Biomedical subjects

M Jia

Publications and source records attributed to M Jia.

41 records · Page 3Linked to original sources

PubMed1986

Evidence for interactions between batrachotoxin-modified channels in hybrid neuroblastoma cells.

Current records from voltage-clamped membrane patches containing two batrachotoxin-modified sodium channels were analyzed to determine whether these channels are identical and independent. In most two-channel patches, the experimentally observed probabilities that zero, one, or two channels are open differ from the binomial distribution, demonstrating that the two channels are nonidentical or nonindependent or both. From the same current records, we also determined the rate for the transition from two open channels to one open channel and for the transition from one open channel to zero open channels. These data are consistent with closing rates for the two channels that are equal and independent. Both probability and closing rate data can be fit by a model wherein the channels are identical, the closing rates are independent, and the opening rate is greater when the other channel is closed than when it is open. The implications of this model for analyzing noise spectra and current variance are examined.

Animals↗

PubMed1986

Calcium currents and transmitter output in cultured spinal cord and dorsal root ganglion neurons.

The effects of repetitive activation upon voltage-dependent calcium currents (ICa) and transmitter release were studied in dissociated cell cultures of fetal mouse spinal cord and dorsal root ganglion. Sodium and potassium currents were suppressed with tetrodotoxin (TTX) and tetraethylammonium (TEA) ions, 4-aminopyridine (4-AP), and cesium sulfate. Calcium currents were compared under voltage clamp before and after a series of depolarizing clamp pulses in spinal cord (SC) and dorsal root ganglion (DRG) neurons. Repetitive activation resulted in an exponential decline in ICa, with the decrease in ICa being much more marked in DRG compared with SC neurons. Both voltage-dependent inactivation and inactivation related to the intracellular movement of Ca2+ appeared to be involved in the decrement in ICa with repetitive activation. A decrease in transmitter output occurred with repetitive activation in DRG neurons but not in SC neurons (either excitatory or inhibitory). DRG neuron synaptic boutons had fewer mitochondria than did the boutons of either excitatory or inhibitory of SC neurons. The decrement in both ICa and synaptic transmitter output in DRG neurons could last for prolonged periods (at least minutes) following repetitive activation. We hypothesize that this vulnerability of DRG neurons to repetitive activation may be related, at least in part, to a relative incapacity to maintain a low intracellular calcium ion concentration [Ca]i during periods of increased calcium ingress associated with excitation. Such an incapacity to buffer [Ca]i may be one mechanism leading to the inactive synapses seen in some studies in vitro and in vivo of synaptic transmission.

Animals↗

PubMed1985

The interaction between sex hormone binding globulin and levonorgestrel released from vaginal rings in women.

The levels of levonorgestrel (L-NOG), progesterone and estradiol were measured in plasma samples of 17 normally menstruating women during a control cycle and during a subsequent period (90 days) with a L-NOG-releasing vaginal ring. During days 38-66 after the insertion of the vaginal ring the concentrations of sex hormone binding globulin binding sites (hereafter: SHBG levels) were also assayed. Significant correlations were found not only between the corresponding levels of SHBG and L-NOG during exposure to the latter compound (r = 0.44; P less than 0.05), but also between the levels of SHBG in the control cycle and the levels of L-NOG measured during exposure (r = 0.60; P less than 0.01). Furthermore, the decrease in SHBG levels during the vaginal administration of L-NOG was directly proportional to the levels of SHBG in the pretreatment cycle (r = 0.64; P less than 0.01). A significant relationship was found between the levels of L-NOG (and, hence - indirectly - the levels of SHBG) and the degree of suppression of ovarian function. Thus the levels of L-NOG were lower (P less than 0.01) in the subjects (n = 8) with an apparently normal or partially suppressed ovulatory-like pattern of progesterone than in those subjects (n = 9) in whom progesterone levels were completely suppressed.

Adult↗

PubMedDate not supplied

Opiate peptide receptor types on cultured mouse spinal neurons.

mu, delta and kappa opioid receptor agonists, morphiceptin, Leu-enkephalin and dynorphin reduced monosynaptic EPSPs evoked in spinal cord neurons by stimulation of spinal cord neurons in a mouse cell culture system. The incidence of the cell pairs which responded to morphiceptin, Leu-enkephalin and dynorphin was 3%, 63% and 37% respectively. Statistical analysis showed the effect of Leu-enkephalin was presynaptic. When tested with Leu-enkephalin and dynorphin, 6 cell pairs responded to both Leu-enkephalin and dynorphin, 5 cell pairs only responded to Leu-enkephalin, none of the cell pairs responded only to dynorphin (n = 18). It is suggested that some cells have only delta receptors, but kappa receptors coexist with delta receptors. Opiate receptors of the mu type are rare on SC neurons.

Analgesics↗

PubMedDate not supplied

A presynaptic locus of the action of Met-enkephalin demonstrated in mouse spinal cord cultures.

Monosynaptic excitatory post-synaptic potentials (EPSPs) evoked in spinal cord (SC) neurons by stimulation of dorsal root ganglion (DRG) neurons in cell cultures were reduced by perfusion application of the opiate peptide, Met-enkephalin (2-4 microM). In about 2/3 of cases examined, EPSPs evoked by stimulation of spinal cord cells were also reduced by Met-enkephalin. The effects were antagonized by concomitant perfusion with naloxone (1-2 microM) and recovered when perfusion with Met-enkephalin was stopped. Statistical analysis of synaptic responses indicated that the reduction of EPSP amplitude was due, at least to a major extent, to a decrease in presynaptic transmitter release.

Animals↗