Gustatory functions, sodium appetite, and conditioned taste aversion survive excitotoxic lesions of the thalamic taste area

Rats with bilateral, electrophysiologically guided, ibotenic acid lesions of the gustatory thalamus (THLX) were tested for their ability to perform a variety of taste-guided behaviors. First, in daily 30-min sessions, the rats were given repeated 10-s access periods to a range of concentrations of sucrose, NaCl, or QHCl, plus water. Both the control and the THLX rats exhibited similar concentration-response functions, regardless of hydrational state. Next, on 3 trials, the rats were given 15 min access to 0.3 M l-alanine and then injected with LiCl (0.15 M, 1.33 ml/100 g body weight ip). All rats learned a taste aversion following 1 pairing with LiCl. Finally, on 3 separate occasions, the rats were injected with furosemide, and Na+-appetite was evaluated 24 hr later. All rats expressed an equivalent sodium appetite after the first furosemide injection, but only the control rats increased intake of 0.51 M NaCl with repeated sodium depletions. These observations reinforce prior data implying that an intact gustatory thalamus is not necessary for the expression of some taste-guided behaviors

Role of gustatory thalamus in anticipation and comparison of rewards over time in rats

Rats reduce intake of a palatable saccharin solution when it is followed by access to a preferred sucrose solution. This phenomenon, referred to as an anticipatory contrast effect ( ACE), is thought to occur because the value of the saccharin conditioned stimulus pales in comparison to the highly rewarding sucrose unconditioned stimulus expected in the near future. Although relatively little is known about the underlying neural substrates, lesions of the gustatory thalamus fully disrupt the phenomenon (Reilly S, Bornovalova M, and Trifunovic R. Behav Neurosci 118: 365-376, 2004; Reilly S and Pritchard TC. Behav Neurosci 110: 746-759, 1996). The present set of experiments revisited this issue to determine the nature of this deficit. Rats with bilateral ibotenic acid lesions of the gustatory thalamus were given 3-min access to 0.15% saccharin and, after a 0-s or 5-min interval, were given 3-min access to either the same saccharin solution or a highly preferred 1.0 M sucrose solution. In experiment 1, ACE testing began with the 5-min interstimulus interval (ISI) and then switched to the 0-s ISI. For experiment 2, the order of ISI testing was reversed. The results show that axon-sparing, neurotoxic lesions of the gustatory thalamus prevent ACEs with a 0-s ISI and lead to a reversal (i.e., a reinforcement effect) with a 5-min ISI. Together, the results suggest that the lesion leads to a specific reward comparison deficit, whereby the rats fail to compare the value of an available reward with the memory of a preferred reward that is anticipated in the near future

Amphetamine-induced taste aversion learning in young and old F-344 rats following exposure to 56Fe particles

Exposure to 56Fe particles produces changes in dopaminergic function and in dopamine-dependent behaviors, including amphetamine-induced conditioned taste aversion (CTA) learning. Because many of these changes are characteristic of the changes that accompany the aging process, the present study was designed to determine whether or not there would be an interaction between age and exposure to 56Fe particles in the disruption of an amphetamine-induced CTA. One hundred and forty F-344 male rats 2-, 7-, 12-, and 16-months old, were radiated with 56Fe particles (0.25–2.00 Gy, 1 GeV/n) at Brookhaven National Laboratory. Three days following irradiation, the rats were tested for the effects of radiation on the acquisition of a CTA produced by injection of amphetamine (3 mg/kg, i.p.). The main effect of age was to produce a significant decrease in conditioning day sucrose intake; there was no affect of age on the acquisition of the amphetamine-induced CTA. Exposing rats to 56Fe particles disrupted the acquisition of the CTA produced by injection of amphetamine only in the 2-month-old rats. These results do not support the hypothesis of an interaction between age and exposure to 56Fe particles in producing a disruption of amphetamine-induced CTA learning. As such, these results suggest that the aging produced by exposure to 56Fe particles may be endpoint specific