Abstract: This paper proposes an extension of scientific horizons in the study of animal behavior and cognition to include conscious experiences. From this perspective animals are best appreciated as actors rather than passive objects. A major adaptive function of their central nervous systems may be simple, but conscious and rational, thinking about alternative actions and choosing those the animal believes will get what it wants, or avoid what it dislikes or fears. Versatile adjustment of behavior in response to unpredictable challenges provides strongly suggestive evidence of simple but conscious thinking. And especially significant objective data about animal thoughts and feelings are already available, once communicative signals are recognized as evidence of the subjective experiences they often convey to others. The scientific investigation of human consciousness has undergone a renaissance in the 1990s, as exemplified by numerous symposia, books and two new journals. The neural correlates of cognition appear to be basically similar in all central nervous systems. Therefore other species equipped with very similar neurons, synapses, and glia may well be conscious. Simple perceptual and rational conscious thinking may be at least as important for small animals as for those with large enough brains to store extensive libraries of behavioral rules. Perhaps only in “megabrains” is most of the information processing unconscious.

Abstract: The position advanced in this paper is that the bedrock of emotional feelings is contained within the evolved emotional action apparatus of mammalian brains. This dual-aspect monism approach to brain-mind functions, which asserts that emotional feelings may reflect the neurodynamics of brain systems that generate instinctual emotional behaviors, saves us from various conceptual conundrums. In coarse form, primary process affective consciousness seems to be fundamentally an unconditional “gift of nature” rather than an acquired skill, even though those systems facilitate skill acquisition via various felt reinforcements. Affective consciousness, being a comparatively intrinsic function of the brain, shared homologously by all mammalian species, should be the easiest variant of consciousness to study in animals. This is not to deny that some secondary processes (e.g., awareness of feelings in the generation of behavioral choices) cannot be evaluated in animals with sufficiently clever behavioral learning procedures, as with place-preference procedures and the analysis of changes in learned behaviors after one has induced re-valuation of incentives. Rather, the claim is that a direct neuroscientific study of primary process emotional/affective states is best achieved through the study of the intrinsic (“instinctual”), albeit experientially refined, emotional action tendencies of other animals. In this view, core emotional feelings may reflect the neurodynamic attractor landscapes of a variety of extended trans-diencephalic, limbic emotional action systems-including SEEKING, FEAR, RAGE, LUST, CARE, PANIC, and PLAY. Through a study of these brain systems, the neural infrastructure of human and animal affective consciousness may be revealed. Emotional feelings are instantiated in large-scale neurodynamics that can be most effectively monitored via the ethological analysis of emotional action tendencies and the accompanying brain neurochemical/electrical changes. The intrinsic coherence of such emotional responses is demonstrated by the fact that they can be provoked by electrical and chemical stimulation of specific brain zones-effects that are affectively laden. For substantive progress in this emerging research arena, animal brain researchers need to discuss affective brain functions more openly. Secondary awareness processes, because of their more conditional, contextually situated nature, are more difficult to understand in any neuroscientific detail. In other words, the information-processing brain functions, critical for cognitive consciousness, are harder to study in other animals than the more homologous emotional/motivational affective state functions of the brain.

Abstract: OBJECTIVE: To assess the effects of a single intravenous dose of butorphanol (0.1 mg kg(-1)) on the nociceptive withdrawal reflex (NWR) using threshold, suprathreshold and repeated subthreshold electrical stimuli in conscious horses. STUDY DESIGN: 'Unblinded', prospective experimental study. ANIMALS: Ten adult horses, five geldings and five mares, mean body mass 517 kg (range 487-569 kg). METHODS: The NWR was elicited using single transcutaneous electrical stimulation of the palmar digital nerve. Repeated stimulations were applied to evoke temporal summation. Surface electromyography was performed to record and quantify the responses of the common digital extensor muscle to stimulation and behavioural reactions were scored. Before butorphanol administration and at fixed time points up to 2 hours after injection, baseline threshold intensities for NWR and temporal summation were defined and single suprathreshold stimulations applied. Friedman repeated-measures analysis of variance on ranks and Wilcoxon signed-rank test were used with the Student-Newman-Keul's method applied post-hoc. The level of significance (alpha) was set at 0.05. RESULTS: Butorphanol did not modify either the thresholds for NWR and temporal summation or the reaction scores, but the difference between suprathreshold and threshold reflex amplitudes was reduced when single stimulation was applied. Upon repeated stimulation after butorphanol administration, a significant decrease in the relative amplitude was calculated for both the 30-80 and the 80-200 millisecond intervals after each stimulus, and for the whole post-stimulation interval in the right thoracic limb. In the left thoracic limb a decrease in the relative amplitude was found only in the 30-80 millisecond epoch. CONCLUSION: Butorphanol at 0.1 mg kg(-1) has no direct action on spinal Adelta nociceptive activity but may have some supraspinal effects that reduce the gain of the nociceptive system. CLINICAL RELEVANCE: Butorphanol has minimal effect on sharp immediate Adelta-mediated pain but may alter spinal processing and decrease the delayed sensations of pain.

Abstract: Six ponies were used to investigate the effect of tolazoline antagonism of detomidine on physiological responses, behavior, epinephrine, norepinephrine, cortisol, glucose, and free fatty acids in awake ponies. Each pony had a catheter inserted into a jugular vein 1 hour before beginning the study. Awake ponies were administered detomidine (0.04 mg/kg intravenously [i.v.]) followed 20 minutes later by either tolazoline (4.0 mg/kg i.v.) or saline. Blood samples were drawn from the catheter 5 minutes before detomidine administration (baseline), 5 minutes after detomidine administration, 20 minutes before detomidine administration which was immediately before the administration of tolazoline or saline (time [T] = 0), and at 5, 30, and 60 minutes after injections of tolazoline or saline (T = 5, 30, and 60 minutes, respectively). Compared with heart rate at T = 0, tolazoline antagonism increased heart rate 45% at 5 minutes. There was no difference in heart rate between treatments at 30 minutes. Blood pressure remained stable after tolazoline, while it decreased over time after saline. Compared with concentrations at T = 0, tolazoline antagonism of detomidine in awake ponies resulted in a 55% increase in cortisol at 30 minutes and a 52% increase in glucose at 5 minutes. The change in free fatty acids was different for tolazoline and saline over time. Free fatty acids decreased after detomidine administration. Free fatty acids did not change after saline administration. After tolazoline administration, free fatty acids increased transiently. Tolazoline tended to decrease sedation and analgesia at 15 and 60 minutes postantagonism. Antagonism of detomidine-induced physiological and behavioral effects with tolazoline in awake ponies that were not experiencing pain appears to precipitate a stress response as measured by cortisol, glucose, and free fatty acids. If antagonism of an alpha-agonist is contemplated, the potential effect on hormones and metabolites should be considered.