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Aim: To establish the prevalence of incisor hypomineralisation (IH) in a cohort of 12-year-old children in Northern England and to relate the prevalence to gender, socioeconomic status, and the prevalence of molar incisor hypomineralisation (MIH). Method: The study population comprised 12-year-old children participating in the 2008-2009 National Dental Epidemiological Programme in five regions in Northern England. Participating dentists were trained and calibrated in the use of the modified Developmental Defects of Enamel Index. Children were examined at school under direct vision with the aid of a dental mirror. First permanent molars and incisors were recorded for the presence and type of enamel defects greater than 2 mm. A diagnosis of MIH was ascribed to any child with a demarcated defect in any first permanent molar. A diagnosis of IH was ascribed to any child with a demarcated defect in an incisor but with molar sparing. Results: 3,233 children were examined. The prevalence of IH was 11.0 % (95 % CI 11.0-12.2 %). There was a strong positive correlation between the prevalence of MIH and IH in different regions which reached significance ( r = 0.9, p = 0.037) according to Spearman's rho test of correlation. There was a similar pattern of prevalence in the different socioeconomic quintiles although this correlation did not reach significance. The most common teeth affected in IH were the maxillary central incisors, followed by the maxillary lateral incisors and followed by the mandibular incisors. There was no difference in the prevalence of IH by gender. Conclusions: The prevalence of IH was 11.0 %. The variation of prevalence between regions and socioeconomic groups and the distribution of lesions in the teeth were very similar to observations seen in MIH children from the same cohort. [ABSTRACT FROM AUTHOR]

Hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels belong to the superfamily of voltage-gated pore loop channels. HCN channels are unique among vertebrate voltage-gated ion channels, in that they have a reverse voltage-dependence that leads to activation upon hyperpolarization. In addition, voltage-dependent opening of these channels is directly regulated by the binding of cAMP. HCN channels are encoded by four genes (HCN1–4) and are widely expressed throughout the heart and the central nervous system. The current flowing through HCN channels, designated Ih or If, plays a key role in the control of cardiac and neuronal rhythmicity (“pacemaker current”). In addition, Ih contributes to several other neuronal processes, including determination of resting membrane potential, dendritic integration and synaptic transmission. In this review we give an overview on structure, function and regulation of HCN channels. Particular emphasis will be laid on the complex roles of these channels for neuronal function and cardiac rhythmicity. [ABSTRACT FROM AUTHOR]

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A hyperpolarization-activated current recorded from the pyramidal cells of the dorsal cochlear nucleus was investigated in the present study by using 150- to 200-μm-thick brain slices prepared from 6- to 14-day-old Wistar rats. The pyramidal neurones exhibited a slowly activating inward current on hyperpolarization. The reversal potential of this component was –32 ± 3 mV (mean ± SE, n = 6), while its half-activation voltage was –99 ± 1 mV with a slope factor of 10.9 ± 0.4 mV (n = 27). This current was highly sensitive to the extracellular application of both 1 mM Cs+ and 10 μM ZD7288. The electrophysiological properties and the pharmacological sensitivity of this current indicated that it corresponded to a hyperpolarization-activated non-specific cationic current (Ih). Our experiments showed that there was a correlation between the availability of the h-current and the spontaneous activity of the pyramidal cells, suggesting that this conductance acts as a pacemaker current in these neurones. Immunocytochemical experiments were also conducted on freshly isolated pyramidal cells to demonstrate the possible subunit composition of the channels responsible for the genesis of the pyramidal h-current. These investigations indicated the presence of HCN1, HCN2 and HCN4 subunits in the pyramidal cells. [ABSTRACT FROM AUTHOR]

Effects of the bradycardiac agent zatebradine (UL-FS 49) were determined in intracellular and patch-clamp experiments of amphibian rod photoreceptors. Zatebradine (0.3–100 µM) greatly enhanced the bright-light-induced hyperpolarization of membrane potential in frog retinal rods and caused damped oscillations during the membrane potential recovery phase. In inner segments of the rod photoreceptor cells, the hyperpolarization-activated inward current (Ih) contributes to the recovery of the photoresponse. Patch-clamp recordings from newt rod photoreceptor cells revealed that zatebradine caused use- and concentration-dependent (0.1–100 µM) inhibition of Ih: conductance was reduced without effects on the reversal potential or activation voltage. Our data confirmed that the pharmacological properties of Ih in rod photoreceptors were similar to those of Ih in cardiac myocytes. In addition, zatebradine inhibited voltage-gated outward K+ currents (IK), but did not affect L-type Ca2+ currents (ICa). These results are consistent with the inhibition of IK and Ih by zatebradine in other cells, and may explain the oscillations evoked during the recovery phase of the membrane potential. These multiple actions of zatebradine on channels in rod photoreceptors may explain its effects on the electroretinogram (ERG) in vivo and its adverse effects on vision in clinical studies. [ABSTRACT FROM AUTHOR]

The properties of hyperpolarization-activated current in pregnant rat uterus (17–19 days gestation) were investigated using microelectrode and patch-clamp techniques, and isometric tension recording. The resting membrane potentials were –58.4 mV and –48.5 mV in longitudinal and circular muscle cells, respectively. Application of hyperpolarizing current pulses produced a time-dependent anomalous inward rectification of membrane potential only in circular muscle cells. Under voltage-clamp conditions, inward currents (Ih) were activated by long hyperpolarizing pulses below –60 mV in circular but not in longitudinal muscle cells. Application of extracellular but not intracellular Cs+ reduced the amplitude of Ih in a concentration-dependent manner (an IC50 of 0.15 mM). The reversal potential for Ih was –26.2 mV and the slope conductance was 5 nS/pF. Changes in [K+]o and [Na+]o shifted the reversal potential, and Ih amplitude increased with excess [K+]o and decreased with low [Na+]o. The steady-state activation of Ih was well fitted by a Boltzmann equation with a half-activation potential of –84.3 mV and a slope factor of 9.6 mV. Time courses of activation and deactivation of the current strongly depended on membrane potential, and were well fitted by a single exponential function. The activation time constant of Ih was dependent on temperature. In isometric tension recording, application of extracellular Cs+ to the circular muscles reduced the frequency, but not the amplitude, of spontaneous contractions in a concentration-dependent manner. It is concluded that in pregnant rat uterus Ih channels are predominantly distributed in smooth muscle cells from the circular layer. Since Ih is activated at the resting membrane potential, it is likely that this current contributes to the maintenance of resting membrane potential and spontaneous activity in circular smooth muscle cells of late pregnant rats. [ABSTRACT FROM AUTHOR]

Using perforated-patch voltage-clamp recording, a prominent hyperpolarization-activated inward cation current ( Ih) has been identified in dissociated, cultured and replated, superior cervical sympathetic (SCG) neurones from 17-day-old rats. Ih was identified as a slowly activated inward current on hyperpolarizing from –60 mV, with an extrapolated null potential (in 3 mM [K+]out) of –42 mV. The activation range for Ih was –40 to –100 mV, with a half-activation voltage ( V0.5) of –63 mV. The current was suppressed by 1 mM Cs+ but not by 1 mM Ba2+. The reversal potential for the current change induced by Cs+ agreed with the null potential for Ih. Ih conferred strong inward rectification to the current-voltage curve negative to –55 mV in both voltage-clamp and current-clamp recording. This inward rectification was reduced by 1 mM Cs+. In a sample of eight cells with initial resting membrane potentials between –51 and –64 mV, Cs+ increased the resting potential of all cells by between 2.5 and 21 mV. These results indicate that Ih contributes a tonic inward (depolarizing) component to the maintenance of the resting membrane potential in SCG neurones. [ABSTRACT FROM AUTHOR]

In mouse dorsal root ganglion (DRG) neurons the activation curve of the hyperpolarization-activated current ( Ih) shifted towards depolarized potentials when cAMP was present in the pipette. The relation between the midpoint potential and cAMP concentration could be described by a Hill function with a half-maximal concentration of 0.55 μM cAMP, reflecting a direct action of cAMP on the channel. With 5 mM ATP and a saturating concentration of cAMP an additional shift of the midpoint potential is observed which can be explained by phosphorylation. Application of Rp-cAMPS and Sp-cAMPS support the hypothesis of both a phosphorylation pathway and a direct effect exhibited by these molecules. The bell-shaped curves, relating the time constants for the slow and fast current components to the voltage, shifted towards positive membrane potentials when cAMP and ATP were in the pipette. The fully activated Ih/voltage relation and the reversal potential were not dependent on the presence of cAMP or ATP in the pipette. The mean resting membrane potential of –59 mV, using the perforated-patch configuration, hyperpolarized in the presence of extracellular CsCl. In the whole-cell configuration the resting membrane potential was significantly more negative at 0 μM cAMP (–61 mV) than at 100 μM cAMP (–57 mV). Thus, the activation of Ih, regulated by both the intracellular cAMP and the ATP concentration, may influence the excitability of DRG neurons. [ABSTRACT FROM AUTHOR]