Application of Cerebrolysin (0.1 /rg per 1 ml) by a fast microperfusion system induced an inward current of 0.2 to 1 nA in all neurones from newborn mouse hippocampi held at —30 mV membrane potential. Cerebrolysin- induced currents were reduced by the GABAa antagonist bicuculline (2 /¿M) by 65 %, by the NMDA antagonist aminophosphovaleric acid (APV, 10 /¿M) by 27 %, and by the non-NMDA antagonist cyanonitroquinoxalinedione (CNQX, 10 ¡utA) by 20 %. Cerebrolysin dialyzed through a 3.6 kD gut did not induce any transmembrane current but potentiated the response induced by GABA (10 /utA) to 135 %. We conclude that, in addition to amino acids which activate GABAa, NMDA and non-NMDA receptors, Cerebrolysin also contains a peptide which potentiates the GABAa receptor response.
At 20oC, both quantal and non-quantal spontaneous acetylcholine release (expressed as miniature endplate potential frequency [f-MEPPs] and the H-effect, respectively) increased during the first 30 min of hypoxia in solution with normal extracellular calcium ([Ca2+]o = 2.0 mM). The hypoxia-induced tenfold increase of the f-MEPPs was virtually
absent in low calcium solution ([Ca2+]o = 0.4 mM) whereas there was still a significant increment of non-quantal release. This indicates that each of these two processes of acetylcholine release is influenced by mechanisms with different oxygen sensitivity. The rise of f-MEPPs during the onset of hypoxia apparently requires Ca2+ entry into the nerve terminal, whereas the non-quantal release can be increased by another factors such as a lower level of ATP.