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

Long-term potentiation of synaptic efficacy following tetanic synaptic inputs was described originally in the hippocampus, and it has been studied extensively based on the hypothesis that it represents a synaptic model of learning and memory in the brain. In the cerebral neocortex, studies on LTP have burgeoned later, and have progressed less rapidly than those in the hippocampus. Recently, however, experimental data describing the phenomenology and the mechanisms underlying LTP have accumulated in the neocortex, particularly in the visual, somatosensory, and motor cortices. In the developing visual cortex, LTP has been induced by afferent tetanic stimulation at relatively low frequencies, for long duration. Thus, particular attention has been given to parameters of the tetanus optimal for the induction of cortical LTP, and the differences between these and those effective in inducing hippocampal LTP have been reviewed. In the motor cortex, the associative LTP following combined activation of separate sites as well as homosynaptic LTP following activation of single pathways have been reported and these types of synaptic plasticity have been suggested as being a basis for a certain type of motor learning. Long-lasting depression (LTD) of synaptic efficacy also has been reported in the developing visual cortex and suggested as a neural basis for experience-dependent modifications of visual cortical neurons. LTD has been found in other areas of the neocortex as well, although the probability of its induction is relatively low and its functional significance is not yet clear. Among the possible mechanisms for the induction of LTP and LTD, those including the involvement of NMDA receptors, protein kinase C, Ca2+/calmodulin-dependent kinase II, and membrane-associated cytoskeletal proteins have been reviewed, although the results obtained so far are only fragmentary and are premature for definitive conclusions to be drawn.
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PMID:Long-term potentiation and depression in the cerebral neocortex. 196 84

Previous studies have demonstrated that tetanization of hippocampal mossy fibers induces a long-term potentiation of non-tetanized (heterosynaptic) non-mossy fiber afferents (Schaffer collateral/commissural and fimbrial fibers). Tetanization of these non-mossy fiber afferents, in contrast, does not induce mossy fiber long-term potentiation, but induces a long-term depression of mossy fiber responses (Bradler and Barrionuevo, Synapse 4, 132-142, 1989). The synaptic activity necessary to evoke these heterosynaptic alterations of efficacy is not known. Specifically, the dependence of heterosynaptic efficacy on the activation of N-methyl-D-aspartate receptors has not been assessed. In addition, the capability of different afferents to CA3 neurons to support alterations in heterosynaptic efficacy remains largely unknown. In the present study, heterosynaptic alterations of efficacy in the rat did not require the activation of N-methyl-D-aspartate receptors. Mossy fibers supported N-methyl-D-aspartate receptor-independent heterosynaptic long-term depression, and N-methyl-D-aspartate receptor-independent long-term potentiation. In contrast, non-mossy fiber afferents expressed N-methyl-D-aspartate receptor-independent heterosynaptic long-term potentiation induced by a mossy fiber tetanus, and an N-methyl-D-aspartate receptor-independent long-term depression, in addition to N-methyl-D-aspartate receptor-dependent homosynaptic long-term potentiation. The possibility that non-N-methyl-D-aspartate receptor activity in non-tetanized afferents is necessary for heterosynaptic long-term potentiation induction is discussed. Heterosynaptic long-term depression was induced in the absence of homosynaptic long-term potentiation, suggesting that these concomitant forms of synaptic plasticity rely on different mechanisms.
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PMID:Heterosynaptic correlates of long-term potentiation induction in hippocampal CA3 neurons. 197 27

Adult cats were used to study the recovery of muscles that had become altered by long-term electrical stimulation. Chronic activation was delivered to the deafferented common peroneal nerve (no pain, no reflexes), and contractile properties were measured for peroneus longus muscle. After 4 wk of great daily amounts of treatment at moderately high pulse rates (30-40 Hz delivered during 50% of daily time), the peroneus longus became considerably weaker, demonstrated a longer time course of twitches and a slower rate of rise of tetanic force, and became less fatigable. Furthermore, its twitch-to-tetanus ratio decreased, and there was no longer any depression of electromyogram (EMG) amplitude during fatigue tests. After 4 wk of subsequent rest it was found that 1) twitch speed and maximum tetanic force had returned to nearly normal values, 2) fatigue resistance showed some return toward normal but was still significantly enhanced, and 3) no significant recovery had yet occurred of the altered twitch-to-tetanus ratio, the abolished EMG depression, or the slowed rate of rise of tetanic tension. During the poststimulation recovery period, the progressive increase of isometric twitch speed was not promoted by the administration of small daily amounts of high-rate stimulation (100-Hz bursts). The results support the conclusions that 1) the time course of recovery differs among physiological properties, 2) the EMG and force reactions that occur during a fatigue test are not strongly coupled, as demonstrated by the alterations of their relationship during poststimulation recovery, and 3) in cat's fast muscles, there is still no evidence for rate-specific effects of chronic stimulation on isometric twitch speed.
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PMID:Recovery after intense chronic stimulation: a physiological study of cat's fast muscle. 205 55

mRNAs encoding the light chain of tetanus and botulinum neurotoxins were transcribed, in vitro, from the cloned and specifically truncated genes of Clostridium tetani and Clostridium botulinum, respectively, and injected into presynaptic identified cholinergic neurons of the buccal ganglia of Aplysia californica. The size of the current response measured in the voltage clamped postsynaptic neuron was taken as indicator of the quantity of acetylcholine released. Depression of neurotransmitter release similar to that observed when native light chains of the two toxins were injected but needing an additional delay of 30 to 40 minutes, demonstrated a successful expression of a foreign mRNA injected into a neuron in situ.
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PMID:Molecular biology of Clostridial toxins: expression of mRNAs encoding tetanus and botulinum neurotoxins in Aplysia neurons. 207 64

The Complement is one of the major effectors of the humoral aspecific immune system building up a defence mechanism of the organism. As it is known that some hormonal substances like gonadotropin (hCG) and some hormone-like substances (PGE2) influence the entire immunitary system, we wanted to see if they had specific action on the Complement. The measurement of CH50 was carried out using Mayer's method, derived by Ferrazzi and modified by us. Fractions C3 and C4 were measured by means of immunochemistry using Beckman nephelometer. The treatment with hCG (1,000 U + 10 Lf tetanus toxoid) caused an increase in the CH50 and in the fraction C3, while the fraction C4 was not modified. The treatment with PGE2 (0.25 microgram/rat/die) caused a higher increase of CH50 and C3 fraction. It seems possible to acknowledge C3 involvement in the variation of the Complement's haemolytic activity and this could confirm the intervention of the "alternative pathway". The notable increase in the activity of the Complement induced by hCG and PGE2 could indicate an alternative mechanism of activation of the aspecific humoral immunity in the defence of the organism in all those physio-pathological situations where these substances cause a state of depression of cellular mediated activity.
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PMID:Modification of the complement induced by PGE2 and gonadotropins. 212 14

An entry of Ca2+ into postsynaptic sites may play a role in the induction of long-term potentiation (LTP) of synaptic transmission in the visual cortex. To test this hypothesis, a Ca(2+)-chelator was injected into layer II/III neurons of sliced visual cortex obtained from young rats, and excitatory postsynaptic potentials (EPSPs) of these cells to test stimulation of the white matter were observed before and after tetanic stimulation of the same site. To confirm the effectiveness of the tetanus, field potentials reflecting the activities of many cells were recorded with another extracellular electrode. The chelator injection led to long-term depression (LTD) of EPSPs following tetanic stimuli which simultaneously induced LTP of field potentials derived from unchelated cells in most of the slices tested. This suggests that a low concentration of post-synaptic, free Ca2+, when associated with tetanic inputs, may lead to LTD while a rise of Ca2+ may lead to LTP.
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PMID:Long-term depression but not potentiation is induced in Ca(2+)-chelated visual cortex neurons. 212 60

Injection of exogenous mRNA purified from various tissue preparations into cellular translation systems such as Xenopus oocytes has allowed expression of complex proteins (e.g., receptors for neurotransmitters). No evidence for expression of injected exogenous mRNA, however, has been reported in terminally differentiated neurons. If achieved, it would allow the study of long-lasting changes of properties of nerve cells in their functional context. To obtain evidence of such expression, we chose two proteins that produce a detectable effect even at very low intracellular concentrations. Tetanus toxin and botulinum neurotoxin fulfill this criterion, being the most potent neurotoxins known. Both toxins block neurotransmitter release at nanomolar intracellular concentrations. These di-chain proteins, consisting of a light chain and a heavy chain, have recently been sequenced. Their active sites are located (or partly located) on the light chain. mRNAs encoding the light chain of either toxin were transcribed in vitro from the cloned and specifically truncated genes of Clostridium tetani and Clostridium botulinum, respectively, and injected into presynaptic cholinergic neurons of the buccal ganglia of Aplysia californica. Depression of neurotransmitter release appeared in less than 1 hr, demonstrating successful expression of foreign mRNA injected into a neuron in situ.
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PMID:Exogenous mRNA encoding tetanus or botulinum neurotoxins expressed in Aplysia neurons. 223

The effect of the cholinergic agonist carbachol on a putative substrate for memory (long-term potentiation; LTP) was investigated in slices of rat hippocampus (CA1 region). Carbachol (5 microM) increased LTP when the presynaptic depression of the EPSP was controlled. The results indicate that carbachol enhances the effectiveness of the tetanus, probably through postsynaptic mechanisms. This effect may have implications for the role of acetylcholine in memory and the use of cholinergics in memory disorders.
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PMID:Cholinergic stimulation enhances long-term potentiation in the CA1 region of rat hippocampus. 228 Aug 95

Tetanic mossy fiber stimulation transiently reduced recurrent inhibition in the rat dentate gyrus. The post-tetanic depression of inhibition was maximal 200 ms after the tetanus and typically lasted for about 2 s. Phaclofen, a selective gamma-aminobutyric acid-B (GABAB) receptor antagonist, significantly increased the post-tetanic level of inhibition. These results suggest that GABAB receptor activation is important for the development of post tetanic disinhibition. We suggest that GABA released during repetitive firing acts on GABAB receptors on inhibitory interneurons to suppress recurrent inhibition.
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PMID:Phaclofen antagonizes post-tetanic disinhibition in the rat dentate gyrus. 232 80

Piglets less than 8 wk of age that are known by genotype to be malignant hyperthermia-susceptible (MHS) do not usually develop characteristic hyperthermia and limb muscle rigidity in response to a brief halothane exposure (5 min of 3%). To determine whether a malignant hyperthermia (MH) episode could nevertheless be provoked by a more rigorous challenge, both genetically MHS (Pietrain) and normal (Yorkshire) 5-wk-old piglets were exposed to a combined halothane-succinylcholine challenge. Only two of eight MHS piglets developed limb rigidity; however, all MHS piglets (and no normal piglets) developed clinical signs of MH episode initiation during the 30-min challenge. Temperatures rose from 37.4 to 38.6 degrees C in MHS piglets while falling slightly in normal piglets. In MHS piglets, venous pH fell from 7.46 +/- 0.02 to 6.88 +/- 0.07, PVCO2 rose from 36 +/- 2 to 126 +/- 17 mmHg, and plasma concentration of K+ rose from 4.0 +/- 0.1 to 7.1 +/- 0.6 mM, whereas all values remained stable in normal piglets. Muscles removed from the same piglets before the halothane-succinylcholine challenge were exposed to halothane in vitro. The muscles from genetically MHS piglets responded to halothane with characteristic depression of tetanic tension and prolonged tetanus relaxation time but did not develop halothane-induced contractures. We conclude that, in the absence of either halothane-induced limb rigidity or in vitro contractures, these young animals were still susceptible to potentially fatal MH episodes on exposure to appropriate triggering agents. The MH defect is apparently partially masked in piglets and expressed fully only in older pigs.
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PMID:Halothane sensitivity of young pigs in vivo and in vitro. 237 22


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