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)

Heterosynaptic interactions between the perforant path and Schaffer's collaterals in the field CA1 and between the perforant path and dentate mossy fibres in the field CA3 were investigated in guinea pig hippocampal slices. Using the method of paired stimuli, space-time summation (for 20--50 ms) was observed in both systems with stimuli sub-threshold for spike generation. Spike responses of the neurons to testing stimulation of afferents synapsing upon the terminal parts of apical dendrites (perforant path) were depressed after spike discharge to conditioning stimulation of proximal afferents (for about 20 ms in CA1, and for about 300 ms in CA3). With inverse combination of the stimuli the period of suppression was much shorter (3--8 ms). Tetanization of the mossy fibres was followed by prolonged (2--30 min) depression of the CA3 responses to the perforant path stimulation. No other reliable long-lasting posttetanic heterosynaptic effects were observed.
 ...
PMID:[Heterosynaptic interactions in fields CA1 and CA3 of the hippocampus in vitro]. 22 31

Comparative analysis of functional characteristics of connection between the fields CA3 and CA1 (Schaffer's collaterals) was performed in experiments in vivo (unanaesthetized rabbits) and in vitro (hippocampal slices of guinea-pigs) with extracellular recording of the unitary activity in the field CA1. Weakness of postexcitatory inhibition, absence of responses of the form of suppression of spontaneous activity, higher effectiveness of low-frequency stimulation of Schaffer's collaterals were observed in experiments in vitro. Posttetanic effects were more frequently observed and lasted longer in vitro than in vivo. The dominating effect in vivo was posttetanic depression and in vitro--posttetanic potentiation. The possible reasons for these differences are discussed.
 ...
PMID:[Functional characteristics of connections: Schaffer's collaterals to the CA1 field of the hippocampus in experiments in vivo and in vitro]. 46 Apr 92

This study was a follow-up to our earlier data which indicated that the hippocampus was one of the brain areas in which ethanol had a preferential action. Rabbits were chronically implanted with electrodes in 9 brain areas associated with the hippocampus. The EEG and multiple-unit activity were recorded simultaneously in each area before and for 15 min after i.p. injection of ethanol at dosages of 0, 150, 300, or 600 mg/kg, given in random order. Subjective evaluation of EEG tracings from all brain areas did not disclose any regional differences. The incidence of hippocampal theta rhythm was depressed transiently at the 2 lower doses and was increased in some rabbits at later post-injection times after the largest dose. Quantitative analysis of the unit activity revealed several major effects of ethanol. Individual rabbits varied significantly in their degree of response. The effects of ethanol included phasic decreases and increases, which varied with the brain area and the dose. A predominant depression of MUA occurred in the septum, fimbria/fornix, entorhinal cortex, and CA1 zone of the hippocampus. Large transient increases in MUA were noted in the CA1, hippocampal commissure, and entorhinal cortex. Overall, regional differences in unit activity consisted of a relatively greater effect in the septum, CA1, and the entorhinal cortex. Conspicuously smaller effects were evident in the CA3 and dentate zones of the hippocampus.
 ...
PMID:Differential effects of low doses of ethanol on the impulse activity in various regions of the limbic system. 82 52

Subregions of the rat hippocampal slice were investigated in relation to (a) the presence of long-term potentiation and (b) responsiveness to low-frequency stimulation. Long-term potentiation was observed in CA1, CA3 and dentate. The effect occasionally lasted up to 6 h, developed gradually, and depended upon repeated low-frequency tetani for maximal effect. To low-frequency monosynaptic stimulation, areas CA3 and CA1 exhibit response facilitation whereas the dentate gyrus exhibits response depression. Reponsiveness in all areas was influenced by stimulus frequency. Recovery was rapid in all areas.
 ...
PMID:Long-term and short-term plasticity in the CA1, CA3, and dentate regions of the rat hippocampal slice. 94 67

Field excitatory postsynaptic potentials were recorded in stratum radiatum of CA1 and CA3 in submerged hippocampal slices from adult or newborn (postnatal days 5-25) Wistar rats. In adult slices, excitatory postsynaptic potentials were depressed by glucose removal ("aglycemia") more rapidly and to a greater extent in CA1 than in CA3 [respective mean times to 50% reduction in peak amplitude were 7.5 +/- 0.83 (standard error) min and 12.5 +/- 0.27 (standard error) min]. Subsequent recovery of excitatory postsynaptic potentials in normoglycemic medium was correspondingly quicker in CA3 than in CA1. Transmission failure at the synapses was indicated by the preservation of the afferent volley, and sharp depression of synaptic input-output plots. In the early postnatal period, CA1 excitatory postsynaptic potentials were much more resistant to aglycemia, substantially persisting for as long as 75 min, with full subsequent recovery in normoglycemic medium. The higher resistance of slices from newborn rats progressively disappeared over the first two postnatal weeks.
 ...
PMID:Developmental and regional differences in the vulnerability of rat hippocampal slices to lack of glucose. 131 67

The selective agonist of metabotropic glutamate receptors, t-ACPD (trans-1-aminocyclopentyl-1,3-dicarboxylic acid) (100-250 microM), reversibly inhibited extracellularly recorded EPSP (excitatory postsynaptic potentials) in the CA1 layer of rat hippocampus. This effect was accompanied by depression of electrical excitability of CA1 neurons as revealed by their antidromic stimulation. The excitability of CA3 neurons remained uneffected. Peculiarly, excitatory postsynaptic currents recorded in voltage clamped, internally perfused CA1 cells remained unaltered. Selective depolarization of CA1 neurons may account for the phenomena described.
 ...
PMID:Trans-ACPD selectively inhibits excitability of hippocampal CA1 neurones. 131 17

Dephosphorylation processes of target proteins are critical to the reversible regulation of intracellular signal transduction systems. Further, brain damage such as ischemic insult induces marked changes in protein kinase activity. To study these changes more thoroughly, specific monoclonal antibodies of the A and B subunits of calcineurin (protein phosphatase 2B) were raised, and regional alterations in the immunoreactivity of calcineurin in the rat hippocampus were investigated after a transient forebrain ischemic insult causing selective and delayed hippocampal CA1 pyramidal cell damage. In normal rats it was found that both the calcineurin A and the B subunits showed high immunoreactivity in the dendritic fields of the hippocampal formation. The immunoreactivity of subunit A in the strata oriens, the radiatum of the CA1 subfield and in the stratum lucidum of the CA3 subfield was most intense, whereas the immunoreactivity in the other CA3 subfields and in the dentate gyrus was relatively low. In contrast, the dendritic fields of the hippocampal formation were equally immunoreactive to calcineurin subunit B, although the stratum lucidum of the CA3, where the mossy fibers from the dentate granule cells terminate, showed a very high immunoreactivity of the B subunit. After transient forebrain ischemia in the CA1 subfield, where selective pyramidal cell death occurred two days after this ischemia, a marked loss of immunoreactivity in both subunits was observed, along with morphological pyramidal cell damage. A recovery of the immunoreactivity of A and B subunits in the strata oriens and radiatum was later noted 30 days after ischemia. In the stratum lucidum of the CA3, the immunoreactivity of both the A and B subunits was transiently depressed from 6 to 24 h, followed by a marked immunoreactivity enhancement from four to 30 days after ischemia. Further, in the histologically intact dentate gyrus, both the immunoreactivity of the A and B subunits in the molecular layer were transiently enhanced from four to 14 days after ischemia, particularly in the supragranular layer. The results clearly indicate that the protein dephosphorylation systems were markedly altered in the whole hippocampal formation during the recirculation period following ischemia. Further, the transient depression in the calcineurin immunoreactivity seen in the mossy fiber terminals may reflect modulated synaptic activity of the dentate granule cells, which may play a pivotal role in the delayed and selective death of the CA1 pyramidal cells. Thus, calcineurin appears to be an excellent marker enzyme for the detection of neuronal activity and synaptic plasticity after brain damage, such as an ischemic insult.
 ...
PMID:Alteration in the immunoreactivity of the calcineurin subunits after ischemic hippocampal damage. 132 5

Spontaneous episodes of spreading depression (SD) were observed in the CA3 subfield of immature or young (2-30 days postnatally) hippocampal slices perfused with medium containing 4-aminopyridine (4-AP, 50 microM). SD appeared in 34% of the hippocampal slices examined and was more frequently observed in slices obtained from 11 to 20-day-old animals. SD studied with extracellular field potential recordings consisted of large amplitude (18.7 +/- 1.1 mV, mean +/- S.E.M.) negative DC shifts that lasted 30-250 s. Unlike the epileptiform activity that was concomitantly seen during 4-AP application, SD was blocked by the NMDA receptor antagonist 3-((RS)-2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid (CPP, 2-10 microM). In contrast, 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX, 5 microM), a non-NMDA-type receptor antagonist, blocked the epileptiform activity but only increased the interval between SD episodes. These results demonstrate that immature hippocampal tissue is susceptible to SD episodes, when perfused with 4-AP-containing medium, and that the occurrence of these episodes presumably depends on the activation of the NMDA receptor. In addition these findings indicate that SD shows a sensitivity to excitatory amino acid receptor antagonists that differs from that of the epileptiform activity recorded simultaneously.
 ...
PMID:CPP, an NMDA-receptor antagonist, blocks 4-aminopyridine-induced spreading depression episodes but not epileptiform activity in immature rat hippocampal slices. 134 14

A few mouse minimum lethal doses (MLD) of tetanus toxin injected into rat hippocampus triggers prolonged changes in neuronal function. Spontaneously recurring epileptic discharges arise in both the injected and the contralateral, uninjected hippocampus. The seizures remit after about 6 weeks, to be succeeded by a permanent depression of hippocampal neuronal responses. There is no evidence of any loss of pyramidal cells at this low dose of toxin. Here we studied presumptive inhibitory, GABAergic neurons, using in situ hybridization (ISH) with a probe directed against the mRNA encoding glutamic acid decarboxylase (GAD), at each of 1, 2, 4 and 8 weeks after injection of tetanus toxin. Epileptic activity was recorded from hippocampal slices prepared from both injected and contralateral hippocampi of rats at each time point, unexpectedly persisting until 8 weeks. There were no significant differences in the numbers of neurons containing GAD mRNA between toxin- and vehicle-injected and control rats in any hippocampal subfield, at any survival time, except for an apparently transient loss of hilar signal in vehicle-injected rats at 1 and 2 weeks which we attribute to a significant, transient loss of neuronal GAD mRNA to below the threshold for detection by ISH using this probe. In contrast there was a marked increase in GAD mRNA in the toxin-injected group, which reached a peak at 4 weeks, and returned to control levels by 8 weeks. The changes were bilateral and were most marked in the hilus of the dentate area, but were also significant in CA3 and CA1. Upregulation of GAD mRNA was preceded by an increase in the levels of the mRNA for the alpha subunit of the GTP binding protein, Gs (Gs alpha), at 2 weeks which affected the GABAergic neurons selectively, and not the pyramidal or granule cells. These marked changes in GAD mRNA may contribute to putative adaptive responses within GABAergic neurons, which would help contain epileptic activity in these chronic foci. The changes in GAD expression may be due to mechanisms acting through an increase in mRNA encoding Gs alpha.
 ...
PMID:Increased expression of GAD mRNA during the chronic epileptic syndrome due to intrahippocampal tetanus toxin. 139 47

1. We used simulations of the in vitro CA3 region of the hippocampus to analyse the 5 Hz population oscillations recorded experimentally in carbachol. 2. A simulation model of the in vitro CA3 region was constructed with 1000 pyramidal neurones and 200 inhibitory neurones (100 producing fast inhibitory postsynaptic potentials (IPSPs) and 100 producing slow IPSPs of delayed onset). Each neurone contained nineteen soma-dendritic compartments. Pyramidal neurones contained six voltage- and/or calcium-dependent ionic currents, whose kinetics were consistent with voltage-clamp data. The connectivity and waveform of unitary synaptic events for excitatory and fast inhibitory synapses were consistent with dual intracellular recordings. This network was shown to generate previously described network oscillations, including synchronized bursts recorded in the presence of GABAA blockers, and synchronized synaptic potentials observed during partial blockade of GABAA inhibition. 3. The model generated 5 Hz oscillations as recorded in carbachol under the following conditions: (a) excitatory synaptic conductance was within a limited range; (b) there was blockade of fast and slow IPSPs (consistent with the experimental lack of effect of bicuculline and phaclofen on carbachol oscillations and the known depression of IPSPs by acetylcholine); (c) the after hyperpolarization (AHP) conductance was reduced (consistent with the known pharmacology of carbachol); (d) the apical dendrites of the pyramidal cells were depolarized, as suggested by the carbachol-induced depolarization of pyramidal neurones. Each oscillation was associated in pyramidal cells with a burst of action potentials riding on a depolarizing wave. The N-methyl-D-aspartate (NMDA) type of excitatory synapse was not necessary for the oscillations to occur. 4. Progressive reduction of excitatory synaptic strength led to an oscillation of the same frequency, with bursts riding on smaller EPSPs (consistent with the experiment). Further reduction of excitatory synaptic strength abolished the population oscillation by uncoupling the neurones. When excitatory synaptic conductance was too large, population oscillations were attenuated as the cells switched from a bursting mode to a repetitively firing mode. 5. Increasing the AHP conductance prolonged the interburst interval as expected. Inclusion of slow IPSPs exerted a similar effect. 6. When fast IPSPs were included, an oscillation with different characteristics emerged: a 10 Hz oscillation that was gated by compound GABAA IPSPs. On any oscillatory wave, few pyramidal neurones fired, and the firing of individual neurones was irregular.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Computer simulation of carbachol-driven rhythmic population oscillations in the CA3 region of the in vitro rat hippocampus. 140 30


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