A comparison of taste reactivity changes induced by ventromedial hypothalamic lesions and stria terminalis transections.

A hyperreactivity to the sensory qualities of a food, i.e., finickiness, is a defining feature of the ventromedial hypothalamic (VMH) lesion syndrome. The precise anatomical locus mediating this disturbance has not been determined. This study examines the hypothesis that interruption of amygdalo-hypothalamic connections (either ascending or descending) via the stria terminalis (ST) is involved in VMH lesion-induced finickiness. Taste reactivity was assessed in animals with VMH lesions, ST knife cuts, combined VMH/ST damage, and controls. In sham feeding tests of taste reactivity, ST and VMH rats were equally hyperreactive compared to controls. Rats with combined VMH and ST damage, however, were more reactive than both these groups. None of the brain lesions resulted in an overreactivity to quinine adulteration of the diet. In contrast to sham feeding, ST rats were not hyperphagic when feeding normally, although VMH rats were. In fact, ST damage attenuated VMH-induced hyperphagia and weight gain. We conclude that the taste reactivity changes induced by VMH lesions and ST transections are independent and additive indicating that VMH finickiness does not involve disruption of amygdalo-hypothalamic connections. Nonetheless, disruption of the ST produces a dramatic change in taste reactivity and the properties and origins of this disturbance are discussed.