Tongue Extension Research Articles

Oral motor performance following central dopamine receptor blockade

Oral motor responses were recorded in water-deprived rats receiving injections of spiroperidol, the dopamine blocker, into the nucleus accumbens and caudate nucleus. Spiroperidol injected into the nucleus accumbens resulted in dose dependent decreases in lap volume and tongue extension. Injections of spiroperidol into adjacent sites or into the caudate nucleus did not significantly reduce lap volume even with an 8 fold larger dose administered into the caudate. These observations implicate the mesolimbic dopaminergic projections to the nucleus accumbens in oral motor responses and indicate the need for systematic comparisons of the contributions of mesolimbic and nigrostriatal dopaminergic systems to ingestive behaviors.

Oral motor deficits following lesions of the central nervous system in the rat.

The effects of lesions of the zona incerta (ZI), globus pallidus (GP), midlateral and far lateral hypothalamus (MLH and FLH), and the central amygdaloid complex (CAC) on oral motor deficits were investigated. Lesions of the ZI, GP, and CAC resulted in a significant reduction in tongue extension and lap volume. MLH lesions significantly reduced tongue extension whereas FLH lesions significantly reduced both tongue extension and lap volume. Injections of 6-hydroxydopamine into the GP, MLH, and CAC also significantly reduced tongue extension and lap volume. Water and/or food intakes were reduced in some of the lesioned groups but the oral motor deficits were observed both in the presence and in the absence of reduced water and food intakes. The possibility that oral motor deficits are associated with damage to striatal and non-striatal dopamine neurons needs further investigation.

Aphagia, behavior sequencing and body weight set point following orbital frontal lesions in rats

Discrete lesions were made in the orbital frontal neocortex of rats and eating, drinking, sensorimotor responsiveness, and sequencing of motor acts were studied. Duration of aphagia was related to palatability/texture of food. Rats were aphagic for a mean of two days to palatable cookie mash presented on a spatula, six days to a high fat diet mash presented in a 4 cm high dish and for seven days to dry laboratory food. Water drinking was resumed with injestion of dry food. Rats presurgically fattened to 120% of body weight appeared stuporous and akinetic for 2–3 postoperative days, and the period for acceptance of food in tall tests was protracted. Rats presurgically dieted to 80% of normal body weight did not show accelerated recovery of feeding. Preoperatively normal, fattened and dieted rats assumed a chronic postoperative body weight level 25% lower than control rats. Rats with lesions showed sensorimotor neglect when tested on an open table top, but did not show neglect when tested in their home cages. In grooming tests, rats with lesions showed all of the components of normal grooming, but failed to exhibit the long chains of grooming characteristics of control rats. They also showed attenuated tongue extension and had difficulty manipulating food with the forepaws. The experiments suggest that following orbital frontal lesions, motor impairments, motor sequencing dysfunctions, change in body weight set point, and depending upon the test situation, sensorimotor neglect, may all be contributing factors to aphagia. The orbital frontal cortex may influence feeding and other behaviors via descending neural projections to the hypothalamus and brainstem.