Pediatric ultrasound: a personal experience during the period 1991-1994.

The ultrasound examination of the eye with A and B scan has become one of the principal diagnostic methods for detecting ocular abnormalities in children because it is a non invasive technique and can be performed without resorting to general anesthesia. The authors report the most unusual and interesting cases from 1,226 examinations performed in the Department of Ophthalmology, Istituto G. Gaslini, Genova, Italy, between January 1991 and December 1994.

Electrocortical desynchronization after microinfusion of kainic acid into the locus coeruleus in rats.

Receptors for the endogenous excitatory amino acid, 1-glutamate, occur in the rat locus coeruleus (LC), an area of the brain involved in the control of sleep/arousal mechanisms and other behavioral functions. However, the functional role of this neurotransmitter system in the LC has yet to be clarified. Therefore, to address this question we have studied the gross behavioral changes and the effects on the electrocortical (ECoG) spectrum power in rats receiving focal injections into the LC of kainic acid, an agonist at the non-N-methyl-D-aspartate (non-NMDA) glutamate receptor subtype. Unilateral injection of kainic acid (25, 50, 100 and 200 pmol) into the rat LC produced contralateral turning, circling and stereotypes; these effects were accompanied by dose-dependent ECoG desynchronization and by a significant decrease in total voltage power and in 6-9, 9-12 and 12-16 Hz bands of the ECoG spectrum. A pretreatment (15 min before) with 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX) (50 and 100 pmol), a competitive non-NMDA receptor antagonist, or with dizocilpine meleate (MK-801) (1 pmol) and 3-(2-carboxy-piperazine-4-yl)-1-propenyl-1-phosphonic acid) (CP-Pene) (10 pmol), two selective NMDA receptor antagonists, injected directly into the LC, abolished the behavioral and ECoG spectrum power effects typically elicited by kainic acid (50 pmol). Similar results were observed in rats pretreated with diazepam (0.5 mg/kg given i.p. 15 min before kainic acid).(ABSTRACT TRUNCATED AT 250 WORDS)

Neuroblastoma IV-S in a patient with bilateral microphthalmia.

Neuroblastoma, a tumor of post-ganglionic sympathetic neurons, may be associated with a variety of genetic defects and congenital malformations (1). We report a case of neuroblastoma (NB) stage IV-S (2) in an infant with bilateral microphthalmia and other ocular malformations.

Panic-like attack induced by microinfusion into the locus coeruleus of antagonists and inverse agonists at GABAA-receptors in rodents.

The microinfusion of drugs inhibiting GABA-ergic transmission into the locus coeruleus (LC) of rats and mice produced a dramatic pattern of behavioural stimulation accompanied by marked electrocortical (ECoG) desynchronization. In rats, unilateral microinfusion into the LC of bicuculline (0.5-4 pmol) produced dose-dependent behavioural stimulation culminating in a panic-like attack, ECoG desynchronization and marked changes in ECoG spectrum power. These effects were prevented by a pretreatment into the same site with muscimol. Similarly, in mice, the microinfusion of ethyl-beta-carboline-3-carboxylate (beta-CCE, 4.1 nmol) into the LC of C57BL/6 mice produced an intense state of behavioural stimulation accompanied by intense stereotyped movements and increased excitability to external stimuli; these effects were prevented by prior microinfusion of diazepam or flumazenil into the same site. In conclusion, the present experiments show that in rodents drug manipulations leading to a decrease in the activity of GABA-benzodiazepine receptor complex in the LC are responsible for the occurrence of panic-like attacks.

Inhibition by pertussis toxin of the soporific effects induced by stimulation of dopamine D2 autoreceptors in the ventral tegmental area in rats.

The behavioural and ECoG spectrum power effects of agonists at dopamine D2 autoreceptors, both after systemic or intracerebral administration, were studied in rats. It was shown that the bilateral injection of apomorphine or (+) 3PPP (0.1, 0.5 and 1.0 nmol for each compound) into the ventral tegmental area produced behavioural and ECoG sleep, accompanied by a statistically-significant increase in ECoG total spectrum power. These effects were completely antagonized by a pretreatment (24, 48 or 72 hr before) with pertussis toxin (0.34 and 3.4 micrograms), given into the same site. Similarly, behavioural sleep and an increase in ECoG total voltage power, produced by systemic administration of apomorphine (263 nmol/kg i.p.), were abolished by pertussis toxin (3.4 micrograms) injected bilaterally into the ventral tegmental area 24, 48 or 72 hr before. In conclusion, the present results suggest that behavioural and ECoG spectrum power effects, triggered by stimulation of dopamine D2 autoreceptors in the ventral tegmental area of rats, seem to be linked to the inhibition of adenylate cyclase activity through a Gi protein and or to other biochemical events linked to Gi proteins.

Age-dependent ECoG spectrum power alterations are reduced by phosphatidylserine in rats.

The present experiments were carried out in order to characterize the changes in ECoG spectrum power occurring in old compared with young rats. In addition, it was planned to ascertain whether chronic treatment with phosphatidylserine affected possible ECoG changes occurring in aged animals. In comparison to 3 months-old rats, the ECoG activity of 13-15 months-old rats showed spontaneous single or bursts of monophasic and biphasic spikes. In addition, spectrum analysis revealed a significant increase in the power of the lowest frequency band (0.25-3 Hz), accompanied by a decrease in 6-9, 9-12 and 12-16 Hz power. Chronic oral or parenteral treatment with phosphatidylserine gradually reversed the changes in ECoG spectrum power occurring in old rats and produced, at the ECoG level, a distribution pattern of single frequency, bands similar to that observed in young animals.

Ventral tegmental area: site through which dopamine D2-receptor agonists evoke behavioural and electrocortical sleep in rats.

1. In freely moving rats the effects on behaviour and electrocortical (ECoG) spectrum power of some dopamine agonists, i.e. apomorphine and (+)-3PPP, given directly into different areas of the rat brain were studied. In particular, dopamine agonists were microinfused in the ventral tegmental area (VTA) and substantia nigra (SN) or into the caudate nucleus, n. accumbens and prefrontal cortex. The ECoG spectrum power effects were continuously analysed by means of a computerized Berg-Fourier analyser as total spectrum power and power in preselected frequency bands. 2. Apomorphine and (+)-3PPP (0.01, 0.1 and 1.0 nmol) given bilaterally into the VTA produced behavioural and ECoG sleep in a dose-dependent fashion. A statistically significant (P less than 0.01) increase in ECoG total spectrum power with a predominant increase in the lower frequency bands (0.25-3, 3-6 and 6-9 Hz) occurred. No behavioural and ECoG changes were evoked by the same doses of apomorphine bilaterally microinfused into the SN or into the caudate nucleus or by (+)-3PPP (1.0 nml) microinjected into the n. accumbens or applied onto the prefrontal cortex. 3. Behavioural and ECoG sleep was also induced in rats after systemic administration of apomorphine (263 nmol kg-1, i.p.). 4. The behavioural and ECoG spectrum power effects of apomorphine (1.0 nmol) bilaterally micro-infused into the VTA were prevented by a previous microinjection into the same site of (-)-sulpiride (9.8 nmol). Similarly, behavioural and ECoG effects evoked by (+)-3PPP (0.1 nmol) given bilaterally into the VTA, were completely antagonized by a previous injection into the same site of haloperidol (16 pmol given 10 min before). In contrast, pretreatment with SCH 23390 (50 pgkg-1, s.c.), a selective antagonist at dopamine Dl-receptors, was unable to antagonize the behavioural and ECoG spectrum power effects of ( +)-3PPP. 5. Soporific effects induced by systemic administration of apomorphine were antagonized by (-)- sulpiride (9.8 nmol) given bilaterally into the VTA 10min before, whereas, yohimbine (1.3 nmol), (an antagonist at alpha 2-adrenoceptors) bilaterally microinfused into the VTA, was ineffective in this respect. 6. The present experiments provide evidence suggesting that stimulation of dopamine D2-receptors located at the cell body level and/or the dendrites of dopaminergic neurones in the VTA may represent the mechanism through which apomorphine or (+)-3PPP exert their soporific effects in rats.