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We evaluated simultaneously leukocyte and platelet aggregation in 40 untreated patients soon after atherothrombotic stroke and in 40 healthy controls matched for age, sex and risk factors. Both leukocyte and platelet aggregation were significantly increased in patients relative to controls (p < 0.01 and p < 0.02, respectively). However, whereas leukocyte aggregation was positive in a significantly higher proportion of patients with subsequent major neurological deficit compared to those with minor deficit (71% vs. 19%; p = 0.04), platelet aggregation was similar in the two patient groups. These data suggest different patterns of activation of leukocyte and platelet aggregation in patients with ischemic stroke. This finding may have pathophysiological and clinical implications.

A peculiar deficit of electrophysiological retinal responses to pattern reversal grating stimuli has been reported in Parkinson's disease (PD) patients. A similar abnormality has been reproduced by means of non-selective dopaminergic antagonists in normal humans. Aim of this study was to verify, by means of a selective D2 antagonist (sulpiride) administered to normal subjects, whether a D2 blockade affects the visual electrophysiological performances with the same trend as observed in PD patients. Patterns electroretinogram (PERG) responses to 1 cycle per degree (c/d) of spatial frequency at 1 (transient) and 7.5 (steady state) Hz of temporal modulation of a square-wave grating pattern reversal have been recorded in 19 healthy volunteers before and after the administration of 100 mg i.m. of sulpiride. The data are consistent for the following conclusion: a selective D2 antagonist reduces steady state and delays transient retinal responses as expected for a PD mimicking agent.

A 10-min bilateral carotid occlusion (BCO) in Mongolian gerbils induces transient generalized epileptic discharges in the hippocampal and cortical regions, which are followed by long lasting interictal spiking activity. An initial peak of this activity occurs within 18-36 h after BCO, then it decreases slowly and completely disappears by the 6th-7th day. On the 7th day, morphological evidence shows a selective loss of CA1 hippocampal neurons. 4-(3-Phosphonopropyl)-2-piperazine-carboxylic acid (CPP), a competitive antagonist of the N-methyl-D-aspartate (NMDA) receptor was administered (7 or 15 mg/kg i.p.) immediately after clamping, and again every 12 h for 3 consecutive days. It induced a dose-related depression of epileptic activity, while, on the other hand, at both dosages, it always prevented the loss of CA1 neurons. The results are discussed in view of the different mechanisms mediating cell damage and epileptic activity.

A Collet-Sicard syndrome was observed in a 53-year-old patient with a coiling of the left internal carotid artery just below the skull base. Although impairment of cranial nerves by tortuous vessel compression has frequently been reported, a combined palsy of the last four cranial nerves related to such a mechanism has never been described before.

The effects of bilateral carotid occlusion (BCO) on electroencephalographic (EEG) activity and hippocampal structural integrity was studied in 25 Mongolian gerbils. During BCO EEG became flat in frontal cortex and hippocampus but bilateral spikes and motor signs were recorded during this period. Following release of clamping EEG gradually recovered within 36 h but interictal activity persisted disappearing on the 6th-7th day. At the end of 7 days a selective necrosis of CA1 hippocampal neurons was observed. The results indicate that 10 min cerebral ischemia induces a transient epileptic activity followed by the CA1 neuronal loss. Mechanisms underlying ischemic damage are complex and probably they involve an altered synaptic transmission.

Retinal and occipital visual evoked potentials and event-related potentials (P300) have been recorded in normal human subjects before and after the administration of the dopaminergic receptor antagonist, haloperidol, and/or the dopaminergic precursor L-DOPA. The data show that either retinal or occipital visual potentials and P300 are delayed by haloperidol. These findings are consistent with the hypothesis that haloperidol in healthy subjects mimicks the electrophysiological abnormalities observed in Parkinson's disease. On the other hand, L-DOPA does not generally modify these latencies in normals, while it is known to decrease the same parameters in parkinsonian patients. This is in accord with the involvement of a specific mechanism in the recovery observed in parkinsonian patients after L-DOPA therapy. Our data confirm that the alterations of visual and cognitive potentials observed in Parkinson's disease are closely related to the impairment of dopaminergic transmission.

Electrical stimulation of the ventral tegmental area and substantia nigra produces monosynaptic and polysynaptic excitatory postsynaptic potentials in rat frontal neurons that can be recorded intracellularly. The electrophysiological characteristics of the monosynaptic responses and the possibility that dopamine (DA) mediates these events are discussed.

We describe a case of essential thrombocythemia in a patient with a mild heart failure. The only clinical manifestation consisted of neurologic symptoms. Cerebral CT was able to show boundary zone infarcts. A possible pathogenetic mechanism for the unusual clinical and radiological finding is proposed.

In the present study we analyze whether glycine satisfies some electrophysiological and biochemical criteria to consider it as a putative transmitter in the rat cerebral cortex. Intracellular recordings from rat sensory-motor cortex showed that in 15-20% of the tested neurons glycine hyperpolarized the cell membrane, decreased the firing rate and flattened the evoked EPSP-IPSP sequence by increasing the membrane conductance. The iontophoretic application of strychnine antagonized the block of 'spontaneous' firing and the membrane hyperpolarization induced by glycine. Moreover, in a group of neurons, strychnine decreased the amplitude and duration of the IPSP and brought back the membrane potential to resting values. Previously accumulated [3H]glycine and endogenous glycine were released from cortical synaptosomal preparations by depolarizing stimuli in a Ca2+-dependent way. The release pattern of glycine was qualitatively similar in cortical and in spinal synaptosomes. [14C]Glycine was rapidly synthetized from [14C]serine in cortical synaptosomal preparations, and the newly formed [14C]glycine was released by depolarizing stimuli in a Ca2+-dependent way. It is concluded that glycine, which is generally considered as an inhibitory neurotransmitter in the spinal cord, medulla and pons, may also have a transmitter role in a discrete number of cortical neurons of some mammalian species.U

Intracellular recordings were obtained from rat neostriatal slices. Bath-applied dopamine (1-10 microM) produced a reversible inhibition of the action potentials evoked by direct stimulation and a decrease in the amplitude of the intrastriatally evoked depolarizing postsynaptic potentials. No change in membrane potential was detected during the application of 1-10 microM dopamine. Dopamine application also produced a decrease in anomalous rectification in the depolarizing direction. This subthreshold inward rectification was abolished by tetrodotoxin, but not by calcium-free and cadmium (0.1-1 mM)-containing solutions. The dopamine-induced decrease in excitatory postsynaptic potential amplitude was evident at resting membrane potential or at more positive levels, but was absent at hyperpolarized values of the membrane potential. Addition of bicuculline (50-500 microM) to the medium did not affect the inhibitory action of dopamine. The inhibitory action of dopamine also persisted in calcium-free and cadmium-containing solutions. The adenosine 3',5'-cyclic monophosphate analogue, 8-bromo-adenosine 3',5'-cyclic monophosphate (0.1-1 mM), mimicked the effects produced by D1 receptor activation. Bath application of 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine (SKF 38393) (1-10 microM), a selective D1 dopaminergic agonist, mimicked the effects of micromolar concentrations of dopamine. The D2 dopaminergic agonists, 4,4a,5,6,7,8,8a,9-octahydro-5-n-propyl-2H-pyrazolo-3,4-g-quinoline (LY 171555) and bromocriptine (both at 10 nM-10 microM), had no effects on neostriatal cells. The inhibition induced by micromolar doses of dopamine or SKF 38393 was antagonized by bath applications of R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepin++ +-7-ol (SCH 23390; 0.1-10 microM), a D1-selective antagonist, but not by sulpiride (10 nM-10 microM), a D2 antagonist. We conclude that the inhibitory effect of dopamine on rat striatal neurons is postsynaptically mediated by the activation of D1 dopaminergic receptors via the reduction of a voltage-dependent tetrodotoxin-sensitive inward conductance.

The actions of GABA and glycine (Gly), iontophoretically applied to rat cortical neurons, were compared. These amino acids hyperpolarized the membrane cell, decreasing the membrane resistance. The results show that the ionic mechanisms involved in the inhibitory actions of GABA and Gly are probably the same in contrast with the results obtained in cat cortical neurons.