dynamical synapses in the network have the short-term plasticity. Here, we show that synapses with short-term depression can be realized by a magnetic tunnel junction, which perfectly reproduces the dynamics of the synaptic weight in a widely applied mathematical model. Then, these dynamical synapses are incorporated into one-dimensional and two-dimensional CANNs, which are demonstrated to have the ability to predict a moving object via micromagnetic simulations. This portable spintronics-based hardware for neuromorphic computing needs no training and is therefore very promising for the tracking technology for moving targets.