Time-dependent effects of repeated amphetamine treatment on norepinephrine in the hypothalamus and hippocampus assessed with in vivo microdialysis

The effects of repeated amphetamine (AMPH) pretreatment on norepinephrine (NE) neurotransmission in the hypothalamus and hippocampus were assessed using in vivo microdialysis. Rats were pretreated with either saline or an escalating-dose AMPH regimen (1-->10 mg/kg) over 10 consecutive days, and then were withdrawn from AMPH for either 1 day or 30 days, at which time the animals underwent two consecutive days of testing. As expected, repeated treatment with AMPH resulted in time-dependent changes in both spontaneous locomotor activity and in the psychomotor response to a subsequent challenge injection of AMPH. In addition, repeated exposure to AMPH resulted in time-dependent and regionally-specific changes in the basal concentrations of NE in dialysate, and in the NE response to an AMPH challenge. For example, AMPH pretreatment produced a persistent (at least one month) increase in the basal concentration of NE in the hippocampus, but not the hypothalamus, although the response to an AMPH challenge was altered in both structures. It is suggested that AMPH treatment produces adaptations in NE systems that far outlast the acute effects of the drug, and that these may contribute to both transient and more persistent behavioral sequelae associated with the discontinuation of chronic AMPH use.     

Progressive aneurysmal degeneration of cortical venous drainage of dural arteriovenous malformations: case report

OBJECTIVE AND IMPORTANCE: The development of a venous aneurysm associated with dural arteriovenous malformations rarely has been documented in the literature. CLINICAL PRESENTATION: A 64-year-old man with known dural arteriovenous malformations developed a venous aneurysms, as shown on sequential angiograms obtained during 2 years. INTERVENTION: The dural arteriovenous malformations were treated with neuroendovascular embolization and then surgical excision. CONCLUSION: The clinical presentation, diagnosis, and treatment of this unusual case are presented.     

Direct recording of nicotinic responses in presynaptic nerve terminals

Nicotinic acetylcholine receptors are widely expressed in the nervous system, but their functions remain poorly understood. One attractive hypothesis is that the receptors act presynaptically to modulate synaptic transmission. We provide a direct demonstration of presynaptic nicotinic receptors in situ by using whole-cell patch-clamp techniques to record currents in large presynaptic calyces that midbrain neurons form on ciliary neurons. Bath application of nicotine induced inward currents in the calyces capable of generating action potentials that overrode the limited space clamp achievable. The inward currents reversed near 0 mV and showed inward rectification common for neuronal nicotinic receptors. Tetrodotoxin (TTX) blocked the action potentials but not the inward currents. alpha-Bungarotoxin blocked both, consistent with the presynaptic receptors containing alpha7 subunits. Recording from the postsynaptic ciliary neurons during nicotine exposure revealed EPSCs that TTX blocked, presumably by blocking presynaptic action potentials. The postsynaptic cells also displayed bimodal inward currents caused by their own nicotinic receptors; the bimodal currents were not blocked by TTX but were blocked partially by alpha-bungarotoxin and completely by D-tubocurarine. Dye-filling with Lucifer yellow from the recording pipette confirmed the identity of patched structures and showed no dye transfer between calyx and ciliary neuron. When calyces or ciliary neurons were labeled en mass with neurobiotin and biocytin through nerve roots, dye transfer was rarely observed. Thus, electrical synapses were infrequent and unlikely to influence calyx responses. Immunochemical analysis of preganglionic nerve extracts identified receptors that bind alpha-bungarotoxin and contain alpha7 subunits. The results unambiguously document the existence of functional presynaptic nicotinic receptors.     

Cross-language synonyms in the lexicons of bilingual infants: one language or two?

This study tests the widely-cited claim from Volterra & Taeschner (1978), which is reinforced by Clark's PRINCIPLE OF CONTRAST (1987), that young simultaneous bilingual children reject cross-language synonyms in their earliest lexicons. The rejection of translation equivalents is taken by Volterra & Taeschner as support for the idea that the bilingual child possesses a single-language system which includes elements from both languages. We examine first the accuracy of the empirical claim and then its adequacy as support for the argument that bilingual children do not have independent lexical systems in each language. The vocabularies of 27 developing bilinguals were recorded at varying intervals between ages 0;8 and 2;6 using the MacArthur CDI, a standardized parent report form in English and Spanish. The two single-language vocabularies of each bilingual child were compared to determine how many pairs of translation equivalents (TEs) were reported for each child at different stages of development. TEs were observed for all children but one, with an average of 30% of all words coded in the two languages, both at early stages (in vocabularies of 2-12 words) and later (up to 500 words). Thus, Volterra & Taeschner's empirical claim was not upheld. Further, the number of TEs in the bilinguals' two lexicons was shown to be similar to the number of lexical items which co-occurred in the monolingual lexicons of two different children, as observed in 34 random pairings for between-child comparisons. It remains to be shown, therefore, that the bilinguals' lexicons are not composed of two independent systems at a very early age. Furthermore, the results appear to rule out the operation of a strong principle of contrast across languages in early bilingualism.     

Polycyclic aromatic hydrocarbon-DNA adducts in human placenta and modulation by CYP1A1 induction and genotype

This study investigated the relationship in human placenta between polycyclic aromatic hydrocabon (PAH)-DNA adduct levels and two biomarkers of cytochrome P4501A1 (CYP1A1): gene induction evidenced by CYP1A1 mRNA, and a genetic polymorphism, the CYP1A1 MspI RFLP. CYP1A1 codes for an inducible enzyme system that catalyzes the bioactivation of PAHs. Prior research found a high correlation in human lung tissue between CYP1A1 activity and DNA damage from PAHs. The CYP1A1 Mspi RFLP has been linked in some studies to risk of lung cancer. The relationships in human placenta between DNA damage, CYP1A1 activity and genotype have not been well characterized and may be relevant to risks from transplacental PAH exposure. The study cohort consisted of 70 newborns from Krakow, Poland, a city with elevated air pollution, and 90 newborns from nearby Limanowa, an area with lower air pollution but greater indoor coal use. Contrary to results seen previously in lung tissue, CYP1A1 mRNA was not significantly correlated with PAH-DNA adduct levels in the placenta. Smoking (self-reported maternal and infant plasma cotinine) was significantly associated with CYP1A1 mRNA levels (P < 0.01), but not with PAH-DNA adduct levels. Placental PAH-DNA adduct levels were significantly higher in infants with the CYP1A1 MspI restriction site compared with infants without the restriction site (P < 0.01), implicating a genetic factor in inter-individual variation in DNA damage in human placenta. Further studies are needed to determine the relevance of this finding to risk of transplacental carcinogenesis.