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The authors immunocytochemically identified mesopontine cholinergic and rostral raphe serotonergic neurons in brains obtained at autopsy from four patients with multiple system atrophy (MSA) and four matched controls. There was a severe depletion of cholinergic neurons in the pedunculopontine (20 +/- 2 vs 81 +/- 10 cells/section, p< 0.001) and laterodorsal tegmental nucleus (18 +/- 3 vs 47 +/- 4 cells/section, p < 0.001) in MSA. Whereas there was also depletion of locus ceruleus neurons, there was a striking preservation of rostral raphe neurons in MSA.

Sleep disorders increase with ageing. The serotonergic system has been linked with sleep regulation. In fatal familial insomnia, a prion disease with insomnia as one major clinical feature, we recently observed a disturbance in the serotonergic system as likely substrate of typical symptoms. Using immunohistochemistry for the serotonin synthesizing enzyme, tryptophan hydroxylase, we investigated the serotonergic median raphe nuclei (dorsal raphe nucleus, superior central nucleus, and raphe obscurus nucleus) in brains of an older (n = 12; age range 62-84 years) and a younger group (n = 10; age range 5-29 years). We found no significant difference between age groups in the percentage of neurons able to synthesize serotonin. Other changes might relate to sleep disturbances in the elderly.

A pre-embedding double immunostaining technique was used to determine the role of beta-endorphin in synapse, particularly in neurons with a postsynaptic membrane containing micro-1 or delta-1 opioid receptors. A small number of beta-endorphin immunoreactive axon terminals in the dorsal raphe nucleus was found to make direct synapses on micro-1 or delta-1 opioid receptor-immunoreactive dendrites, some of which showed immunostaining of their postsynaptic membranes, although with low frequencies. These results suggest that beta-endorphin can play a direct role through the micro-1 or delta-1 opioid receptors at synapses, but the main route would be through other opioid receptor at the synapse or even not through the synapse.

We report for the first time, modulation of cytosolic calcium in response to glutamate and specific glutamate receptor agonists in early embryonic rat brain cells (raphe cells taken at gestation days 13 or 14). Metabotropic as well as ionotropic agonists were effective. Cells responding to kainic acid were particularly prominent in caudal raphe. We used very short post-plating delays (2 to 6 h); it may therefore be assumed that functional receptors already exist in the intact embryonic brain by gestation day 13. Since many developmental processes are influenced by cytosolic calcium modulation, glutamate receptors may play a key role in brain development, well before the extensively studied postnatal peak in receptor density.