The Relationship between Self-Efficacy, Other-Efficacy, and Relation-Inferred Self-Efficacy with Performance in Soccer

This study assessed the relationships between other-efficacy, relation-inferred self-efficacy, self-efficacy, and performance. The participants were three head coaches and 40 athletes from three NCAA women’s soccer teams. New measures of self-efficacy, other-efficacy, and relation-inferred self-efficacy were developed using Bandura’s guidelines. Performance was measured by the number of times the athletes completed a soccer task successfully. Analysis indicated that none of the efficacy measures could predict performance. Results did show a significant con-elation between relation-inferred self-efficacy and the self-efficacy measures, indicating that the self-efficacy an athlete has to perfonn a task was similar to what they perceived their coaches’ perceptions would be

Mechanisms Of Dopaminergic, Histaminergic, And Glutamatergic Neuromodulation Within The Medial Entorhinal Cortex

The medial entorhinal cortex (MEC) is a critical region for both limbic functions as well as learning and memory. In addition to these normal processes, the MEC is also implicated in several disorders including epilepsy, Alzheimer’s disease, and several neuropsychiatric disorders. The MEC’s function and role in various disorders is intimately related to its underlying cellular activity. The primary neuronal cell types in this region consist of glutamatergic principle cells and GABAergic local inhibitory interneurons. This dissertation consists of three aims related to the neuromodulation of these cells located in the superficial layers of the MEC—the primary input source to the hippocampus. The first aim addresses how dopamine (DA) alters GABAergic transmission. The second aim also considers GABAergic transmission but examines its modulation by histamine (HA). Finally, the third aim investigates mechanisms of group I metabotropic glutamate receptor(mGluR)-induced increases in layer III principal cell excitability. For Study 1, exogenous application of DA increases spontaneous inhibitory postsynaptic currents (sIPSCs) recorded from layer II neurons. This increase is mediated by a promiscuous interaction with the α1 adrenergic receptors (α1 ARs) found on the MEC interneurons. Application of amphetamine to elevate extracellular DA concentrations mimic theses effects in an α1 AR-dependent fashion. Activation of interneuron α1 AR-induced depolarization is mediated by inhibition of inwardly rectifying K+ channels (Kirs). For Study 2, exogenous application of HA increases sIPSCs recorded from layer II principal neurons. This increase requires both H1 and H2 receptors located on GABAergic interneurons. The magnitude of HA-induced depolarization is significantly larger within one class of tested interneurons and HA-induced depolarization of interneurons involves both the inhibition of (Kirs) and activation of a TTX-insensitive Na+ current. For Study 3, activation of group I mGluRs increases action potential firing, depolarization and generation of inward currents in layer III pyramidal neurons. This increase is sensitive to antagonists for both mGluR1 and mGluR5, indicating the functional presence of both receptors. The mGluR-induced currents are mediated by a non-selective cation channel that contains TRPC4 and TRPC5 subunits

Optimization and validation of the NeuroLux wireless optoelectronics system for optogenetics

Utilizing light and genetic engineering, optogenetics permits the manipulation of events within cells via light using the light-sensitive properties of single-component microbial opsins. Microbial opsins are activated by a light source, such as lasers, light-emitting diodes, and incandescent sources that deliver light to the region of interest either directly or indirectly, such as through fiberoptics. In classical in vivo optogenetics, the wiring of optic fibers necessitates tethering of animals by the optic fiber to the light source. The novel NeuroLux wireless optoelectronic system for optogenetics circumvents issues pertaining to classical optogenetics by utilizing near-field power transfer via magnetic coil antennae to power miniature, subdermal, and flexible optoelectronic implants, including an LED light sources. Furthermore, features of the NeuroLux system overcome issues posed by other wireless systems, including interference. This preliminary study sought to validate and optimize the novel NeuroLux system setup by stimulating the cornu ammonis 2 (CA2) region of the hippocampus in transgenic mice that express Cre recombinase from the vasopressin 1b receptor promoter. Following experimentation, distinct stimulation, indicated by quantified cFos expression, was noted in the CA2 region, thereby validating the use of the NeuroLux wireless optoelectronics system for future optogenetics studies

NMDA Receptor in Vasopressin 1b Neurons Is Not Required for Short-Term Social Memory, Object Memory or Aggression

This work is licensed under a Creative Commons Attribution 4.0 International License.The arginine vasopressin 1b receptor (Avpr1b) plays an important role in social behaviors including aggression, social learning and memory. Genetic removal of Avpr1b from mouse models results in deficits in aggression and short-term social recognition in adults. Avpr1b gene expression is highly enriched in the pyramidal neurons of the hippocampal cornu ammonis 2 (CA2) region. Activity of the hippocampal CA2 has been shown to be required for normal short-term social recognition and aggressive behaviors. Vasopressin acts to enhance synaptic responses of CA2 neurons through a NMDA-receptor dependent mechanism. Genetic removal of the obligatory subunit of the NMDA receptor (Grin1) within distinct hippocampal regions impairs non-social learning and memory. However, the question of a direct role for NMDA receptor activity in Avpr1b neurons to modulate social behavior remains unclear. To answer this question, we first created a novel transgenic mouse line with Cre recombinase knocked into the Avpr1b coding region to genetically target Avpr1b neurons. We confirmed this line has dense Cre expression throughout the dorsal and ventral CA2 regions of the hippocampus, along with scattered expression within the caudate-putamen and olfactory bulb (OB). Conditional removal of the NMDA receptor was achieved by crossing our line to an available floxed Grin1 line. The resulting mice were measured on a battery of social and memory behavioral tests. Surprisingly, we did not observe any differences between Avpr1b-Grin1 knockout mice and their wildtype siblings. We conclude that mice without typical NMDA receptor function in Avpr1b neurons can develop normal aggression as well as short-term social and object memory performance

Dopamine acting at D1-like, D2-like and α1-adrenergic receptors differentially modulates theta and gamma oscillatory activity in primary motor cortex

The loss of dopamine (DA) in Parkinson’s is accompanied by the emergence of exaggerated theta and beta frequency neuronal oscillatory activity in the primary motor cortex (M1) and basal ganglia. DA replacement therapy or deep brain stimulation reduces the power of these oscillations and this is coincident with an improvement in motor performance implying a causal relationship. Here we provide in vitro evidence for the differential modulation of theta and gamma activity in M1 by DA acting at receptors exhibiting conventional and non-conventional DA pharmacology. Recording local field potentials in deep layer V of rat M1, co-application of carbachol (CCh, 5 μM) and kainic acid (KA, 150 nM) elicited simultaneous oscillations at a frequency of 6.49 ± 0.18 Hz (theta, n = 84) and 34.97 ± 0.39 Hz (gamma, n = 84). Bath application of DA resulted in a decrease in gamma power with no change in theta power. However, application of either the D1-like receptor agonist SKF38393 or the D2-like agonist quinpirole increased the power of both theta and gamma suggesting that the DA-mediated inhibition of oscillatory power is by action at other sites other than classical DA receptors. Application of amphetamine, which promotes endogenous amine neurotransmitter release, or the adrenergic α1-selective agonist phenylephrine mimicked the action of DA and reduced gamma power, a result unaffected by prior co-application of D1 and D2 receptor antagonists SCH23390 and sulpiride. Finally, application of the α1-adrenergic receptor antagonist prazosin blocked the action of DA on gamma power suggestive of interaction between α1 and DA receptors. These results show that DA mediates complex actions acting at dopamine D1-like and D2-like receptors, α1 adrenergic receptors and possibly DA/α1 heteromultimeric receptors to differentially modulate theta and gamma activity in M1

A protocol for preparation and transfection of rat entorhinal cortex organotypic cultures for electrophysiological whole-cell recordings

Understanding how neuromodulators influence synaptic transmission and intrinsic excitability within the entorhinal cortex (EC) is critical to furthering our understanding of the molecular and cellular aspects of this region. Organotypic cultures can provide a cost-effective means to employ selective molecular biological strategies in elucidating cellular mechanisms of neuromodulation in the EC. We therefore adapted our acute slice model for organotypic culture applications and optimized a protocol for the preparation and biolistic transfection of cultured horizontal EC slices. Here, we present our detailed protocol for culturing EC slices. Using an n-methyl-d-glucamine (NMDG)-containing cutting solution, we obtain healthy EC slice cultures for electrophysiological recordings. We also present our protocol for the preparation of “bullets” carrying one or more constructs and demonstrate successful transfection of EC slices. We build upon previous methods and highlight specific aspects in our method that greatly improved the quality of our results. We validate our methods using immunohistochemical, imaging, and electrophysiological techniques. The novelty of this method is that it provides a description of culturing and transfection of EC neurons for specifically addressing their functionality. This method will enable researchers interested in entorhinal function to quickly adopt a similar slice culture transfection system for their own investigations

Adenosinergic depression of glutamatergic transmission in the entorhinal cortex of juvenile rats via reduction of glutamate release probability and the number of releasable vesicles.

Adenosine is an inhibitory neuromodulator that exerts antiepileptic effects in the brain and the entorhinal cortex (EC) is an essential structure involved in temporal lobe epilepsy. Whereas microinjection of adenosine into the EC has been shown to exert powerful antiepileptic effects, the underlying cellular and molecular mechanisms in the EC have not been determined yet. We tested the hypothesis that adenosine-mediated modulation of synaptic transmission contributes to its antiepileptic effects in the EC. Our results demonstrate that adenosine reversibly inhibited glutamatergic transmission via activation of adenosine A1 receptors without effects on GABAergic transmission in layer III pyramidal neurons in the EC. Adenosine-induced depression of glutamatergic transmission was mediated by inhibiting presynaptic glutamate release probability and decreasing the number of readily releasable vesicles. Bath application of adenosine also reduced the frequency of the miniature EPSCs recorded in the presence of TTX suggesting that adenosine may interact with the exocytosis processes downstream of Ca(2+) influx. Both Gαi/o proteins and the protein kinase A pathway were required for adenosine-induced depression of glutamatergic transmission. We further showed that bath application of picrotoxin to the EC slices induced stable epileptiform activity and bath application of adenosine dose-dependently inhibited the epileptiform activity in this seizure model. Adenosine-mediated depression of epileptiform activity was mediated by activation of adenosine A1 receptors and required the functions of Gαi/o proteins and protein kinase A pathway. Our results suggest that the depression of glutamatergic transmission induced by adenosine contributes to its antiepileptic effects in the EC

Adenosine-induced depression of seizure activity is mediated by activation of A₁ ARs and requires the functions of Gα_i proteins and PKA.

<p><b>A,</b> Seizure events induced by bath application of picrotoxin at the saturated concentration (100 µM) in a rat slice at different times. An extracellular electrode containing ACSF was placed in layer III of the EC to record the seizure events. <b>B,</b> Time course of picrotoxin-induced seizure events (n = 7 slices). <b>C,</b> Seizure events recorded before, during and after the application of adenosine (100 µM). <b>D,</b> Summarized time course of adenosine-induced inhibition of seizure activity (n = 10 slices, p<0.001 vs. baseline, paired t-test). <b>E,</b> Concentration-response curve of adenosine-induced depression of seizure activity. Numbers in the parenthesis are the number of slices recorded from. <b>F,</b> Prior bath application of the A₁ AR inhibitor, DPCPX, blocked adenosine-induced depression of seizure events (n = 12 slices, p = 0.89 vs. baseline, paired t-test). <b>G,</b> Bath application of the A₁ AR agonist, NCPA, irreversibly suppressed the seizure events (n = 6 slices, p<0.001 vs. baseline, paired t-test). <b>H,</b> Application of antagonists to other ARs except A₁ ARs did not block adenosine-induced depression of epileptiform activity (One-way ANOVA followed by Dunnett test, *** p<0.001 vs. adenosine alone). <b>I,</b> Bath application of adenosine failed to depress significantly picrotoxin-induced seizure events in slices pretreated with PTX (n = 8 slices, p = 0.45 vs. baseline, paired t-test). <b>J,</b> Pretreatment of slices with and continuous bath application of the membrane permeable PKA inhibitor, KT5720, blocked adenosine-induced depression of seizure events (n = 8 slices, p = 0.7 vs. baseline, paired t-test).</p