Ectopic parathyroid adenoma in the submandibular region: a case report.

Ectopic parathyroid adenomas that affect the submandibular region have not been widely reported. We describe a 34-year-old man who presented with a painless swelling of the submandibular region. The identification of hypercalcaemia encouraged us to engage a multidisciplinary team to evaluate further serum changes. Parathyroid hormone analysis, 99mTc-methoxy-isobutyl-isonitrile (99mTc-MIBI) scintigraphy, and single-photon emission computed tomography (SPECT-CT) were done to rule out hyperparathyroidism. Raised parathyroid hormone together with 99mTc-MIBI and SPECT-CT examination were consistent with a tumour caused by the hyperparathyroidism. Removal of the lesion resulted in rapid improvement in serum calcium and parathyroid hormone, and the normalisation of the serum creatinine, concentrations. Histopathological analysis confirmed a parathyroid adenoma. We conclude that ectopic parathyroid adenomas should be considered as part of a differential diagnosis for tumours of the submandibular region.

Three electrophysiological phenotypes of cultured human umbilical vein endothelial cells.

The conventional whole cell patch-clamp technique was used to measure the resting membrane conductance and membrane currents of nonstimulated cultured human umbilical vein endothelial cells (HUVECs) in different ionic conditions. Three electrophysiological phenotypes of cultured HUVECs (n = 122) were determined: first, 20% of cells as type I mainly displaying the inwardly rectifying potassium current (IKi); second, 38% of cells as type II in which IKi was super-posed on a TEA-sensitive, delayed rectifying current; third, 27% of cells as type III predominantly displaying the outwardly rectifying current which was sensitive to TEA and slightly inhibited by a chloride channel blocker niflumic acid (N.A.). In cells of type I, the mean zero-current potential (V0) was dependent on extracellular K+ ([K+]o) but not on Cl-, indicating major permeability to K+. Whereas V0 of type II was also affected by extracellular Cl- ([Cl-]o), indicating the contribution of an outward Cl- current in setting V0. The cells of type III were not sensitive to decrease of [Cl-]o and the outward current was activated in a relative stable voltage range. This varying phenotypic expression and multipotential behavior of HUVECs suggests that the electrical features of HUVEC may be primarily determined by embryonic origin and local effect of the microenvironment. This research provided the detailed electrophysiological knowledge of the endothelial cells.

Effects of Fe(2+) on ion channels: Na(+) channel, delayed rectified and transient outward K(+) channels.

The effects of Fe(2+) on the properties of three types of ion channels were studied in acutely dissociated rat hippocampal pyramidal neurons from area CA1 at postnatal ages of 7-14 days using the whole cell patch clamp technique. The results indicated that: (1) in the existence of Fe(2+), the activation voltage threshold of transient outward K(+) currents (I(A)) was decreased. The normalized current-voltage curves of activation were well fitted with a single Boltzmann function, and the V(1/2) was 2.44+/-1.14 mV (n=15) in control, whereas 1.79+/-1.53 (n=15), -2.96+/-0.92 (n=14), -5.11+/-1.31 (n=13), -9.05+/-1.64 mV (n=12) in 1, 10, 100 and 1000 microM Fe(2+), respectively. Differences between two groups were significant (P<0.05, n=12-15), except for that between the control and 1 microM (P>0.05, n=15). (2) Fe(2+) caused a left shift of the current-voltage curves of steady-state inactivation of I(A) in a concentration-dependent manner. The curves were well fitted with a single Boltzmann function with similar slope (P>0.05, n=10-13). The V(1/2) were -70.71+/-1.23 (n=13), -71.14+/-1.37 (n=13), -78.21+/-1.17 (n=11), -84.61+/-1.34 (n=12), and -89.68+/-2.59 mV (n=10) in control, 1, 10, 100 and 1000 microM Fe(2+), respectively. Fe(2+) also shifted the current-voltage curves of Na(+) channel steady-state inactivation to more negative depolarization potentials in parallel, with V(1/2), -67.37+/-1.33 mV (n=12) in control, and -67.52+/-1.28 mV (n=12), -68.24+/-1.61 mV (n=10), -71.58+/-1.45 mV (n=10), -76.65+/-1.76 mV (n=9) in 1, 10, 100 and 1000 microM Fe(2+) solutions, respectively. (3) In Fe(2+) solutions, the recovery from inactivation of I(A) was slowed. (4) With application of different concentrations of Fe(2+), the voltage threshold of activation of delayed rectified outward K(+) currents (I(K)) was decreased, while Fe(2+) showed a little inhibition at more positive depolarization. Briefly, the results demonstrated that Fe(2+) is a dose- and voltage-dependent, reversible modulator of I(A), I(K) and Na(+) channels. The results will be helpful to explain the mechanism of Fe(2+) physiological function and Fe(2+) intoxication in the central nervous system.

Two components of long-term depression are impaired by chronic lead exposure in area CA1 and dentate gyrus of rat hippocampus in vitro.

Previous studies have demonstrated that low-level lead exposure can impair the induction of long-term depression (LTD) in area CA1 and dentate gyrus (DG) of rat hippocampus in vitro and in vivo. The induction of LTD in area CA1 and DG has been shown to associate with N-methyl-D-aspartate receptors (NMDARs) and voltage-gated calcium channel (VGCC). In this study, the relative contributions of NMDARs-dependent and VGCC-dependent components in the induction of LTD in the hippocampus and the impairments of these two components of LTD by chronic low-level lead exposure were investigated. Neonatal Wistar rats were exposed to lead from parturition to weaning via milk of dams drinking 0.2% lead acetate solution. Field excitatory postsynaptic potentials (EPSPs) were recorded in area CA1 and DG before and after two 15-min trains of 1-Hz low-frequency stimulation (LFS) (2x900 pulses). In area CA1, the amplitude of NMDARs-dependent LTD (NMDA-LTD), in the presence of 10 microM nimodipine (a blocker of L-type Ca(2+) channels), was 80.05+/-2.54% (n=8) and 94.58+/-10.57% (n=8) in the control and lead-exposed rats, respectively. The amplitude of VGCC-dependent LTD (VGCC-LTD), in the presence of 50 microM (-)-2-amino-5-phosphonopentanoic acid (AP5), was 80.36+/-4.08% (n=10) and 93.91+/-7.85% (n=10) in the control and lead-exposed rats, respectively. In area DG the amplitude of NMDA-LTD, with both 50 microM Ni(2+) (a blocker of T-type Ca(2+) channels) and 10 microM nimodipine present, in the control rats (79. 97+/-4.30%, n=8) was significantly larger than that in the lead-exposed rats (91.24+/-11.08%, n=10, P<0.001). The amplitude of VGCC-LTD, with 50 microM AP5 present, was significantly larger in the control rats (70.80+/-3.64%, n=9) than that in the lead-exposed rats (87.60+/-9.00%, n=10, P<0.001). The results suggested that chronic lead exposure affected two components of LTD induction in area CA1 and DG. Furthermore, the impairment of two components by lead exposure might be similar in area CA1, while the impairment of VGCC-LTD might be more serious in DG of hippocampus.

Age-related impairment of long-term depression in area CA1 and dentate gyrus of rat hippocampus following developmental lead exposure in vitro.

Chronic developmental lead exposure is known to be associated with cognitive dysfunction in children. Impairment of the induction of long-term depression (LTD) has been reported in area CA1 and dentate gyrus (DG) of rat hippocampus following chronic lead exposure. The present study was carried out to investigate age-related alterations of LTD in area CA1 and DG of rat hippocampus following developmental lead exposure in vitro. Neonatal Wistar rats were exposed to lead from parturition to weaning via milk of dams drinking 0.2% lead acetate solution. Field excitatory postsynaptic potentials (EPSPs) were recorded in hippocampal slices at various postnatal ages: postnatal day (PND) 17-23, 27-33, and 57-63. Following low-frequency stimulation (LFS, 900 pulses/1 Hz), the average magnitude of LTD is age related. In the controls, LTD magnitude in area CA1 decreased with age, whereas in DG it increased with age. In the lead-exposed groups, the magnitude of LTD declined during development in both area CA1 and DG. The differences of LTD magnitude between the control and lead-exposed rats were 27.26 +/- 9.15% (PND 17-23), 21.59 +/- 12.93% (PND 27-33), and 16.96 +/- 9.33% (PND 57-63) in area CA1, and were 6.95 +/- 9.26%, 17.60 +/- 3.91%, and 33.63 +/- 10.47% in DG, respectively. These results demonstrated that the lead-induced impairment of LTD magnitude was an age-related decline in area CA1 and an age-related increase in area DG of rat hippocampus. Published by Elsevier Science Inc.

Effects of chronic lead exposure on short-term and long-term depression in area CA1 of the rat hippocampus in vivo.

Chronic developmental lead (Pb) exposure to the rat has been reported to impair the long-term potentiation (LTP) in area CA1 and DG of the hippocampus. The present study was performed to investigate the effects of chronic Pb exposure on homosynaptic short-term depression (STD) and long-term depression (LTD) of population spikes (PS) in area CA1 of the rat hippocampus in vivo. Neonatal Wistar rats were exposed to Pb from parturition to weaning via the milk of dams fed with 0.2% lead acetate solution. The input/output (I/O) function, paired-pulse reaction (PPR), the PS were measured in the area CA1 in response to low frequency stimulation (LFS). The results showed that the homo-STD amplitude of PS depotentiation in Pb-exposed rats (87.48 +/- 7.44%, n = 14) was less significant than that in control rats (72.34 +/- 6.05%, n = 18, P<0.05), and the homo-LTD amplitude of PS depotentiation in Pb-exposed rats (72.80 +/- 5.86%, n = 14) was even less significant than that in control rats (47.80 +/- 5.03%, n = 18, P<0.01). The results suggest that chronic Pb exposure in neonatal rats caused impairments in the STD and LTD of area CA1 of hippocampus.

The effects of chronic lead exposure on long-term depression in area CA1 and dentate gyrus of rat hippocampus in vitro.

Long-term potentiation (LTP) and long-term depression (LTD), two forms of synaptic plasticity, are believed to underlie the mechanisms of learning and memory. Previous studies have demonstrated that low-level lead exposure can impair the induction and maintenance of LTP in vivo and in vitro. The present study was carried out to investigate whether the low-level lead exposure affected the induction and maintenance of LTD. Neonatal Wistar rats were exposed to lead from parturition to weaning via milk of dams drinking 0.2% lead acetate solution. Field excitatory postsynaptic potentials (EPSPs) were recorded in hippocampal slices in adult rats (50-65 days) to study the alterations of LTD in area CA1 and dentate gyrus (DG) of hippocampus following chronic lead exposure. The input-output (I/O) curves before conditioning in both areas showed no evident alterations in basic synaptic transmission between the control and lead exposure groups. In area CA1, the mean amplitude of EPSP slope in control rats (61+/-11%, n=15) decreased significantly greater than that in lead-exposed rats (78+/-8%, n=8, P<0.05) following low frequency stimulation (LFS, 1 Hz, 15 min), which lasted at least 45 min. In area DG, with application of the same LFS, the LTD was induced in control rats (72+/-22%, n=8), while the LFS failed to induce LTD in lead-exposed rats (100+/-26%, n=8). These results showed that chronic lead exposure affected the induction of LTD in both area CA1 and DG. The effect of lead on synaptic plasticity in area CA1 was also investigated. The alteration of the amplitude of LTP in hippocampal slices caused by lead was reexamined in order to compare with that on LTD (control: 189+/-23, n=5; lead-exposed: 122+/-12, n=10). The result demonstrated that low-level lead exposure could reduce the range of synaptic plasticity, which might underlie the dysfunction of learning and memory caused by chronic lead exposure.