THE ROLE OF BROCA’S AREA IN SYNTAX: A TMS STUDY ON WRITTEN GREEK LANGUAGE

A number of recent papers have addressed the potential of transcranial magnetic stimulation (TMS) to interfere with linguistic processes or speech production. In this paper we present an experiment with TMS to clarify the role of Broca’s area in syntactic processing. An experimental paradigm contrasted sentences that require syntactic and semantic decisions on written Greek language. We found a clue of selective priming effects on syntactic decisions but not on semantic decisions. Our results provide evidence of the involvement of Broca’s area in syntax

Somatostatin, cholecystokinin and neuropeptide Y mRNAs in normal and weaver mouse brain

The distribution of mRNAs encoding for somatostatin, cholecystokinin and neuropeptide Y was determined by in situ hybridization histochemistry in the weaver (wv/wv) mouse, a model of dopamine deficiency as well as in normal (+/+) controls. Weaver mutants did not show any appreciable departure from the normal pattern of expression for mRNA encoding for neuropeptide Y. In contrast, an 82% increase in mRNA encoding for somatostatin was observed in the reticular thalamic nucleus, whereas increases in the order of 20-87% were observed in different hypothalamic nuclei of the weaver brain. In addition, a 47-103% increase of the hybridization signal encoding for choleocystokinin was observed in the cerebral cortex, hippocampus and thalamus of the weaver brain. It can be assumed that the elevated and region-specific somatostatin and choleocystokinin levels observed in the weaver brain may be due to a secondary or compensatory response under conditions of altered neurotransmitter levels.This work was supported by a “Career award in Greece to Greek-speaking researchers living abroad” to K.Z. from the General Secreteriat of Research and Technology of GreecePeer Reviewe

[3H]CNQX and NMDA-sensitive [3H]glutamate binding sites and AMPA receptor subunit RNA transcripts in the striatum of normal and weaver mutant mice and effects of ventral mesencephalic grafts

Levels of excitatory amino acid receptors were studied in the weaver mouse model of DA deficiency after unilateral intrastriatal transplantation of El2 +/+ mesencephalic cell suspensions. Graft integration was verified by turning behavior tests and from the topographical levels of the DA transporter, tagged autoradiographically with 3 nM [3H]GBR 12935 (average increase in grafted dorsal striatum compared to nongrafted side, 60%). Autoradiography of 80 nM [3H]CNQX and 100 nM NMDA-sensitive [3H]glutamate binding was carried out to visualize the topography of non-NMDA and NMDA receptors, respectively, in +/+ mice and in recipient weaver mutants 3 months after grafting. Increases of 30% or more were found for [3H]CNQX binding in the dorsal nongrafted weaver striatum compared to +/+, and a further 6-9% increase in grafted weaver compared to nongrafted side. The added increase of non-NMDA receptors in the transplanted striatum might be explained by a presence of such receptors on DA presynaptic endings of graft origin. A 20% increase in NMDA-sensitive [3H]glutamate binding was measured in the dorsal nongrafted weaver striatum compared to +/+. NMDA-sensitive [3H]glutamate binding in the transplanted side of weaver mutants tended to be slightly higher in all areas of the striatal complex compared to the nongrafted side, without reaching conventional levels of statistical significance. Using in situ hybridization histochemistry with synthetic 32P-labeled oligonucleotide probes, we investigated RNA transcripts encoding the four AMPA receptor subunits. RNA transcripts in the striatum are seen with a decreasing signal intensity in the following order: GluRB > GluRA > GluRC > GluRD. The weaver caudate-putamen shows a 12% increase in GluRA subunit mRNA compared to +/+, whereas mesencephalic neuron transplantation leads to slight increases (3%) in the levels of GluRB mRNA in the nucleus accumbens. The results are placed in the context of the important interaction between the converging glutamatergic corticostriatal and the DAergic nigrostriatal pathways in controlling the functional output of the basal ganglia in Parkinson's disease and in experimental models of DA deficiency.Peer Reviewe