ELECTRICALLY-INDUCED RELEASE OF ENDOGENOUS NORADRENALINE AND DOPAMINEFROM BRAIN-SLICES - PSEUDO-ONE-PULSE STIMULATION UTILIZED TO STUDY PRESYNAPTIC AUTOINHIBITION

Slices of rat hypothalamus (noradrenaline experiments) or rabbit cauda te nucleus (dopamine experiments) were prepared, superfused, and field -stimulated using series of monophasic rectangular pulses. Noradrenali ne, dopamine and the main dopamine metabolite, dihydroxyphenylacetic a cetic acid (DOPAC), were determined using HPLC with electrochemical de tection. Electrical stimulation was performed using the following prot ocols: 1) 4 pulses delivered at 100 Hz; this type of stimulation is re ferred to as pseudo-one-pulse stimulation (POP); its short duration of only 32 ms does not allow the development of autoinhibition; 2) 2 bur sts of 4 pulses at 100 Hz, delivered 1 s apart (2-POP-stimulation); 3) 8 pulses at t Hz (dopamine experiments only); 4) 36 pulses at 3 Hz. N oradrenaline experiments. The alpha2-adrenoceptor antagonist yohimbine (1 mumol/l) did not enhance noradrenaline overflow following POP stim ulation, but enhanced the overflow following 2-POP-stimulation by abou t 50% and that following 36-pulse-stimulation by almost 100%. Dopamine experiments. The D2-dopamine receptor antagonist sulpiride (3 mumol/l ) facilitated the overflow of dopamine elicited with 2-POP-stimulation (66%), 8 pulses/1 Hz (92%), and 36 pulses/3 Hz (140%). It did not sig nificantly facilitate the overflow of dopamine following POP-stimulati on (19%). The overflow of DOPAC was not, or only slightly, increased b y electrical stimulation, and its spontaneous outflow was more than th ree times higher than that of dopamine. Furthermore, the electrically induced overflow of dopamine did not exceed the outflow of DOPAC at an y of the stimulation conditions employed. The results of the present s tudy bear out important claims of the autoreceptor theory and confirm the data obtained in previous experiments using labelled transmitters.