Vasopressin pressor receptor-mediated activation of HPA axis by acute ethanol stress in rats.

The plasma arginine vasopressin (AVP), ACTH, and corticosterone levels and the hypothalamic corticotropin-releasing hormone (CRH) content were measured after oral administration of 1 ml of 75% ethanol to rats, a model known to induce acute gastric erosions and stress. Elevated plasma AVP, ACTH, and corticosterone levels were detected 1 h after ethanol administration. Treatment with the vasopressin pressor (V(1)) receptor antagonist [d(CH(2))(5)Tyr(Me)-AVP] before ethanol administration significantly reduced the ACTH and corticosterone level increases.

Vasopressin receptor antagonist OPC-31260 prevents cerebral oedema after subarachnoid haemorrhage.

The effects of the non-peptide vasopressin V2 receptor antagonist, 5-dimethylamino-1-[4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tetrah ydro-1 H-benzazepine hydrochloride (OPC-31260) on the cerebral oedema induced by subarachnoid haemorrhage were studied in rats. Subarachnoid haemorrhage induced significant water retention after water loading, increased the brain content of water and Na+ and increased plasma vasopressin levels. The water retention and brain water and Na+ accumulation were prevented by OPC-31260 administration, but the plasma vasopressin levels were further enhanced by OPC-31260.

Pharmacological actions of essential (zinc, copper) and toxic metal ions (lead, mercury) on neurons and neuronal synapses of the snail, Helix pomatia L.

Actions of zinc, copper, lead and mercury ions on identified neurons and neuronal synapses of the snail, Helix pomatia L. were examined by use of electrophysiological methods. The studied metal ions depolarized the membrane and decreased the resistance but the neuronal excitability changed differentially.

Comparative electrophysiological aspects of aluminum actions on central neurons and neuronal synapses of invertebrate and vertebrate animals.

Aluminum compounds (Al) increased the membrane potential (Em) and decreased the input resistance (Rin) of identified snail neurons. The neuronal excitability increased after Al withdrawal in the washing period. Cumulative Al applications caused dose-dependent modulation of Em and Rin in most of the studied neurons.

Endogenous vasopressin increases acute endotoxin shock-provoked gastrointestinal mucosal injury in the rat.

Administration of a low dose of endotoxin (from Escherichia coli, 3 mg kg(-1), i.v.), which does not affect vascular permeability or blood pressure over 1 h, leads to the release of endogenous vasopressin and damage to the mucosal microvasculature.

Impaired water metabolism and cerebral oedema following experimental subarachnoid haemorrhage in rats(1.).

The acute phase of subarachnoid haemorrhage (SAH) is frequently associated with an impaired water metabolism and a disposition to cerebral oedema. For study of the pathogenesis of brain oedema following SAH, an experimental model of SAH was created in the rat The diuretic curves after water loading, the brain water and electrolyte contents and the plasma and cerebrospinal fluid arginine vasopressin (AVP) levels were examined in rats with SAH. Following a water load, a significant water retention and increases in brain water and sodium contents were observed after subarachnoid bleeding.

Actions of Zn2+ on spontaneous, stimulus and transmitter evoked events in Helix neurons.

Modulatory actions of Zn2+ (0.05-2 mM) on spontaneous, stimulus evoked excitatory postsynaptic potentials (EPSPs) or currents (EPSCs) and GABA, L-glutamate induced depolarizations were examined in current- and voltage-clamp conditions. Identified and unidentified Helix pomatia L.

Cerebral oedema after subarachnoid haemorrhage. Pathogenetic significance of vasopressin.

The authors report the frequency, characteristic clinical symptoms, laboratory alterations and diagnostic criteria of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after subarachnoid haemorrhage. The data on 290 patients with subarachnoid haemorrhage (SAH) during a period of years at the Division of Neurosurgery, University Medical School, Szeged, are analysed. Twenty-seven (9.

Properties of depolarizing plateau potentials in aminopyridine-induced ictal seizure foci of cat motor cortex.

The mechanisms of generation of self-sustained depolarizing plateau potentials (DPs) were studied in intracellular recordings in aminopyridine-induced ictal seizure foci in the motor cortex of the cat. In some experiments single-electrode voltage clamp techniques were used and intracellular pressure injection of aminopyridine (Ap), phorbol esters (PhEs) and tetraethylammonium (TEA) was carried out. After several ictal episodes, DPs with bursts of action potentials or with spike inactivation developed gradually in the clonic and interictal phases, without synchronism with surface ictal seizure potentials.

Long-lasting potentiation of synaptic transmission requires postsynaptic modifications in the neocortex.

The mechanisms of associative long-lasting potentiation (LLP) of excitatory postsynaptic potentials (EPSPs) were studied in the motor cortex of anesthetized cats. Mono- and oligosynaptic EPSPs were evoked by stimulations of thalamic VL nucleus, pyramidal tract, callosal and somatosensory system and paired with orthodromic, antidromic or current-induced action potentials. EPSP-spike stimulus pairs with 0.