We report on the pathological findings in the brains of 8 Parkinson's disease patients treated with deep brain stimulation (DBS) of the thalamic ventral intermediate nucleus (6 cases) and subthalamic nucleus (2 cases). DBS was performed continuously for up to 70 months. All brains showed well‐preserved neural parenchyma and only mild gliosis around the lead track compatible with reactive changes due to surgical placement of the electrode. We conclude that chronic DBS does not cause damage to adjacent brain tissue. Ann Neurol 2000;48:372–376

SUMMARYSynchronized video and high-frequency audio recordings of two trained harbour porpoises searching for and capturing live fish were used to study swimming and echolocation behaviour. One animal repeated the tasks blindfolded. A splash generated by the fish being thrown into the pool or -in controls -by a boat hook indicated prey and stimulated search behaviour. The echolocation sequences were divided into search and approach phases. In the search phase the porpoises displayed a clear range-locking behaviour on landmarks, indicated by a distance-dependent decrease in click interval. Only in trials with fish was the search phase followed by an approach phase. In the initial part of the approach phase the porpoises used a rather constant click interval of around 50 ms. The terminal part started with a sudden drop in click interval at distances around 2-4 m. Close to the prey the terminal part ended with a buzz, characterized by constant click intervals around 1.5 ms. The lag time in the search and the initial part of the approach phase seems to be long enough for the porpoise to process echo information before emitting the next click (pulse mode). However, we assume that during the buzz lag times are too short for pulse mode processing and that distance information is perceived as a 'pitch' with a 'frequency' corresponding to the inverse of the two-way transit time (pitch mode). The swimming speed of the animal was halved when it was blindfolded, while the click intervals hardly changed, resulting in more clicks emitted per metre swum.

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Chordoid glioma of the third ventricle was recently reported as a novel tumor entity of the central nervous system with characteristic clinical and histopathological features (Brat et al., J Neuropathol Exp Neurol 57: 283-290, 1998). Here, we report on a histopathological, immunohistochemical and molecular genetic analysis of five cases of this rare neoplasm. All tumors were immunohistochemically investigated for the expression of various differentiation antigens, the proliferation marker Ki-67, and a panel of selected proto-oncogene and tumor suppressor gene products. These studies revealed a strong expression of GFAP, vimentin, and CD34. In addition, most tumors contained small fractions of neoplastic cells immunoreactive for epithelial membrane antigen, S-100 protein, or cytokeratins. The percentage of Ki-67 positive cells was generally low (<5%). All tumors showed immunoreactivity for the epidermal growth factor receptor and schwannomin/merlin. There was no nuclear accumulation of the p53, p21 (Waf-1) and Mdm2 proteins. To examine genomic alterations associated with the development of chordoid gliomas, we screened 4 tumors by comparative genomic hybridization (CGH) analysis. No chromosomal imbalances were detected. More focussed molecular genetic analyses revealed neither aberrations of the TP53 and CDKN2A tumor suppressor genes nor amplification of the EGFR, CDK4, and MDM2 proto-oncogenes. Our data strongly support the hypothesis that chordoid glioma of the third ventricle constitutes a novel tumor entity characterized by distinct morphological and immunohistochemical features, as well as a lack of chromosomal and genetic alterations commonly found in other types of gliomas or in meningiomas.

The auxiliary subunit ␣ 2 ␦3 modulates the expression and function of voltage-gated calcium channels. Here we show that ␣ 2 ␦3 mRNA is expressed in spiral ganglion neurons and auditory brainstem nuclei and that the protein is required for normal acoustic responses. Genetic deletion of ␣ 2 ␦3 led to impaired auditory processing, with reduced acoustic startle and distorted auditory brainstem responses. ␣ 2 ␦3 Ϫ/Ϫ mice learned to discriminate pure tones, but they failed to discriminate temporally structured amplitude-modulated tones. Light and electron microscopy analyses revealed reduced levels of presynaptic Ca 2ϩ channels and smaller auditory nerve fiber terminals contacting cochlear nucleus bushy cells. Juxtacellular in vivo recordings of sound-evoked activity in ␣ 2 ␦3 Ϫ/Ϫ mice demonstrated impaired transmission at these synapses. Together, our results identify a novel role for the ␣ 2 ␦3 auxiliary subunit in the structure and function of specific synapses in the mammalian auditory pathway and in auditory processing disorders.

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