Explorations of the neural substrates of conditioned taste aversions (CTAs) have focused principally on diencephalic and telencephalic structures. The nucleus tractus solitarius (NTS) is the initial gustatory relay in the rat's hindbrain. It is worthy of investigation for its part in mediating CTAs in that it is sensitive to several physiological conditions which affect feeding while also being a site of anatomical convergence for vagal afferents from the viscera and centrifugal projections from areas (hypothalamus, amygdala) implicated in emotions and hedonics. We compared single neuron responses from NTS to several taste stimuli in three groups of rats: (1) those receiving exposure to 0.0025 M sodium saccharin without physiological consequences; (2) those made ill through intraperitoneal injections of LiCl but having no obvious gustatory referent for their malaise (sensitization-pseudoconditioning controls); (3) those in which exposure to 0.0025 M sodium saccharin (the CS) was paired with LiCl-induced poisoning (the US), creating a pronounced aversion to the saccharin. According to response profiles, NTS neurons in all three groups could be divided into subsets of about 30%, which showed a sweet-sensitive profile, and 70%, which were primarily sensitive to nonsweet qualities. The major effect of the conditioning procedure was to increase responsiveness to the saccharin CS only among the sweet-sensitive subset. Moreover, the peak of activity which largely accounted for the increase occurred with a latency of 900 msec, perhaps implicating a secondary input to NTS from diencephalic or telencephalic sites. The significance of the results is that: (1) CTAs affect sensory activity at a lower order level than had heretofore been demonstrated; (2) NTS shows sensitivity to yet another physiological condition, reinforcing the involvement of the hindbrain in hedonics and sophisticated taste-related processes; (3) there is a subset of taste neurons, rather distinct according to its sensitivity profile, which is also functionally unique in its response to conditioning by a sweet CS.

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. (1997). Fundam. Appl. Toxicol 38,[75][76][77][78][79][80][81][82][83][84][85][86][87][88] The extent to which cardiorespiratory infirmity and other sublethal effects of saxitoxin (STX) and tetrodotoxin (TTX) can be reversed by 4-aminopyridine (4-AP) was investigated in guinea pigs chronically instrumented for the concurrent electrophysiological recordings of electrocorticogram (ECoG), diaphragmatic electromyogram (DEMG), Lead II electrocardiogram, and neck skeletal muscle electromyogram. Animals were intoxicated with either STX or TTX (2 and 3 /xg/kg, im) to produce a state of progressive cardiorespiratory depression (depicted by decreasing DEMG amplitude, bradypnea, and bradycardia). At the point where cardiorespiratory performance was most seriously compromised («30 min posttoxin), 4-AP (1 or 2 mg/kg, im) was administered. The therapeutic effect of 4-AP was striking in that, within minutes, the toxin-induced diaphragmatic blockade, bradypnea, bradycardia, and depressed cortical activity were all restored to a level either comparable to, or surpassing, that of control. The optimal 4-AP dose level was determined to be 2 mg/kg (im) based on analyses of cardiorespiratory activity profiles throughout the course of intoxication and 4-AP treatment. At the dose levels (either 1 or 2 mg/ kg) used to restore ventilatory function and cardiovascular performance, 4-AP produced no sign of seizures and convulsions. Although less serious secondary effects such as cortical excitant/arousal effect (indicated by ECoG power spectral analysis) and transient periods of skeletal muscle fasciculation were observed, these events were of minor concern particularly in view of the remarkable therapeutic effects of 4-AP. © i»»7 society of Toxicology.Saxitoxin (STX) and tetrodotoxin (TTX) are among the deadliest nonprotein neurotoxins known (lethal dose in guinea pigs «*5 ^g/kg, im; unpublished observations).