Health promotion profile of youth sports clubs in Finland: club officials' and coaches' perceptions

The purpose of this article is to examine the current health promotion orientation of youth sports clubs in Finland in view of the standards created previously for the health promoting sports club (HPSC). Ninety-seven youth sports clubs participated, and 273 sports club officials and 240 coaches answered the questionnaires. To describe clubs health promotion orientations, an HPSC index was created. The HPSC index was formulated on sub-indices by factor analysis. The sub-indices were: policy, ideology, practice and environment indexes. The results indicate that youth sports clubs are fairly health promoting in general. On average, the clubs fulfilled 12 standards for HPSC out of 22. Every fourth club was categorized as higher health promoting (≥ 15 fulfilled standards), and every third as lower health promoting (<11 fulfilled standards). The variation between clubs was wide. The clubs that had been recognized as exemplary and hence certified by the Young Finland Association were more likely to recognize health promotion than non-certified clubs (OR = 2.36, p = 0.016). The sports club officials were twice as likely to evaluate their clubs as higher health promoting than the coaches (OR = 2.04, p = 0.041). Under the sub-indices, ideologies were recognized best, others less. These findings indicate that minority of the youth sports clubs have realized health promotion comprehensively as a part of their activities. There is a lot of need for development, especially in the area of health promotion policies and practices. The instruments used proved valid and reliable and can therefore be recommended for international use

A T-type channel-calmodulin complex triggers αCaMKII activation

Abstract Calmodulin (CaM) is an important signaling molecule that regulates a vast array of cellular functions by activating second messengers involved in cell function and plasticity. Low voltage-activated calcium channels of the Cav3 family have the important role of mediating low threshold calcium influx, but were not believed to interact with CaM. We find a constitutive association between CaM and the Cav3.1 channel at rest that is lost through an activity-dependent and Cav3.1 calcium-dependent CaM dissociation. Moreover, Cav3 calcium influx is sufficient to activate αCaMKII in the cytoplasm in a manner that depends on an intact Cav3.1 C-terminus needed to support the CaM interaction. Our findings thus establish that T-type channel calcium influx invokes a novel dynamic interaction between CaM and Cav3.1 channels to trigger a signaling cascade that leads to αCaMKII activation

Determinants of Synaptic Integration in Cerebellar Neurons

The integration of synaptic inputs by neurons relies on protein channels that conduct specific ions. Cav3 calcium (Ca2+) channels can amplify excitatory postsynaptic potentials (EPSPs) while Ca2+-activated potassium (KCa) channels decrease EPSP amplitude. By comparison, inhibitory postsynaptic potentials (IPSPs) can activate hyperpolarization-activated (HCN) channels that generate a rebound excitatory current at the end of an inhibitory stimulus. This thesis examines how Cav3, KCa, and HCN channels control synaptic integration in cerebellar Purkinje cells and deep cerebellar nuclei (DCN) neurons. These two populations of neurons are central to cerebellar function and represent a dichotomy of synaptic processing, as Purkinje cells receive primarily excitatory inputs, while DCN neurons receive mainly inhibitory inputs. I tested the hypothesis that Cav3-mediated Ca2+ current activates KCa channels to control the summation of parallel fibre EPSPs in Purkinje cells. Patch clamp recordings from in vitro slices of rat cerebellum showed that Cav3 current activates intermediate conductance KCa (KCa3.1) channels, which have previously never been found in central neurons. KCa3.1 channels are activated at hyperpolarized membrane voltages, due to an extended Cav3 channel window current, and suppress summation of low-frequency EPSPs. Dynamic clamp experiments and computer simulations revealed that the Cav3-KCa3.1 complex increases the signal-to-noise ratio for sensory-like parallel fibre inputs undergoing short-term facilitation by selectively suppressing background inputs. In DCN neurons, I tested the hypothesis that Cav3 and HCN channels control the frequency and timing of rebound bursts following inhibition by IPSPs. The results demonstrate that Cav3 and HCN currents are activated during physiological levels of hyperpolarization and modulate rebound bursts. A novel model of a DCN neuron showed that Cav3 current is solely responsible for generation of the rebound burst, while HCN channels increase burst frequency and temporal precision. Together, this research demonstrates how a novel Cav3-KCa3.1 channel complex participates in the processing of excitatory inputs, and identifies a new synergistic interaction between ion channels that enables processing of inhibitory inputs. These findings illustrate the importance of ion channel interactions for signal processing in the cerebellum, with far reaching implications for neural circuits throughout the brain

Signal processing by T-type calcium channel interactions in the cerebellum

T-type calcium channels of the Cav3 family are unique among voltage-gated calcium channels due to their low activation voltage, rapid inactivation, and small single channel conductance. These special properties allow Cav3 calcium channels to regulate neuronal processing in the subthreshold voltage range. Here, we review two different subthreshold ion channel interactions involving Cav3 channels and explore the ability of these interactions to expand the functional roles of Cav3 channels. In cerebellar Purkinje cells, Cav3 and intermediate conductance calcium-activated potassium (IKCa) channels form a novel complex which creates a low voltage-activated, transient outward current capable of suppressing temporal summation of excitatory postsynaptic potentials (EPSPs). In large diameter neurons of the deep cerebellar nuclei, Cav3-mediated calcium current (IT) and hyperpolarization-activated cation current (IH) are activated during trains of IPSPs. These currents have distinct, and yet synergistic, roles in the subthreshold domain with IT generating a rebound burst and IH controlling first spike latency and rebound spike precision. However, by shortening the membrane time constant the membrane returns towards resting value at a faster rate, allowing IH to increase the efficacy of IT, and increase the range of burst frequencies that can be generated. The net effect of Cav3 channels thus depends on the channels with which they are paired. When expressed in a complex with a KCa channel, Cav3 channels reduce excitability when processing excitatory inputs. If functionally coupled with an HCN channel, the depolarizing effect of Cav3 channels is accentuated, allowing for efficient inversion of inhibitory inputs to generate a rebound burst output. Therefore, signal processing relies not only on the activity of individual subtypes of channels but also on complex interactions between ion channels whether based on a physical complex or by indirect effects on membrane properties