Effects of medial forebrain bundle lesions on the responsiveness of brain histamine receptors: biochemical and electrophysiological studies [proceedings].
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Biomedical subjects
Publications and source records attributed to H L Haas.
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Responses of neurones in different regions of the rat and cat brain to micro-electrophoretically applied histamine and some related substances including antagonists are reported. Histamine excites most neurones in the hypothalamus but depresses the vast majority of neurones in other structures. Depressant actions of histamine and some inhibitions in the cortex and hippocampus of the rat are antagonized by metiamide, an H2-receptor antagonist. The results lend strong support to the idea of histaminergic transmission in the mammalian brain.
The effects of two diazepines (diazepam and Ro 11-7800) and 3 barbiturates (thiamylal, pentobarbitol and phenobarbital) on GABA-mediated recurrent inhibition were assessed on single hippocampal pyramidal cells and on population spikes using extracellular recording techniques. Recurrent inhibition was evoked in spontaneously active CA1 pyramidal cells by stimulation of the fimbria or the alveus with single shocks. Microiontophoretic application of Ro 11-7800 or systemic application of diazepines or barbiturates resulted in an increase of the duration of the inhibition and in a concomitant depression of the spontaneous firing in most neurones tested. When the firing rates were kept constant artificially, using excitant amino acids, a prolongation of the recurrent inhibition was observed with barbiturates but not with diazepines. The duration of the inhibition, which was assessed from CA1 population spikes elicited by double shocks to the fimbria, was prolonged following systemic application of diazepines or barbiturates. It is concluded that both diazepines and barbiturates are able to potentiate GABAergic recurrent inhibition in the hippocampus. The demonstration of this effect appears to depend critically on certain experimental conditions.
1 The action of iontophoretically administered lithium was studied on spinal Renshaw cells an interneurones and on supraspinal neurones in cerebral cortex, thalamus, hypothalamus and brain stem in anaesthetized cats and rats. 2 There was a correlation between the effects of Li+ and those of acetylcholine (ACh), although rather more cells were unaffected by Li+ than by ACh. 3 The usual effect was an excitation of rather slow onset, but occasionally effects were produced with time courses similar to those of ACh. The excitation was blocked by ACh antagonists and was best demonstrated with dihydro-beta-erythroidine on Renshaw cells. 4 The postsynaptic excitant action of ACh on Renshaw cells was reduced by Li+. 5 Depressant actions of Li+ were encountered on cells also depressed by ACh. 6 It is concluded that Li+ may facilitate cholinergic transmission at some sites in the CNS by increasing the release of ACh by an unknown mechanism. Similar effects at non-cholinergic synapses might also occur but would appear to be of less importance. Since facilitation of neuronal firing with Li+ was usually observed, the depressant effects on postsynaptic responses to ACh may be of little consequence.
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