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At least 1,603 records · Page 89Linked to original sources
PubMed1975

Chloralose induced alteration of visually evoked response from specific and non-specific regions of cat neocortex.

Visually evoked response (VER) and EEG from the motor cortex (precruciate gyrus) and the visual cortex (marginal gyrus) of cats were recorded from 4 to 7 h after the injection of anesthetic doses of alpha-chloralose. During the recording period the VER from the precruciat gyrus showed a 200-300% increase in amplitude while the VER from the marginal gyrus rarely varied more than 50% in amplitude, and did so independent of the changes in the VER from the precruciate gyrus. The number of large amplitude spikes in the EEG from the precruciate gyrus also increased dramatically during the recording period, but no definite correlation between changes in VER amplitude and in the number of spikes in the EEG could be demonstrated. These observations suggest a functional separation between specific and nonspecific sensory pathways, with the latter showing a considerably greater sensitivity to level of anesthesia.

Animals↗
PubMed1976

Visual evoked potentials during the development of a spiking cobalt focus in rat neocortex.

Averaged visual evoked potentials recorded from three electrode placements in visual cortex in response to single and paired light flashes were acquired from rats with epileptogenic cobalt implants or with stainless-steel control implants. Evoked potentials acquired after computer-detected epileptic spikes were also recorded from rats in the cobalt group. Epileptic spiking began between the 6th and 9th postoperative days and flashes then began to evoke epileptic spikes. Excitability cycles were assessed. On the day showing the maximum rate of spiking, excitability at the site of the cobalt was markedly reduced following flash-triggered or spontaneous epileptic spikes in almost all cases. By contrast, the electrode placement in contralateral homotopic cortex showed nearly normal excitability despite the presence of large amplitude epileptiform spikes and sharp waves projected from the site of the cobalt. The results are discussed with reference to other experimental findings.

Animals↗
PubMed1991

Lesions of nucleus basalis alter ChAT activity and EEG in rat frontal neocortex.

The EEG was recorded from frontal, parietal and visual cortices of sham-operated control rats and rats having ibotenic acid lesions of the nucleus basalis. Recordings were made during a period of rest and during stimulus-evoked desynchronization. Spectral power was determined using a Fast Fourier Transform routine; 3 artifact-free 4 sec epochs of resting activity and two 4 sec epochs of activated EEG were analyzed. Choline acetyltransferase activity (ChAT) was measured in each cortical area and was reduced in lesioned animals an average of 25% in frontal cortex, 19% in the parietal region and 10% in visual cortex. The percent of low frequency activity (1-12 Hz) in the frontal EEG was significantly greater in lesioned animals than in the control group during quiet rest; a significant correlation was found between ChAT activity and power in this band. Desynchronized activity was largely unaffected except for a reduction in 25-31 Hz activity in the frontal cortex of lesioned animals. EEG activity in both the parietal and visual areas was unchanged from control values.

Animals↗
PubMed1978

Adenosine modulates depolarization-induced release of 3H-noradrenaline from slices of rat brain neocortex.

The effects of adenosine and some related purines on the K+-induced release of 3H-noradrenaline from rat cerebral cortex slices were determined in a superfusion system. Adenosine and ATP caused a dose-dependent inhibition of 3H-NA release with a maximal effect of 35% at 10(-4) M. Theophylline, 10(-4) M, antagonized the inhibitory effect of adenosine. The results support the hypothesis that at least some of the central stimulant effects of the methylxanthines could be related to blockade of a purinergic inhibitory tone on noradrenergic synaptic output.

Adenosine↗
PubMed1981

Reversal of noradrenaline denervation-induced increase of beta-adrenoreceptor binding in rat neocortex by noradrenaline infusion.

The effect of intraventricular infusion of (-)-noradrenaline (NA) on beta-receptor binding in vitro to homogenates from 6-hydroxydopamine (6-OH-DA)-denervated and from normal rat cerebral cortex was studied. NA was infused with osmotic minipumps connected to cannulas placed in the right lateral ventricle, delivering 1 or 5 microgram (-)-NA/h continuously for 9 days. One day later the rats were sacrificed and cortical tissue taken for beta-receptor (using [3H]dihydroalprenolol ([3H]DHA) as radioligand) and NA assay. The NA level in the cerebral cortex of 6-OH-DA treated rats was decreased to 70-80% of that of controls. No substantial change in the NA level was observed after infusion of 1 microgram (-)-NA/h, whereas infusion of 5 microgram/h led to a 40-60% increase compared to that of control rats infused with vehicle alone. Infusion of vehicle alone into control rats did not cause any change in [3H]DHA binding, whereas in denervated rats there was a 30-50% increase in [3H]DHA binding compared to that of controls. This increase was completely counteracted by infusion of 1 or 5 microgram (-)-NA/h. Infusion of 1 microgram (-)-NA/h to control rats did not cause any change, while infusion of 5 microgram (-)NA/h led to a significant decrease (-24%) in [3]DHA binding. The present results further support the view that the availability of NA at the receptors controls the number of beta-adrenergic receptors, thereby probably regulating the NA sensitivity of cells with beta-receptors.

Animals↗
PubMed1985

Localisation and pharmacological characterisation of D-2 dopamine receptors in rat cerebral neocortex and cerebellum using [125I]iodosulpride.

Dopamine D-2 receptors were characterised in membranes from all areas of rat cerebral cortex and from cerebellum tested, by using [125I]iodosulpride, a highly selective ligand. The IC50 values of a large variety of dopaminergic and non-dopaminergic agents against [125I]iodosulpride binding in parietal cortex or cerebellum were highly correlated with their IC50 values against [125I]iodosulpride (or [3H]domperidone) binding in striatum. Moreover in the presence of a guanylnucleotide, 5'-guanylylimidodiphosphate (GppNHp), the dopamine inhibition curves of [125I]iodosulpride binding were shifted similarly to the right in the three regions. The density of D-2 receptors in cerebellum and in most areas of the cerebral cortex represented about 1% and 2%, respectively, of their density in striatum whereas the corresponding value in frontal cortex was 4%. Labelling on autoradiographic sections was localised to superficial (I-III) and deep layers (V) of the parietal cortex and to the molecular layer of the cerebellum.

Animals↗
PubMed1995

Neonatal damage to neocortex abolishes the anxiolytic action of diazepam in adult rats.

A neonatal cerebral cortical lesion was made in rats and the effects of diazepam on ultrasonic isolation calls in pups and footshock-elicited ultrasonic distress calls in young adult rats were assessed. There was no indication that the cortical lesion influenced the production of the ultrasonic distress calls in either pups or adults. Diazepam attenuated the ultrasonic isolation calls in all the pups with and without cortical lesion, and the distress calls in normal adult rats. However, diazepam failed to exert the effect in rats which received a neonatal cortical lesion. 8-Hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT), another anxiolytic, was effective to diminish the distress calls even in the adult rats which had had the neonatal damage to the cortex. These findings indicate that the intact cerebral cortex is not always required for production of ultrasonic distress calls; however, the development of the neuronal mechanism involving benzodiazepine receptors to inhibit the ultrasonic expression of anxiety or fear in adult rats is dependent on the integrity of the cerebral cortex.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1994

Characterization of the GABA autoreceptor in human neocortex as a pharmacological subtype of the GABAB receptor.

Release-regulating gamma-aminobutyric acidB (GABAB) autoreceptors were studied in synaptosomes from fresh specimens of human cerebral cortex. The K+ (12 mM)-evoked overflow of [3H]GABA was inhibited by the GABAB receptor agonists (-)-baclofen (EC50 = 1.48 microM) and 3-aminopropylphosphinic acid (3-APPA; EC50 = 0.034 microM). The effect of 10 microM (-)-baclofen was differentially reduced by the three GABAB receptor antagonists CGP 52432 ([3-[[(3,4-dichlorophenyl)methyl)amino]propyl]-(diethoxymethyl)- phosphinic acid), phaclofen and CGP 35348 (3-aminopropyl-(diethoxymethyl)- phosphinic acid). CGP 52432 was by far the most potent antagonist (IC50 = 0.09 microM). Phaclofen was about 700-fold less potent than CGP 52432 (IC50 = 70.0 microM) while CGP 35348 was ineffective up to 100 microM. The present results suggest that human and rat GABAB neocortical autoreceptors have similar pharmacological characteristics.

Adolescent↗