Experience-dependent learning of behavioral laterality in the scale-eating cichlid Perissodus microlepis occurs during the early developmental stage

Behavioral laterality—typically represented by human handedness—is widely observed among animals. However, how laterality is acquired during development remains largely unknown. Here, we examined the effect of behavioral experience on the acquisition of lateralized predation at different developmental stages of the scale-eating cichlid fish Perissodus microlepis. Naïve juvenile fish without previous scale-eating experience showed motivated attacks on prey goldfish and an innate attack side preference. Following short-term predation experience, naïve juveniles learned a pronounced lateralized attack using their slightly skewed mouth morphology, and improved the velocity and amplitude of body flexion to succeed in foraging scales during dominant-side attack. Naïve young fish, however, did not improve the dynamics of flexion movement, but progressively developed attack side preference and speed to approach the prey through predation experience. Thus, the cichlid learns different aspects of predation behavior at different developmental stages. In contrast, naïve adults lost the inherent laterality, and they neither developed the lateralized motions nor increased their success rate of predation, indicating that they missed appropriate learning opportunities for scale-eating skills. Therefore, we conclude that behavioral laterality of the cichlid fish requires the integration of genetic basis and behavioral experiences during early developmental stages, immediately after they start scale-eating.

The Effect of Learning Methods and Cognitive Style on Student Learning Achievement

The purpose of this study was to examine: The effect of discussion and recitation methods on learning achievement, the effect of independent and dependent cognitive styles on learning achievement, the interaction between learning methods and cognitive style on learning achievement, whether learning achievement by using the discussion method with independent cognitive style was higher than the recitation learning method, whether learning achievement using the discussion method with a dependent cognitive style was higher than the recitation method. This research used quantitative research methods, the type of research was quasi-experimental factorial 2x2 with a population of 173 students and the sample was 61 students. The data collection technique used was a test of cognitive style and learning achievement. The analysis technique used two way ANOVA test and t-test. The results of hypothesis testing concluded: There was an influence of discussion learning methods and recitation learning methods on learning achievement, there was an influence of cognitive style on learning achievement, there was an interaction between learning methods and cognitive styles on student learning achievement, learning achievement using the discussion method of students who had independent cognitive style was higher than the dependent, learning achievement using the recitation method of students who had an independent cognitive style was not higher than the independent.

BDNF-induced BDNF release mediates presynaptic LTP and is regulated by cannabinoids

Although brain-derived neurotrophic factor (BDNF) and its effector, Tropomyosin receptor kinase B (TrkB), are implicated in activity-dependent synaptic plasticity, the precise underlying mechanisms remain unclear. In the dentate gyrus, a hippocampal input region that expresses uniquely high levels of BDNF, repetitive activation of mossy cells (MCs) induces a presynaptic, BDNF/TrkB-dependent form of LTP at MC to granule cell (GC) synapses. Here, we report that activity-induced BDNF release from MC axons in mice elicits postsynaptic BDNF release in a TrkB- and calcium-dependent manner, and that BDNF-induced BDNF release is essential for LTP induction. Suppression of BDNF release by tonic and phasic activity of presynaptic type-1 cannabinoid receptors dampened LTP, revealing an unprecedented role of these receptors in controlling neuropeptide release. Lastly, BDNF-mediated MC-GC LTP can be elicited in vivo. Thus, BDNF-induced BDNF release emerges as a mechanism for activity-dependent LTP that may contribute to dentate gyrus-dependent learning, epilepsy, and neuropsychiatric disorders.

Opioid withdrawal abruptly disrupts amygdala circuit function by reducing peptide actions

Opioid withdrawal drives relapse and contributes to compulsive drug use through disruption of endogenous opioid dependent learning circuits in the amygdala. Normally, endogenous opioids control these circuits by inhibiting glutamate release from basolateral amygdala principal neurons onto GABAergic intercalated cells. Using patch-clamp electrophysiology in rat brain slices, we reveal that opioid withdrawal dials down this endogenous opioid inhibition of synaptic transmission. Peptide activity is dialled down due to a protein kinase A dependent increase in the activity of the peptidase, neprilysin. This disrupts peptidergic control of both GABAergic and glutamatergic transmission through multiple amygdala circuits, including reward-related outputs to the nucleus accumbens. This likely disrupts peptide-dependent learning processes in the amygdala during withdrawal. and may direct behaviour towards compulsive drug use. Restoration of endogenous peptide activity during withdrawal may be a viable option to normalise synaptic transmission in the amygdala and restore normal reward learning.

FosGFP expression does not capture a sensory learning-related engram in superficial layers of mouse barrel cortex

Immediate-early gene (IEG) expression has been used to identify small neural ensembles linked to a particular experience, based on the principle that a selective subset of activated neurons will encode specific memories or behavioral responses. The majority of these studies have focused on “engrams” in higher-order brain areas where more abstract or convergent sensory information is represented, such as the hippocampus, prefrontal cortex, or amygdala. In primary sensory cortex, IEG expression can label neurons that are responsive to specific sensory stimuli, but experience-dependent shaping of neural ensembles marked by IEG expression has not been demonstrated. Here, we use a fosGFP transgenic mouse to longitudinally monitor in vivo expression of the activity-dependent gene c-fos in superficial layers (L2/3) of primary somatosensory cortex (S1) during a whisker-dependent learning task. We find that sensory association training does not detectably alter fosGFP expression in L2/3 neurons. Although training broadly enhances thalamocortical synaptic strength in pyramidal neurons, we find that synapses onto fosGFP+ neurons are not selectively increased by training; rather, synaptic strengthening is concentrated in fosGFP− neurons. Taken together, these data indicate that expression of the IEG reporter fosGFP does not facilitate identification of a learning-specific engram in L2/3 in barrel cortex during whisker-dependent sensory association learning.

Long-Term Pharmacological Inhibition of the Activity of All NOS Isoforms Rather Than Genetic Knock-Out of Endothelial NOS Leads to Impaired Spatial Learning and Memory in C57BL/6 Mice

Increasing epidemiological and experimental evidence points to a link between arterial stiffness and rapid cognitive decline. However, the underlying mechanism linking the two diseases is still unknown. The importance of nitric oxide synthases in both diseases is well-defined. In this study, we introduced arterial stiffness in both genetic (eNOS−/−, endothelial nitric oxide synthase knockout) and pharmacological (N(G)-nitro-L-arginine methyl ester (L-NAME) treatment) NO dysfunction models to study their association with cognitive decline. Our findings demonstrate that the non-selective inhibition of NOS activity with L-NAME induces cardiac dysfunction, arterial stiffness, and a decline in hippocampal-dependent learning and memory. This outcome demonstrates the importance of neuronal NOS (nNOS) in both cardiovascular and neurological pathophysiology and its potential contribution in the convergence between arterial stiffness and cognitive decline.

Online Linear Programming: Dual Convergence, New Algorithms, and Regret Bounds

We study an online linear programming (OLP) problem under a random input model in which the columns of the constraint matrix along with the corresponding coefficients in the objective function are independently and identically drawn from an unknown distribution and revealed sequentially over time. Virtually all existing online algorithms were based on learning the dual optimal solutions/prices of the linear programs (LPs), and their analyses were focused on the aggregate objective value and solving the packing LP, where all coefficients in the constraint matrix and objective are nonnegative. However, two major open questions were as follows. (i) Does the set of LP optimal dual prices learned in the existing algorithms converge to those of the “offline” LP? (ii) Could the results be extended to general LP problems where the coefficients can be either positive or negative? We resolve these two questions by establishing convergence results for the dual prices under moderate regularity conditions for general LP problems. Specifically, we identify an equivalent form of the dual problem that relates the dual LP with a sample average approximation to a stochastic program. Furthermore, we propose a new type of OLP algorithm, action-history-dependent learning algorithm, which improves the previous algorithm performances by taking into account the past input data and the past decisions/actions. We derive an [Formula: see text] regret bound (under a locally strong convexity and smoothness condition) for the proposed algorithm, against the [Formula: see text] bound for typical dual-price learning algorithms, where n is the number of decision variables. Numerical experiments demonstrate the effectiveness of the proposed algorithm and the action-history-dependent design.

A Noradrenergic Lesion Attenuates Surgery-Induced Cognitive Impairment in Rats by Suppressing Neuroinflammation

Postoperative cognitive dysfunction (POCD) is a common postoperative neurocognitive complication in elderly patients. However, the specific pathogenesis is unknown, and it has been demonstrated that neuroinflammation plays a key role in POCD. Recently, increasing evidence has proven that the locus coeruleus noradrenergic (LCNE) system participates in regulating neuroinflammation in some neurodegenerative disorders. We hypothesize that LCNE plays an important role in the neuroinflammation of POCD. In this study, 400 μg of N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) was injected intracerebroventricularly into each rat 7 days before anesthesia/surgery to deplete the locus coeruleus (LC) noradrenaline (NE). We applied a simple laparotomy and brief upper mesenteric artery clamping surgery as the rat POCD model. The open field test, novel objection and novel location (NL) recognition, and Morris water maze (MWM) were performed to assess postoperative cognition. High-performance liquid chromatography (HPLC) was used to measure the level of NE in plasma and brain tissues, and immunofluorescence staining was applied to evaluate the activation of microglia and astrocytes. We also used enzyme-linked immune-sorbent assay (ELISA) to assess the levels of inflammatory cytokines and brain-derived neurotrophic factor (BDNF). Pretreatment with DSP-4 decreased the levels of systemic and central NE, increased the level of interleukin-6 (IL-6) in the plasma at 6 h after the surgery, decreased the concentration of IL-6 in the prefrontal cortex and hippocampus, and decreased the level of interleukin-1β (IL-1β) in the plasma, prefrontal cortex, and hippocampus at 1 week postoperatively. In addition, DSP-4 treatment attenuated hippocampal-dependent learning and memory impairment in rats with POCD, with a downregulation of the activation of microglia and astrocytes in the prefrontal cortex and hippocampus. In conclusion, these findings provide evidence of the effects of LCNE in modulating neuroinflammation in rats with POCD and provide a new perspective in the prevention and treatment of POCD.