The milk-ejection reflex after different lesions of the sensory system was studied by mechanical milking of the ewe. Only animals with lesions which did not produce locomotor ataxia were investigated. Section of the dorsal tract of the spinal cord at different thoracic levels blocked the mi l k\x=req-\ ejection reflex. This was not due to postoperative shock, because the same type of lesion made at the sacral level was without effect. Moreover, unilateral section of this tract blocked the reflex when milking was limited to the ipsilateral mammary gland. At the cervical level, the interruption of the dorsal tract was ineffective, which can probably be explained by the existence, in sheep, of the spino-cervico-thalamic tract. The latter becomes ventral at the cervical level. Lesions of the lemniscal system in the mesencephalon (bilateral coagulation of the medial lemniscus) and in the thalamus (bilateral destruction of the ventral posterolateral nucleus) do not inhibit the milk-ejection reflex.The role of the spinal lemniscal system is discussed in relation to the work of others and to the electrophysiological results obtained by one of us. It is suggested that two sensory systems (lemniscal and extralemniscal) have to interact to induce the release of oxytocin evoked by the stimuli of mammary origin during milking.

Electrical stimulation of fimbria-fornix (fi-fx) fibers monosynaptically activated many of the neurons tested in the lateral septal complex (LSC) of the rat. The orthodromically activated LSC neurons were classified as "strongly" orthodromically activated (SOA) or "weakly" orthodromically activated ( WOA ) cells according to their threshold for eliciting a response, stability of the response latency, frequency following and the stimulus-response ratio. Microiontophoretically applied glutamate (GLU) could excite both SOA and WOA neurons. However, the expelling currents needed to activate the SOA cells were often considerably lower than those necessary to excite the WOA cells suggesting higher sensitivity to GLU of those cells which receive a strong fi-fx innervation. Iontophoretically administered glutamic acid diethylester (GDEE) in general reversibly attenuated excitatory responses of LSC cells to GLU but not to acetylcholine. GDEE was also effective in blocking the synaptic responses of SOA septal cells to fi-fx stimuli. In addition, GDEE administered topically reversibly suppressed the field potential induced in the LSC by fi-fx stimulation. These electrophysiological and pharmacological results support recent biochemical observations suggesting that the excitatory innervation of LSC neurons by fi-fx fibers is mediated by GLU or a closely related excitatory amino acid.

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