AIMThe effects of morphine on the potassium ionic currents of caudate nucleus neurons of neonatal rat were studied.

METHODSUsing of whole cell voltage clamp technique on caudate nucleus neurons, applied morphine chronically or acutely on it. In order to research the effects of morphine for voltage-gated of potassium ionic currents.

RESULTSThe amplitude of potassium ionic currents are increased by applied morphine acutely in caudate nucleus from (2.6 +/- 0.4) nA to (3.3 +/- 0.5) Na, naloxone can block the effect of morphine on K+ current and the currents are decreased to (2.4 +/- 0.4) nA. If applied morphine in caudate nucleus chronically, the amplitude of potassium ionic currents are increased from (2.6 +/- 0.4) nA to (3.1 +/- 0. 5) nA. After applied naloxone, the currents are decreased to (2.4 +/- 0.4) nA.

CONCLUSIONThe effects of morphine increased potassium ionic currents by micro-opioid receptor mediated and induced the hyper polarization of neurons, leading to inhibition of neural activity.

Animals ; Caudate Nucleus ; cytology ; drug effects ; physiology ; Morphine ; pharmacology ; Neurons ; drug effects ; physiology ; Patch-Clamp Techniques ; Potassium Channels ; drug effects ; physiology ; Rats ; Rats, Wistar

Animals ; Heart ; growth & development ; Myocardium ; metabolism ; Nerve Growth Factors ; genetics ; metabolism ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley

AIMTo make approach to the relationship between the changes of free zinc and ischemic neuronal damage in hippocampus after forebrain ischemia/reperfusion.

METHODSThe models of forebrain ischemia/reperfusion were established in rats. The contents of free Zn2+ were measured by TSQ fluorescence method. The Zn2+ chelator (CaEDTA) was injected into lateral ventricles in order to evaluate the effect of free Zn2+ on ischemic neuronal damage.

RESULTS(1) Zn2+ fluorescence in the hilus of dentate gyrus, CA3 region and the stratum radiatum and stratum oriens of CA1 decreased slightly at forty-eight hours after reperfusion. From seventy-two hours to ninety-six hour after reperfusion, the decreased fluorescence gradually returned to the normal level, but some fluorescence dots were found in pyramidal neurons of CA1 and the hilus of dentate gyrus. Seven days after reperfusion, all the changes of the fluorescence almost recovered. (2) The cell membrane-impermeable Zn2+ chelator CaEDTA could reduce the intracellular concentration of free Zn2+ and reduced neuronal damage after forebrain ischemia/reperfusion.

CONCLUSION(1) The synaptic vesicle Zn2+ released and then translocated into postsynaptic neurons after forebrain ischemia/reperfusion and played a role in ischemic neuronal damage. (2) The cell membrane-impermeable chelator CaEDTA could provide neuroprotection.

Animals ; Brain Ischemia ; metabolism ; pathology ; Hippocampus ; pathology ; Male ; Neurons ; metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; pathology ; Zinc ; metabolism

AIM AND METHODSThe parameters of low frequency stimulation (LFS) were altered systematically (frequencies of 1, 3 or 5 Hz; number of pulses of pulses of 300 or 900; and time lag after high frequency stimulation (HFS) of 20 or 100 min) and examined their effects on depotentiation (DP) of long-term potentiation (LTP) of synaptic transmission in CA1 neurons in hippocampal slices of rat.

RESULTSLTP could be induced by HFS (two trains of 100 Hz, 100 pulses, separated by 30 s) and be reversed to produce DP by a train of LFS of 900 pulses at 3 Hz given 20 min after HFS. DP induced by LFS could be blocked by NMDA receptor antagonist AP5 (50 micromol/L). And significantly reduced effect was observed for LFS at 1 Hz or 5 Hz, with smaller numbers of pulses or a longer time lag from LFS to HFS.

CONCLUSIONThe above results indicate that DP induced in CA1 neurons of rat hippocampal slices is strongly dependent on the parameters of LFS, and the process may be mediated through the NMDA receptor.

Animals ; Electric Stimulation ; methods ; Hippocampus ; cytology ; physiology ; In Vitro Techniques ; Long-Term Potentiation ; Male ; Neurons ; physiology ; Rats ; Rats, Sprague-Dawley ; Synapses ; physiology ; Synaptic Transmission ; physiology

AIMTo investigate the effects of anoxia/reoxygenation on Fos and Jun expression and apoptosis in cultured rat hippocampal neurons.

METHODSThe hippocampal neurons cultured for 12 d were exposed to anoxia environment (90% N2 + 10% CO2) for 4 h and then reoxygenated for 24 h and 72 h. The neurons were immunocytochemically stained using the antiserum against Fos and Jun, and the apoptosis were detected by using the terminal deoxynucleotidyl transferase mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL) method and flow cytometric analysis.

RESULTSThe percentage of Fos and Jun positive neurons and apoptosis neurons in cultured hippocampal neurons after anoxia/reoxygenation increased than those in control.

CONCLUSIONThe occurrence of neurons apoptosis is related to the increase in Fos and Jun expression in cultured hippocampal neurons after anoxia/reoxygenation.

Animals ; Apoptosis ; Cell Hypoxia ; Cells, Cultured ; Genes, fos ; Genes, jun ; Hippocampus ; metabolism ; Neurons ; metabolism ; Oxygen ; metabolism ; Rats ; Rats, Wistar

Animals ; Aorta ; Cells, Cultured ; Chloride Channels ; physiology ; Male ; Muscle, Smooth, Vascular ; drug effects ; metabolism ; physiology ; Pyrazines ; pharmacology ; Rats ; Rats, Sprague-Dawley

AIMTo compare the drinking behavior and c-fos expression induced by chemical or electrical stimulation of subfornical organ (SFO) in rat brain.

METHODSL-glutamic acid microinjection and constant electrical current were used as chemical and electrical stimulation of SFO, respectively. The water intake over 1 h was recorded and Fos expression was examined immunohistochemically.

RESULTSA similar volume of water intake and Fos expression pattern were induced by both methods of stimulation of SFO. These include 11 forebrain areas (organum vasculosum of the lamina terminalis, median preoptic nucleus, hypothalamic paraventricular nucleus, supraoptic nucleus and lateral hypothalamic area, paraventricular nucleus, reunions nucleus and central medial nucleus of thalamus, bed nucleus of the stria terminalis, perifornical dorsal area and substantia innominata) and 4 areas of hindbrain (area postrema, nucleus solitary tract, lateral parabrachial nucleus and dorsal raphe nucleus).

CONCLUSIONThe drinking behavior and Fos expression in brain induced by SFO stimulation are the results of activation of the neuronal bodies in SFO.

Animals ; Brain ; drug effects ; metabolism ; Drinking Behavior ; Electric Stimulation ; Glutamic Acid ; pharmacology ; Male ; Proto-Oncogene Proteins c-fos ; metabolism ; Rats ; Rats, Sprague-Dawley ; Subfornical Organ ; metabolism ; physiology

Animals ; Epilepsy ; immunology ; metabolism ; Hippocampus ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; gamma-Aminobutyric Acid ; immunology ; metabolism

Bronchi ; cytology ; Cell Culture Techniques ; Cells, Cultured ; Humans ; Myocytes, Smooth Muscle ; cytology

Adenosine Triphosphate ; pharmacology ; Animals ; Burns ; metabolism ; Calcium ; metabolism ; Female ; Male ; Mitochondria, Heart ; metabolism ; Rats