Facilitation of synaptic transmission by general anaesthetics.

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Abstract
The actions of 5 structurally different i.v. and inhalation anesthetics (alphaxalone/alphadolone, halothane, ketamine, methohexitone, and pentobarbitone) were studied on synaptic transmission through the cuneate nucleus of the dorsal column-lemniscal afferent pathway in the decerebrate cat. Synaptic input and output were estimated from antidromic and orthodromic potentials, which were evoked by either afferent volleys from the periphery or micro-electrode excitation of the presynaptic fiber terminals in the cuneate and recorded at forelimb nerves and the medial lemniscus. Each of the anesthetic agents potentiated the efficiency of synaptic transmission, as shown by the elevation of input-output curves constructed from the integrals of the potentials evoked by varying intensities of either peripheral or cuneate stimulation. The excitability of the afferent terminals, as measured at the peripheral nerves by the antidromic responses to micro-electrode stimulation, was depressed by the anesthetics. Post-synaptic excitability, which was assessed from the direct lemniscal response to intra-nuclear stimulation, did not appear to change. Hypotensive states (mean arterial levels .mchlt. 60 torr) produced depolarization of presynaptic terminals and depression of synaptic efficiency and transmissions; these changes opposed the primary effects of the general anesthetics. Apparently, anesthetics do not depress activity at all synapses of the CNS. Their facilitatory action on cuneate transmission is attributed to an enhanced release of excitatory transmitter; the underlying mechanism may be hyperpolarization of the primary afferent terminals, secondary to an increase in K+ conductance.