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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exposure of the submerged hippocampal slice to in vitro ischemic conditions (superfusion with hypoxic medium lacking glucose) resulted in a progression of changes in the orthodromically evoked response recorded from the CA1 pyramidal region. There was an early depression of the population spike with no change in the presynaptic fiber volley, followed by a transient return of the population spike and, finally, a complete loss of both the population spike and fiber volley. The adenosine A1 subtype-selective antagonists, 8-phenyltheophylline (8-PT) and 8-cyclopentyltheophylline (8-CPT), greatly attenuated the early depression of the population spike such that the initial loss of the population spike was associated with the loss of the fiber volley. This result suggests that the initial loss of synaptic function in the hippocampal slice during exposure to in vitro ischemic conditions is due to increased levels of the inhibitory neuromodulator, adenosine.
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PMID:Adenosine antagonists alter the synaptic response to in vitro ischemia in the rat hippocampus. 232 29

The action of various concentrations of bicuculline and picrotoxin on fast- and slow-rise IPSPs (fast and slow IPSPs) was studied in CA1 region of hippocampal slice preparations. Antidromic stimulation evoked in neurons studied preferentially fast IPSPs but the orthodromic one was followed by fast and slow IPSPs combined frequently in two-component IPSP. Both types of IPSPs recorded not only in soma but also in apical dendrites of the nerve cell were blocked reversibly by bicuculline and picrotoxine. The degree of their depression depended on the drug dose and duration of the drug action. Slow IPSPs were much more resistant to the action of these blockers than the fast ones. At the same effective concentration of bicuculline or picrotoxin the slow IPSPs were inhibited later and recovered after perfusion with the standard solution earlier than the fast IPSPs. Under tetanic stimulation the difference between the blocking effect of the drugs on the fast and slow IPSPs remained, however IPSPs amplitude reduced much more rapidly than in response to single stimulation. The reason of this phenomenon as well as peculiarities of GABA-receptors that mediated the slow IPSPs are discussed.
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PMID:[The action of bicuculline and picrotoxin on the fast and slow IPSPs of the pyramidal neurons in isolated slices of rat hippocampus]. 233 32

In slices of rat hippocampus, a train of conditioning pulses that would produce long-term potentiation (LTP) if applied to afferent inputs was found to produce a long-lasting depression of Schaffer collateral/commissural synapses on CA1 cells when instead it was applied to the CA1 axons. The depression lasted undiminished for up to 2 h (the maximum duration of recording). Intracellular recording showed that long-term depression (LTD) of e.p.s.p. amplitude occurred in 66% of cells when this antidromic conditioning stimulation was delivered in normal medium, and in 100% of cells when the antidromic stimulation was delivered in medium containing sufficient Mg++ to block all synaptic transmission. We infer that the difference is because conditioning stimuli sometimes activated test synapses in normal Mg++ but could not in high Mg++. The fact that LTD could be induced in high Mg++ eliminates enhanced inhibitory feedback as a possible mechanism of the long lasting synaptic depression and demonstrates that the mechanism is probably postsynaptic. Resting membrane potential and cell input resistance were the same before and after conditioning, so persisting changes in these postsynaptic parameters can not be the explanation for LTD. LTD of the sort described in this paper could have significant implications for models of learning and memory.
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PMID:Long-term depression at synapses in slices of rat hippocampus can be induced by bursts of postsynaptic activity. 235 27

The neurotoxic effects of long-term, low-level exposure to the commercially available insecticide, Fenthion, were examined in the present study. Young (2 month) adult, male Long-Evans rats were dermally exposed to Fenthion (25 mg/kg, 3X week) and sampled after 2 and 10 months exposure to assess neurotoxic damage in the hippocampus using morphological and biochemical endpoints. Histopathology, consisting of gliosis, swollen and necrotic neurons, and cell dropout, occurred in the dentate gyrus (DG), CA4 (hilus), and CA3 sectors as early as 2 months postexposure. Acetylcholinesterase (AChE) staining of brain tissues taken at this time was severely reduced in the septal nuclei, the DG molecular layer, the CA4, and the hippocampus proper. After 10 months exposure to Fenthion, cellular necrosis and gliosis intensified in the CA4 and CA3 regions and occasionally involved the CA2. Radiometric assays of AChE activity in the hippocampus indicated a 65 and 85% depression after 2 and 10 months exposure, respectively. Quinuclidinyl benzilate binding for the hippocampal muscarinic receptor was reduced by 6 and 15%, after 2 and 10 months exposure, respectively. A separate group of older (12 month) rats was exposed to the same dosing regimen of Fenthion and examined for neuropathological damage after 2 and 10 months exposure. Aged animals exposed for only 2 months expressed severe hippocampal degeneration in a pattern similar to that seen in the young adult after 10 months exposure (viz., DG, CA4, CA3). Aged animals exposed for 10 months showed more extensive histopathology of the CA4-2 and occasionally CA1. These observations indicate that in both young adult and aged animals, subchronic, low-level exposure to anticholinesterase compounds can result in serious neurotoxic consequences to the mammalian hippocampus.
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PMID:The neurotoxicity of subchronic acetylcholinesterase (AChE) inhibition in rat hippocampus. 238 36

1. The modulatory effect of serotonin on CA1 pyramidal cells in the hamster (Mesocricetus auratus) hippocampus was examined over a range of temperatures. 2. Following repetitive Schaffer collateral/commissural stimulation, changes in the amplitude of population spikes (the synchronous firing of CA1 pyramidal cells) were recorded in the hamster, a hibernator. Amplitudes were measured after 10 microM serotonin was added to and then withdrawn from the perfusing medium with the temperature of the bath fixed at different temperatures. 3. Between 35 degrees C and 15 degrees C a depression in population spike amplitude of at least 10% was seen in 36 of 43 trials, with an average depression of 68%. No significant temperature dependence of the depressive effect was seen. 4. Following the removal of serotonin from the perfusate, the spike amplitude was enhanced over the same range of temperatures, averaging 33% higher than control values. The enhancement was most pronounced at 35 degrees C and 15 degrees C and smallest at 25 degrees C. 5. Thus, over the entire temperature range of 35 degrees C to 15 degrees C, serotonin exerted a dual modulatory effect on the spike amplitude, a depression followed by an enhancement. Serotonin's modulatory effects on pyramidal cell excitation persist over temperatures encountered as the hamster enters hibernation.
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PMID:Thermal dependence of serotonergic modulation of neural activity in the hamster. 238 82

In rat hippocampal slices which were superfused with low calcium (0.2 mM) medium, stimulation of the alvear fibers elicited an extracellularly recorded antidromic population spike in CA1 pyramidal neurons which was followed by 2-4 afterpotentials. Adenosine (20-40 microM) and the A1-adenosine agonist 1-phenylisopropyladenosine (L-PIA) blocked these afterpotentials without affecting the first spike. Addition of up to 5 mM tetraethylammonium to the superfused medium did not interfere with this adenosine action. But the addition of only 50 microM 4-aminopyridine (4-AP) antagonized almost completely the adenosine- or L-PIA-induced depression of antidromically evoked repetitive firing. It is concluded that functioning of 4-AP-sensitive potassium channels is a prerequisite for this 'antiepileptic' adenosine action. Since a similar pharmacological characteristic has been described for the A-current, it is likely that adenosine acts by turning on this particular potassium current.
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PMID:Non-synaptic modulation of repetitive firing by adenosine is antagonized by 4-aminopyridine in a rat hippocampal slice. 242 36

A paired-pulse stimulus protocol was used to measure angular bundle to dentate gyrus paired-pulse inhibition in rats before and after the occurrence of 36 or 72 seizures elicited from the contralateral CA3 region. The seizures showed progressive lengthening. There was a moderate increase in paired-pulse depression 1 h after 36 seizures and a further increase after 72 seizures. These data demonstrate that the same experimental protocol which produced a decrease in paired-pulse inhibition in the CA1 region caused the opposite effect in the dentate gyrus.
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PMID:Repetitive seizures cause an increase in paired-pulse inhibition in the dentate gyrus. 248 90

Intracellular recording from hippocampal CA1 pyramidal cells was used to characterize the pharmacological properties of muscarinic responses. Results obtained with the M1 antagonist pirenzepine and the M2 antagonist gallamine suggest that an M1 muscarinic receptor is involved in the muscarinic-induced membrane depolarization and blockade of the afterhyperpolarization (AHP). On the other hand, an M2 receptor may be involved in the cholinergic depression of the EPSP and the blockade of the potassium current termed the M-current. Pretreatment of hippocampi with pertussis toxin did not prevent any of the muscarinic responses suggesting that a pertussis toxin-sensitive G-protein is not involved. The M-current, in contrast to the other muscarinic actions, was unaffected by muscarinic agonists which are weak at increasing phosphoinositide (PI) turnover and actually blocked the action of full agonists. This finding suggests that stimulation of PI turnover may be involved in the blockade of the M-current. Although activation of protein kinase C with phorbol esters has little effect on the M-current, intracellular application of inositol trisphosphate did reduce the M-current. We were unable to establish any clear relationship between biochemical effector systems and the muscarinic receptor subtypes.
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PMID:Pharmacological characterization of muscarinic responses in rat hippocampal pyramidal cells. 253 6

1. Reversible effects of brief periods of anoxia (replacing 95% O2-5% CO2 with 95% N2-5% CO2 for 2-4 min) were studied in CA1 neurons in hippocampal slices (from Sprague-Dawley rats), kept in an interface-type chamber at 33.5 degree. 2. The predominant voltage change during anoxia (N2) was a hyperpolarization, accompanied by a marked fall in resistance and excitability; synaptic potentials were also depressed, especially inhibitory postsynaptic potentials (IPSPs). 3. In voltage-current (V-I) plots, the N2-evoked hypolarization had a reversal potential below -90mV, even when recording with 2 M KCl electrodes and after substituting 90% of medium Cl- with isethionate. The accompanying fall in input resistance (RN) is therefore probably caused by an increase in K conductance (in agreement with previous reports). There was evidence that anomalous rectification enhances the fall in RN but limits the hyperpolarization. 4. These effects of anoxia were not fully blocked by any of the K-channel antagonists tested, including Cs, TEA, 4-AP, quinine and apamin. 5. Intracellular injections of Ca chelators caused a variable depression of N2-evoked reductions in RN. 6. It is unlikely that N2 activates ATP-sensitive K channels as tolbutamide enhanced rather than depressed the hyperpolarization and fall in RN. 7. When early depletion of cellular ATP was prevented by incubation in creatine (25 mM for greater than 1 h), even longer anoxic periods produced only minor changes in potential, RN, and synaptic transmission. 8. It was concluded that activation of K conductance by a rise in cytosolic-free Ca2+ is the most plausible of several possible underlying mechanisms.
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PMID:Hypoxic changes in hippocampal neurons. 254 34

1. The effects of brief anoxia (2-4 min) on membrane currents--especially the tetrodotoxin (TTX)-insensitive, Cd2+-sensitive slow inward currents, presumed to be Ca2+ currents--were studied by single-electrode voltage clamp in CA1 and CA3 neurons in submerged hippocampal slices from adult and newborn Wistar rats (PN1-13). 2. In mature neurons, anoxia had no effect on Q-type inward relaxations, but slowly activating C-type outward currents were depressed. The most striking change was the suppression of Ca inward currents (especially the slowly inactivating L-type, by greater than 95%). This effect of anoxia was not sensitive to the N-methyl-D-aspartate (NMDA) receptor blocker, D-aminophosphonovalerate. Anoxia also reversibly abolished the NMDA-evoked inward current. 3. In neurons from newborn animals (PN1-6), Q-type inward relaxations and postanoxic outward currents were very small or undetectable. The slow inward (Ca) currents were smaller than in mature cells, but they showed a clearer separation between low-threshold, fast-inactivating and high-threshold, slowly inactivating currents. Both types of current were more resistant to anoxia (mean depression of L-type was by only 53.3 +/- 5.6%, mean +/- SE). 4. In such immature neurons, the NMDA-evoked inward currents were also more resistant to anoxia. 5. By PN7-13, increasing maturation was reflected in 1) larger voltage-dependent inward currents, 2) increasingly evident Q-type relaxations and postanoxic outward currents, and 3) near-complete blockade of inward currents by anoxia (at PN11-13, mean depression of L-type currents was by 98.5 +/- 1.5%).
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PMID:Anoxia on slow inward currents of immature hippocampal neurons. 255 81


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