Dogs are unique among mammals in having a 100-fold range in body weight for nonobese adults. This variation makes the calculation of the power function for metabolic body size and hence the allometry of energy requirements a particularly challenging subject. Several functions have been proposed from W0.68 to W0.88 (W = body weight in kg). In the present study we measured the heat output of 22 dogs representing seven breeds, aged 1-10 y with W from 5.8 to 48.8 kg, using a whole-body calorimeter specifically designed for this purpose. Regression of log energy output against log W gave the equation 678 W0.64 (r = 0.96; P less than 0.001), which is considered to represent resting energy expenditure (REE) as kJ/d. If estimates of the energy cost of activity are added to REE, new equations of 655 W0.69 (low activity) and 643 W0.73 (higher activity) are obtained, depending on the amount of activity included in the calculation. From these results we suggest that the allometry of energy requirements of adult dogs is a function of different exponents for REE and the energy cost of activity. It does not appear to exceed W0.75 and may be nearer to W0.67.

1 The behavioural effects of the intrathecal injection of a thyrotrophin-releasing hormone (TRH) analogue L-orotyl-L-histidyl-prolineamide (CG 3509, 0.5 /g), the non-selective 5-HT, and 5-HT2 receptor agonist 5-methoxy-N,N'-dimethyltryptamine (5-MeODMT, 2-100pg) and the selective 5-HT2 receptor agonist 2,5-dimethoxy-a,4-dimethyl-benzene ethamine hydrochloride (DOM, 2-25 ug) were compared with the response of systemically administered 5-MeODMT (2 mg kg-1, i.p.) in rats, to establish whether the agonist-induced behaviours were mediated by bulbospinal 5-HT, or 5-HT2 receptors. 2 Intrathecal injection of 5-MeODMT or DOM produced dose-related back muscle contractions (a previously undocumented behaviour) and wet-dog shakes which were both markedly attenuated by ritanserin pretreatment (1 mg kg 1, i.p.) indicating the involvement of 5-HT2 receptors. In contrast, reciprocal forepaw treading, flat body posture and Straub-tail were evoked by 5-MeODMT but not by DOM indicating that these behaviours were not produced by 5-HT2 receptor activation alone. However, as ritanserin pretreatment reduced the reciprocal forepaw treading induced by intrathecal 5-MeODMT, this behaviour may be facilitated by 5-HT2 receptor activation.3 Intrathecal 5,7-dihydroxytryptamine (5,7-DHT, 2 x 150pg) treatment decreased thoraco-lumbar spinal cord 5-HT (-95%) and potentiated the back muscle contractions produced by intrathecal DOM injection without altering the wet-dog shake behaviour. None of the components of the 5-HT syndrome produced by 5-MeODMT (2mgkg-1, i.p.), with the exception of a small increase in wet-dog shakes, was significantly altered by intrathecal 5,7-DHT (which reduced thoraco-lumbar spinal cord 5-HT by 84%). Taken together these data suggest that the only 5-HT agonist-induced behaviour mediated by the activation of 5-HT2 receptors located postsynaptic to bulbospinal 5-hydroxytryptaminergic (5-HTergic) neurones was back muscle contractions. 4 The wet-dog shake and forepaw licking behaviors produced by intrathecal CG 3509 (0.5 Mg) were attenuated when ritanserin was administered intrathecally 30 min before, but not when it was given at the same time as CG 3509 and neither behaviour was altered by intrathecal 5,7-DHT. This suggests that bulbospinal 5-HTergic neurones are not involved in the production of these TRH analogue-induced behaviours and that the 5-HT2 receptors which mediate these behaviours are not located in the spinal cord.

No abstract

No abstract

No abstract