Proefschrift Universiteit van Amsterdam. / Met lit. opg. - Met samenvatting in het Nederlands.

Thesis (Ph. D. in Psychology)--Vanderbilt University, May 2005. / Title from title screen. Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1970. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliography.

Ulm, Univ., Diss., 2007.

Thesis (doctoral)--München, 1983.

Issued also as thesis, Paris.

No description available.

No description available.

Compounds that interact with Group II metabotropic glutamate receptors (mGluRs) have antipsychotic effects in animal models. These drugs have also shown efficacy in the treatment of schizophrenia in humans. The mechanism of action is believed to arise from a reduction of glutamatergic transmission in limbic and forebrain regions commonly associated with this disorder. Previous anatomical tracer and lesion studies have revealed that neurons of the paraventricular nucleus of the thalamus (PVT) are an important source of the glutamatergic drive to these specific regions. However, the function of Group II mGluRs in the PVT remains to be determined. Whole-cell recordings from PVT neurons reveal that activation of these receptors has two interesting effects; it reduces calcium entry through voltage-gated calcium channels and it causes neurons to hyperpolarize. These two effects may contribute to affect the excitability of PVT neurons, an action that may underlie the effectiveness of Group II mGluR-activating compounds.

The drug sensitivity of neurones of the Nucleus ventralis lateralis (VL) of the thalamus, and their synaptic activation by electrical stimulation of brachium conjunctivum (BC), precruciate cortex and entopenduncular nucleus, (EN) has been studied in anesthetized and in decerebrate cats. Cells evoked with short latency by BC stimulation were particularly sensitive to excitation by iontophoretically applied acetylcholine (ACh) and L-glutamate (LG) when compared with cells of more dorsal thalamic nuclei. The VL neurones did not exhibit such an enhanced sensitivity to DL-homocysteic acid and N-methyl aspartic acid. The α-methyl derivative of glutamic acid (α-MG) was found in many cases to depress or block the excitation of thalamic neurones by LG, but had no effect on ACh excitation. α-MG sometimes depressed the effects of other excitatory amino acids, but to a lesser degree than those produced by LG. Short latency single action potential and late burst responses evoked in VL by BC or cortical stimulation have been reported by other workers and were confirmed in this study. However, it was found that both cortical and BC stimulus evoked early burst responses which were observed only in anesthetized animals. EN stimulation evoked burst response in VL neurones with latencies of 4-22 msec. Both the early burst and the EN evoked responses could be converted to shorter latency single spikes by iontophoretically applied amino acids and ACh. ACh facilitated synaptic activation by cortical and BC stimuli but could either excite or depress the responses to EN stimulation. Iontophoretically applied atropine and dihydro-β-erythroidine blocked ACh excitation of VL cells but did not alter their synaptic activation, although atropine could reverse the ACh depression of EN evoked responses. Intravenous atropine in doses of 0.5-1.0 mgm/kgm also blocked these ACh effects, but in addition markedly reduced the BC evoked field response in VL without affecting the response to cortical stimulation. It was concluded that the pathways from EN and motor cortex to VL are unlikely to be cholinergically mediated, but that ACh may be the synaptic transmitter for at least part of the cerebello-thalamic pathway. Pentobarbital and α-chloralose were potent blockers of ACh excitation in VL neurones.. It was shown that neurones of EN give rise to collateral axon branches which project to VL and N. centrum-medianum. Stimulation of sensori-motor cortex evoked cell and field responses in the lateral, but not the medial parts of the centrum medianum-Parafascicular complex. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate