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REVERSIBLE EFFECTS OF TETANUS TOXIN ON STRIATAL‐EVOKED RESPONSES AND [ 3 H]‐γ‐AMINOBUTYRIC ACID RELEASE IN THE RAT SUBSTANTIA NIGRA
Author(s) -
COLLINGRIDGE GRAHAM L.,
DAVIES JOHN
Publication year - 1982
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1982.tb09234.x
Subject(s) - substantia nigra , pars compacta , neurotransmission , inhibitory postsynaptic potential , chemistry , striatum , neuroscience , neurotoxin , toxin , midbrain , medicine , globus pallidus , endocrinology , dopamine , pharmacology , biology , biochemistry , basal ganglia , central nervous system , dopaminergic , receptor
1 The effects of sublethal doses of tetanus toxin on γ‐aminobutyric acid (GABA)‐mediated synaptic transmission and [ 3 H]‐GABA release were studied in the rat substantia nigra. 2 Intranigral injections of tetanus toxin at 1–5 times the mouse LD 50 dose produced ipsiversive circling behaviour which was maximal after 1 week and lasted 2–3 weeks. Rats then displayed normal behaviour suggesting that the effects of the toxin were fully reversible. 3 In the treated nigra of circling rats there was a reduction in the striatal‐evoked inhibition of compacta and reticulata neurones, but no change in their spontaneous firing rates. Some forms of striatal‐evoked excitation were also reduced. Once rats had recovered from circling no alterations in the synaptic responses were detected. 4 In circling rats there were no differences in the sensitivities of neurones in the treated and untreated nigra to GABA or to other inhibitory neurotransmitters. 5 The Ca 2+ ‐dependent, K + ‐evoked release of [ 3 H]‐GAB A from slices prepared from the treated nigra of circling rats was less than that from the untreated nigra of circling rats. No differences in nigral [ 3 H]‐GABA release were observed once rats had recovered from the circling behaviour. 6 The results demonstrate that doses of tetanus toxin which produce reversible behavioural effects can interfere reversibly with GABA‐mediated synaptic transmission by a presynaptic mechanism which probably involves a reduction in transmitter release.