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)

In acute experiments on cats under deep Nembutal anesthesia punctures of the cortex caused a prolonged negative shift of its surface potential (up to 15 mv, 5.5 min), which was followed by a prolonged positive shift. During these shifts of the potential, both components of the direct response were depressed. The changes in potential and the depression of electric activity spread over the cortex at a mean rate of 65 micrometers/s. The phenomenon arised when the punctures are made with a pipet 20 micrometers and above in diameter. A puncture of the surface structures was critical; passage of the pipet through the middle and deep layers was ineffective. It is assumed that when cortical punctures are made the SD is caused by K(+) ions which leak out of the destroyed glial structures.
 ...
PMID:Spreading depression resulting from cortical punctures. 121 Dec 54

1. The effects of BRL 34915 (cromakalim), a potassium channel opener, have been tested on the epileptiform activity elicited by high dose/concentrations of some calcium antagonists in in vivo (diltiazem) and in vitro (diltiazem and verapamil) experiments in rats. 2. Diltiazem (150-300 mg kg-1, i.p.) induced behavioural and electroencephalographic (EEG) seizures that were completely prevented by cromakalim (10 nmol/10 microliters, i.c.v.). Whereas, pentobarbitone (5-10 mg kg-1, i.p.) only prevented the behavioural component of the seizures. 3. In hippocampal slices, verapamil (1.5-2.0 mM) produced, within 30-60 min of perfusion, a CA1 epileptiform bursting in 80% of the experiments. This epileptiform activity was prevented by the cromakalim concentration (50 microM) that did not affect the control CA1 synaptic transmission per se. Pentobarbitone also prevented verapamil-induced epileptiform bursting only at the concentration (100 microM) that also reduced control CA1 synaptic transmission. 4. Diltiazem (1.5 mM) produced a biphasic excitatory-depressant effect within 60 min of perfusion. A CA1 epileptiform bursting appeared in 100% of the experiments within 30 min of perfusion. These excitatory effects were followed by a depression phase, characterized by a reduction of the magnitude of CA1 excitatory postsynaptic potentials (e.p.s.ps) and population spike. 5. The diltiazem-induced epileptiform bursting was prevented by cromakalim at a concentration (50 microM) that did not affect the control CA1 synaptic transmission per se. Pentobarbitone also prevented the diltiazem-induced epileptiform bursting only at a concentration (100 microM) that also reduced the control CA1 synaptic transmission. Both cromakalim (50 microM) and pentobarbitone (100 microM) failed to affect the depressant effects of diltiazem on CA1 hippocampal area. On the contrary, high (3.3mM) calcium solutions prevented both the excitatory and the depressant effects of 1.5 mm diltiazem within 60 min.6. These data indicate an involvement of potassium currents in the epileptiform activity elicited by high doses of diltiazem and verapamil.
 ...
PMID:Cromakalim (BRL 34915) counteracts the epileptiform activity elicited by diltiazem and verapamil in rats. 166 91

Locomotor stepping can be elicited by brain stimulation at various diencephalic sites under moderate levels of Nembutal. This study determined if locomotor initiation measured under anesthesia provides a valid measure of the intersite factors which determine initiation in the awake condition. We compared the latencies to initiate locomotor stepping elicited by electrical stimulation (50 microA, 0.5-msec pulses, 10 to 160 Hz) by rats tested while awake and unrestrained in a rotary runway or anesthetized and held in a stereotaxic apparatus. In the latter tests, initial anesthesia was provided by Nembutal (25 mg/kg) and 2% halothane and maintenance anesthesia was provided by 7 mg/kg as needed and local injections of lidocaine. For 30 sites in 16 rats, average locomotor initiation latency in the awake condition and the shortest latencies in the anesthetized condition were positively correlated (r = .78). Locomotion at sites with long latencies in the awake condition was frequently blocked in the anesthetized condition, but sites with short latencies were rarely blocked. The results indicate that the shortest locomotor latencies in the anesthetized condition approximate the latencies measured in the awake condition. It is concluded that the anesthetized condition can provide valid initiation measures, but sites with long latencies in the awake condition are prone to depression under anesthesia.
 ...
PMID:Latency to initiate locomotion elicited by stimulation of the diencephalon positively correlates in awake and anesthetized rats. 221 98

Parameters of electrical stimulation (ES) of the rats cerebral cortex which synaptically induced spreading depression (SD) in deep structures were found. The thalamic SD was regularly triggered by short (0.02-0.05 s) high-frequency (200-500 Hz) ES of the parietal cortical surface. In this case the EEG control showed the absence of any seizure activity in the cortical and subcortical structures. Nembutal (20-40 mg/kg) raised the SD thresholds, but did not prevent the short-latency thalamic SD. The ES of the parietal cortex was not sufficiently effective for SD synaptic excitation in the hippocampus and caudate nucleus. In contrast to the thalamic SD, the hippocampal one was accompanied by the episodes of epileptiform activity at certain SD phases. Thus, the low subseizure threshold of the synaptically triggered cortical and subcortical SD should be taken into account when biological purpose of the SD is discussed.
 ...
PMID:[Spreading depression in the thalamus, hippocampus and caudate nucleus of the rat during electrical stimulation of the parietal area of the cortex]. 233 31

1. A comparison was made between the influences of supramammillary (SUM) and medial septal (MS) nuclei on hippocampal physiology in Nembutal-anesthetized rats. Specifically, the effects of prestimulation of the SUM or MS on the perforant path-dentate field potential, on spontaneous activity of single units, and on perforant path-induced unit activation were assessed. Another series of experiments addressed the issue of whether the SUM and MS effects on the perforant path-dentate field response are independent. 2. Prestimulation of the SUM or MS significantly facilitated the perforant path-dentate population spike with no clear effect on the field excitatory postsynaptic potential (EPSP) recorded in the subgranular zone of the dentate hilus. Prestimulation of either nucleus also reduced the threshold for spike onset. The major differences between the two spike facilitation effects were the magnitude of the change and possibly the optimal interstimulus intervals required to obtain the effects. 3. Acute transection of the ipsilateral column of fornix or dorsal fornix eliminated the SUM population spike facilitation effect. MS lesion or dorsal fornix/fimbria transection eliminated the MS spike facilitation effect. The MS lesion did not alter the effects of SUM prestimulation. Cingulum or medial forebrain bundle transection affected neither SUM- nor MS-mediated spike facilitation. Thus the SUM and MS influences on the dentate field response appear to be independent of one another. The relevant SUM afferents travel through the ipsilateral column of fornix and dorsal fornix, whereas MS afferents project through the dorsal fornix/fimbria. 4. Single units recorded in stratum granulosum (SG) were assessed with respect to several parameters. These included the mean firing rate, whether or not excitation occurred prior to the field population spike and at lower threshold, and whether or not a driven unit responded to a second perforant path stimulus delivered at short latency following the first (during the period of population spike depression). The latter parameter in particular appeared to separate SG cells into two classes. The cells that were not activated during the second field potential were classified as granule cells, whereas those that were activated were classified as basket cells. Based on this distinction, significant differences were also found between the two cell classes on the other parameters. In particular, cells classified as granule cells often had very low firing rates.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:A comparison of supramammillary and medial septal influences on hippocampal field potentials and single-unit activity. 249 75

Excitatory synaptic transmission, induced by electrical stimulation of optic nerve fibres on relay neurones, was recorded from in vitro preparations of the optic tectum of the frog. Bath-applied glutamate (the putative excitatory transmitter of the optic nerve) produced transient enhancement of tectal field potentials, followed by a depression, presumably caused by sustained neuronal depolarization. Pentobarbitone potently antagonized the depressant effect of glutamate, producing an approximate 50% reduction in the response of the tectum to glutamate at 25 microM. Midazolam also decreased the effect of glutamate with an IC50 value of 5 nM. Since, in the optic tectum of the frog, neither pentobarbitone nor midazolam enhance responses to bath-applied GABA, it is suggested that this area of the brain is a useful preparation in which to investigate the interaction of barbiturates and benzodiazepines with glutamate receptor mechanisms, without concurrent interactions with GABAergic processes.
 ...
PMID:Antagonism of the actions of glutamate by pentobarbitone or midazolam in the frog optic tectum in vitro. 281 83

Short latency somatosensory evoked potential (SSEP) was recorded in cats to identify the potentials originating from the cortex and the thalamus, and the following results were obtained. When SSEP was elicited on the bregma by stimulation of the contralateral superficial radial nerve, P2, P4, P4.5, P5.5, P7, P8, N8.5, P11, P9.5, N11.5, N12.5 and N14 were recognized. Of these components N11.5, N12.5 and N14 consisted of large negative potential (LNP). When KCl was applied to the sensorimotor cortex to induce spreading depression, the positive component of the primary evoked potential was markedly decreased and the negative component disappeared. In SSEP, components preceding N8.5 were unchanged. N8.5-P11 and P11-N12.5, however, markedly diminished or disappeared. The latency of the first component of the field potential recorded in the VPL nucleus of the thalamus was about 5 ms. When a small amount of Nembutal was injected into VPL nucleus, components between P2 and P4.5 remained unchanged, but P5.5 disappeared. P7, P8 and N8.5 were preserved. The amplitude of N8.5-P11 was markedly decreased and LNP disappeared. From these results, among various components of SSEP, P5.5 should originate from the thalamus, and P7, P8 and N8.5 from the extralemniscal system. N8.5-P11 should mainly represent post-synaptic potential (PSP) in the deep somatic layer, and P11-N12.5 represent PSP in the apical dentrites of the sensorimotor cortex. N14 probably represents PSP via the diffuse projection system. Thus, LNP should consist of complex potentials of specific and non-specific sensory systems.
 ...
PMID:Origin of short latency somatosensory evoked potential in cats: especially potentials derived from thalamus and cortex. 289 Oct 65

Experiments were carried out on cats under Nembutal anaesthesia. The electrodes were placed on the gyrus suprasylvius. The recording macroelectrode and the K+--sensitive microelectrode were placed between two stimulating electrodes (S1 and S2). A strong stimulus applied through S1 elicited a slow surface negative potential (SNP) and an increase in [K/]0. The change of K+ potential correlated in time with SNP but the decay of K+ potential lasted longer. At this time depression of the dendritic potential (DP)--EPSP of apcial dendrites--evoked by stimulation through S2 took place. The greater the negative shift and the [K/]0 increase the greater was the depression. Tetraethylammonium increased SNP and this correlated with a strong depression of DP. Application of KCl or acetylcholine solutions resulted in DP depression. It may be supposed that the depression of dendritic potentials expresses presynaptic inhibition in the cortical neuropile based on the action of K+ ions.
 ...
PMID:On the process of inhibition in the superficial neuropil of the cerebral cortex. 294 82

Pentobarbitone depresses synaptic excitation in the guinea-pig olfactory cortex slice in vitro. A study has been made to elucidate the possible role of gamma-aminobutyric acid (GABA) in this depression by testing pentobarbitone in the presence of high concentrations of the GABA blockers, i.e. picrotoxin or bicuculline. These blockers reduced the action of pentobarbitone; the dose-depression curve for pentobarbitone was shifted to the right by a factor of 2.3. It is concluded that pentobarbitone has a bimodal action, one action via GABA and another unrelated to GABA or Cl- conductances.
 ...
PMID:gamma-Aminobutyric acid partly mediates the pentobarbitone depression of synaptic excitation in the guinea-pig olfactory cortex in vitro. 298 34

4,6,6-Trimethylcaprolactam antagonised GABAA receptor-mediated contractile responses in guinea-pig isolated ileum, displacing the GABA dose-response curve to the right in a non-parallel manner, and causing a depression of the maximum response. Pentobarbitone not only potentiated the GABAA receptor-mediated contractions but also reversed this non-competitive antagonism by 4,6,6-trimethylcaprolactam, shifting the dose-response curve for GABA to the left and restoring the maximum response. It is conclude that this caprolactam acts at the picrotoxin-barbiturate site on the Cl(-)-ionophore complex.
 ...
PMID:Caprolactam-barbiturate interaction at the GABAA receptor complex in the guinea-pig intestine. 301 60


<< Previous 1 2 3 4 5 Next >>