mise à jour du 23 janvier 2003
Psychopharmacology (Berl) 1979; 65; 3; 317-8
Stretching and yawning: a role of glutamate
Lanthorn TH, Isaacson RL
Department of Psychology, University of Florida, Gainesville, U.S.A


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In the course of work on the behavioral effects of the intraventricular administration of nonneurotoxic doses of kainate, an agonist of the "glutamate-preferring" receptor, we noticed that kainate suppressed the appearance of stretching and yawning (SY) in rats. This was most obvious with repeated exposure to the observation apparatus. The number of SY emitted by normal and saline-injected animals increases with repeated exposures to the observation boxes. By the third or fourth exposure, SY reaches a plateau of seven to eight SY in the hour observation period. Low doses of kainate completely suppressed SY.

Our interest in finding behavioral correlates of changes in glutamate-mediated neurotransmission led us to examine the effect of glutamate antagonist on the occurrence of SY. We now present our findings using glutamate diethyl ester (GDEE), an antagonist of glutamate and aspartate.

Materials and Methods

The subjects were 23 male Long-Evans hooded rats (225-300g). GDEE was rernoved from a freezer and dissolved in saline (0. 15 mmol/mI for the lowest dose and 1 mmol/ml for the rest). GDEE was injected IP within 15 min after it was removed from the freezer so that it had little opportunity to undergo hydrolysis. GDEE was given in doses of 0.15 mmol/kg (N = 5), 1 rnmol/kg) (204mg/kg) (N = 3), 3 mmol/kg (N = 7), and 4.5 mmol/kg (N = 3). Five more rats were injected with 1 ml/kg of saline.

Immediately after injection the subiects were placed in individual observation boxes (30x3Ox2Ocm) as described previously. Up to live animals were observed at one time. SY was recorded for 1 h (six 10-min periods). For the five rats administered 0.15 mmol/kg GDEE, grooming was also recorded for the last 50 min of the session. Grooming was scored in the manner of Gispen et al. (1975).


The systemic injection of GDEE in these doses resulted in the rapid onset (less than 10 min after injection) of very pronounced stretching activity. Stretches were often seen immediately succeeding one another (a "stretching crisis") at the three higher doses. At doses of 0. 15, 1, 3, and 4.5 mmol/kg of GDEE, the mean number of SY induced in 1 h were 13.2, 27, 34.7, and 40, respectively. Saline injection resulted in the occurrence of 1.5 SY in an hour. This was recorded as six 10-min periods and is shown in Fig. The declines of SY in the fifth period for the three higher doses and the sixth period for the 1 mmol/kg group were concomitant with the subjects lying down. They appeared to be asleep.

Out of a total of over 400SY recorded after administration of the three higher doses of GDEE, yawns accotinted for less than 1 of the total. At the 0.15mmol/kg dose, yawns were commonly observed and accompanied a majority of the stretches. There were also more stretches of the front limbs occurring after the lowest dose of GDEE.

At the 0. 15 mmol/kg dose grooming was counted. The mean score (25.2 out of a possible 200) was well within the normal reported range.


The administration to rats of GDEE, an antagonist of both glutamate and aspartate receptors, results in the occurrence of the stretching and yawning syndrome (SYS). Coupled with our previous findings that kainate suppresses naturally occurring SY, the present results suggest a role of glutamate-mediated transmission in the emission of SY. SY can be induced by a variety of chemical agents. These include adrenocorticotrophic hormone (ACTH) and melanocyte-stimulating hormone (MSH) (Ferrari et al., 1963; Izumi et al., 1973; Gispen et al., 1975), zinc (Izumi et al., 1973), recovery from potassium chlorideinduced cortical spoading depression (Huston, 1971), and muscarinic stimulants (Urba-Holmgren et al., 1977). ACTH and GDEE induce an SY pattern in which one stretch may immediately succeed another. Ferrari et al. (1963) termed this pattern a "crisis". Unlike ACTH, however, GDEE does not induce excessive grooming. This difference helps to confirm the suggestions by Gispen et al. (1975) and Colbern et al. (1977) that the neural mechanisms of SY are different from those mediating excessive grooming.