Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. High-threshold, slow inactivating inward Ca2+ currents were studied in CA1 pyramidal neurones from rat hippocampal slices using the single-electrode voltage clamp technique. 2. Kainate (50-400 nM) induced a dose-dependent depression of the amplitude of the slow Ca2+ current. At a dose of 200 nM the current amplitude was reduced from -0.63 +/- -0.06 to -0.32 +/- 0.06 nA. Such an effect of kainate was associated with the development of a small inward current (-0.11 +/- 0.03 nA). Kynurenic acid (1 mM) or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 20 microM) fully prevented these actions of kainate. 3. The structurally related kainate analogue alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA; 200 nM) depressed the slow Ca2+ current by 30 +/- 7%, an effect also blocked by CNQX. 4. In low-Na+ medium slow Ca2+ currents were followed by sustained inward tail currents. Kainate reduced both the steady-state Ca2+ current (from -0.98 +/- 0.14 to -0.63 +/- 0.15 nA) and the tail current (from -0.40 +/- 0.04 to -0.14 +/- 0.03 nA). 5. The inactivation process of the slow Ca2+ current was tested by a double-pulse protocol and was found to be enhanced by kainate. 6. Equimolar replacement of Ca2+ by Ba2+ produced larger inward currents followed by prolonged tails. Kainate reduced the Ba2+ steady-state current from -1.77 +/- 0.18 to -1.44 +/- 0.24 nA and the tail current from -0.47 +/- 0.15 to -0.17 +/- 0.05 nA. 7. In current clamp experiments Ca2+ action potentials were recorded from cells loaded with the Ca2+ chelator BAPTA. In these conditions kainate failed to reduce the Ca2+ action potential, while in the absence of BAPTA kainate shortened the Ca2+ action potentials by 30%. 8. It is suggested that low concentrations of kainate reduced the slow Ca2+ current by promoting its inactivation perhaps through a rise in free intracellular Ca2+.
 ...
PMID:Depression of a sustained calcium current by kainate in rat hippocampal neurones in vitro. 177 Apr 44

The effects of the phorbol ester 4 beta-phorbol-12,13 dibutyrate (PDBu) and the protein kinase (PK) inhibitors H-7 and sphingosine were investigated on the short-term potentiation (STP) of the population excitatory postsynaptic potential (EPSP) induced by perfusion of N-methyl-D-aspartate (NMDA) in the stratum radiatum of CA1 of the rat hippocampal slice. Bath perfusion of 130 microM NMDA for 10 s caused an initial depression of the population EPSP followed by a STP, which averaged 46% and lasted 16 min. PDBu (100 nM) perfused for 2 h completely inhibited the NMDA induced STP, suggesting that the stimulation of PKC inhibited an NMDA receptor activated process which induced the STP. The protein kinase inhibitors H-7 and sphingosine did not alter the NMDA induced STP.
 ...
PMID:Inhibition of an N-methyl-D-aspartate induced short-term potentiation in the rat hippocampal slice. 177 45

Brief (5 min) bilateral carotid occlusion in the gerbil produces forebrain ischemia resulting, as previously reported, in almost complete neuronal loss in the CA1 region of the hippocampus; this neuronal destruction occurs between the 4th and 7th day post-ischemia. Various hippocampal biochemical indices were measured from just after such ischemia to 21 days of recirculation, and the temporal pattern of changes compared with that of cell loss. The level of thiobarbiturate reacting substances (TBARS), a measure of lipid peroxidation, was greatly elevated at 30 min after ischemia, rapidly returned to normal levels (by 60 min), but was again elevated on days 4-14. The beginning of this second period of elevation correlated closely with the onset of neuronal loss and the very abrupt and large (to about 32%) decrease in specific N-methyl-D-aspartate (NMDA) binding sites, measured with radioactive CPP. The number of muscarinic binding sites, measured with radioactive quinuclidinyl benzilate, showed an even greater decrease (to 13%) at 21 days post-ischemia, but the decrease was delayed (starting at day 7) and much more gradual than the loss in NMDA binding. In neither case was there any change in binding affinity at any time studied. Acetylcholine (ACh) concentrations were initially greatly decreased (to about 15% at 5 min), transiently increased (to about 130% at 30 min), and then decreased again (to about 15% at 60 min), after which gradual recovery occurred and was completed by day 14. Since no inhibition of choline acetyltransferase activity was observed at any time, the reversible depression in ACh must depend upon some factor other than loss of this key synthetic enzyme.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Time course of changes in lipid peroxidation, pre- and postsynaptic cholinergic indices, NMDA receptor binding and neuronal death in the gerbil hippocampus following transient ischemia. 182 14

Non-associative long-term depression (LTD) of the stratum radiatum input to area CA1 was studied in rat hippocampal slices. Tetanization of either the alveus or stratum oriens produced greater than 30 min depression of the radiatum field EPSP and population spike, but generally only in the presence of picrotoxin. The spike depression was accounted for by the EPSP depression, and could be blocked by prior administration of an N-methyl-D-aspartate receptor antagonist. These data suggest that the induction of non-associative LTD is depolarization-dependent and involves the N-methyl-D-aspartate receptor/channel complex.
 ...
PMID:Heterosynaptic long-term depression is facilitated by blockade of inhibition in area CA1 of the hippocampus. 182 76

A 10-min bilateral carotid occlusion (BCO) in Mongolian gerbils induces transient generalized epileptic discharges in the hippocampal and cortical regions, which are followed by long lasting interictal spiking activity. An initial peak of this activity occurs within 18-36 h after BCO, then it decreases slowly and completely disappears by the 6th-7th day. On the 7th day, morphological evidence shows a selective loss of CA1 hippocampal neurons. 4-(3-Phosphonopropyl)-2-piperazine-carboxylic acid (CPP), a competitive antagonist of the N-methyl-D-aspartate (NMDA) receptor was administered (7 or 15 mg/kg i.p.) immediately after clamping, and again every 12 h for 3 consecutive days. It induced a dose-related depression of epileptic activity, while, on the other hand, at both dosages, it always prevented the loss of CA1 neurons. The results are discussed in view of the different mechanisms mediating cell damage and epileptic activity.
 ...
PMID:Epileptic activity following cerebral ischemia in Mongolian gerbils is depressed by CPP, a competitive antagonist of the N-methyl-D-aspartate receptor. 183 55

Quantal analysis can provide a quantitative description of important aspects of chemical synaptic transmission and its modification. The technique has recently been applied to excitatory synapses within the hippocampus, especially the form of synaptic plasticity known as long-term potentiation. However, these attempts have met with only limited success, in that the individual quantal amplitudes making up the synaptic response generally could not be resolved. Here we have paid attention to the possible instability of the quantal fluctuation pattern over time. We were able to resolve individual quantal component amplitudes for a high proportion of the experiments, and so demonstrate the quantal nature of excitatory transmission in the CA1 region of the hippocampus. Mean quantal amplitudes for individual excitatory postsynaptic potentials were 84-197 microV, with a mean of 131 +/- 29 microV. For periods during which the fluctuation pattern was stable, the variance associated with individual quantal amplitudes was low. We have also used quantal analysis to show that synaptic depression following prolonged stimulation at these synapses is primarily a presynaptic phenomenon.
 ...
PMID:Quantal analysis of excitatory synaptic action and depression in hippocampal slices. 184 19

The blood-brain barrier was breached in urethane anaesthetized rats by infusing hypertonic mannitol or NaCl at high rate under high pressure into one internal carotid artery. Opening of the blood-brain barrier was confirmed by staining of the perfused hemisphere by intravenous Evans Blue dye. Orthodromic-evoked potentials in CA1 region of hippocampus were transiently extinguished, and the extracellular potential in hippocampus and neocortex shifted in the positive direction during hypertonic infusion. After the hypertonic infusion, the permeability of the barrier to K+ was tested by infusing into the internal carotid artery artificial cerebrospinal fluid in which K+ replaced most of the Na+, raising the concentration of K+ in the blood plasma in the superior sagittal sinus to 13-17 mM. Extracellular potential and interstitial potassium concentration ([K+]O) in hippocampus and neocortex, and evoked potentials in hippocampus, remained unchanged during prolonged infusion of high K+, unless and until spreading depression occurred. After a wave of spreading depression, [K+]O returned to baseline in spite of continued high K+ infusion. We conclude that [K+]O in brain tissue is effectively regulated even when colloidal dye can penetrate the blood-brain barrier, but excess K+ may have entered the cerebral interstitial space in scattered patches outside the region sensed by the ion-selective microelectrodes, triggering spreading depression.
 ...
PMID:Osmotic-hypertensive opening of the blood-brain barrier in rats does not necessarily provide access for potassium to cerebral interstitial fluid. 191 Jul 58

Orthodromically evoked field potentials were recorded in the CA1 region of hippocampal slices while perfusing the slices with media containing lead acetate. High-frequency stimulation (HFS) was applied to the stratum radiatum during lead perfusion. In half of the slices investigated, HFS resulted in an initial increase of the evoked responses which decayed again after about 10 min. In the other half the evoked responses increased only after the washout of lead and this potentiation was comparable to untreated controls. The lead-induced depression of the long-term potentiation might be related to the behavioral deficits observed in chronically lead-exposed mammals.
 ...
PMID:Long-term potentiation in rat hippocampal slices is impaired following acute lead perfusion. 192 37

The effect of local pressure application of N-methyl-D-aspartate (NMDA) in the synaptic layer of CA1 pyramidal cells was investigated in the guinea pig hippocampal slice preparation using extracellular recording technique. Application of NMDA produced a transient depression and a subsequent 30-60 min potentiation of the field excitatory postsynaptic potential (EPSP) seen as an increase of the initial slope and amplitude of the EPSP. The increase in amplitude was consistently greater than that of the initial slope. Prior tetanization that caused saturation of long-term potentiation prevented the generation of an NMDA-induced potentiation of the initial slope for more than 1-2 h, but not the generation of an increase of the amplitude.
 ...
PMID:Synaptic potentiation in the hippocampal CA1 region induced by application of N-methyl-D-aspartate. 193 77

To study the type of adaptive modification (tolerance vs. sensitization) in different organism's indices following intermittent cocaine (COC) administrations, acute COC (2 mg/kg, SC)-induced changes in heart and breathing rate, response to increasing noxious stimulation, spontaneous EEG and event-related evoked and slow brain potentials (ERP) registered from the occipital cortex and hippocampal CA1 region were investigated in naive rabbits and one subchronically treated with COC (6 injections at a same dose). Tolerance developed for bradycardia, depression of noxious responsiveness, cortical desynchronization and increase of main components of cortical ERP, typical to acute COC, while the changes in breathing and hippocampal ERP were stable. These changes as well as a significant increase due to COC administrations of the basal values of an animal's noxious responsiveness and increase in relative changes in main component of cortical ERP (N205) are considered as a consequence of adaptive changes in neurophysiological/neurochemical substrate accepting COC action and mediating phenomena tolerance-sensitization and dependence typical to the drug.
 ...
PMID:Activation-induced changes in evoked and slow brain potentials: effect of cocaine in rabbits previously subchronically treated by cocaine. 195 82


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>