The author comments on the work of G. G. Gallup and S. D. Suarez, specifically focusing on animal rights issues. Gallup and Suarez argue for the status quo in research practices involving nonhuman animals; while K. J. Shapiro and others take a reformist position that the suffering of and the reliance on animals in psychology laboratories can and ought to be diminished. 2012 APA, all rights reserved).
Hypocretin regulates brain reward function and cocaine consumption in rats. The hypocretinergic (Hcrt) system is implicated in energy homeostasis, feeding and sleep regulation. Hypocretinergic cell bodies are located in the lateral hypothalamus (LH) and project throughout the brain. The aim of the present studies was to investigate the role of the Hcrt system in regulating brain reward function and the reinforcing properties of cocaine in rats. Intracranial self-stimulation (ICSS) thresholds provide an accurate measure of brain reward function in rats. Here (...) we show that a single injection of Hcrt-1 (5 µg icv) induced persistent, long-lasting elevations in ICSS thresholds in drug-naïve rats. Indeed, Hrct-1 elevated ICSS thresholds for 36 h, with peak elevations between 6 and 12 hours after injection. Hrct-1-induced threshold elevations were attenuated by an antibody known to neutralize the binding of hcrt-1 to its receptors. Taken together, these observations suggest that Hrct-1 negatively regulates brain reward function in rats. Because Hrct-1 negatively regulates brain reward function, we hypothesized that it may attenuate the increased brain reward function usually observed after cocaine consumption, and thereby alter cocaine self-administration behavior. A daily injection of Hrct-1 (1 µg icv), for 4 consecutive days, slightly increased cocaine self-administration (0.25 mg/infusion) in rats. Overall, these data demonstrate that Hrct-1 negatively regulates brain reward function, and as such may indirectly alter cocaine self-administration. Given the well-established role of hypocretin neurons in regulating feeding behavior and sleep, we hypothesize that hypocretinergic regulation of brain reward function may provide a mechanism by which appropriate and competing behaviors (e.g. sleep or feeding) may be engaged to maintain energy homeostasis. (shrink)
Elevations in brain stimulation reward (BSR) thresholds have been observed in rats undergoing nicotine withdrawal and have been proposed as a sensitive measure of the negative affective state associated with nicotine withdrawal. mGluR are presynaptic autoreceptors that decrease glutamate release when stimulated. The aim of this study was to examine the role of glutamate neurotransmission in nicotine dependence. The mGluR agonist LY314582 (2.5–7.5 mg/kg) precipitated nicotine withdrawal as measured by elevations in BSR thresholds in nicotine-treated rats but not in controls. (...) It was hypothesized that LY314582 precipitated nicotine withdrawal by decreasing glutamatergic tone at postsynaptic glutamate receptors. Therefore, the effects of MPEP (0.5–2 mg/kg), an mGluR antagonist, and MK-801 (0.01–1 mg/kg), an NMDA receptor antagonist, were examined. MPEP elevated BSR thresholds by an equal magnitude in control and nicotine-treated rats. At low doses, MK-801 (0.01–0.2 mg/kg) lowered BSR thresholds to a similar extent in control and nicotine-treated rats. At higher doses, MK-801 (0.25–1 mg/kg) disrupted performance in nicotine-treated and control rats. These data indicate that mGluR and NMDA receptors regulate BSR in opposite directions in non-dependent animals, and chronic nicotine treatment does not alter these effects. Most importantly, the data demonstrate that the mGluR is involved in nicotine dependence, but mGluR and NMDA receptors do not mediate mGluR actions in nicotine dependence. (shrink)
We examine and reject the claim that the past-directed aspect of mental time travel (episodic memory) is unique to humans. Recent work in our laboratory with rats has demonstrated behaviours that resemble judgements about past occasions. Similar to human episodic memory, we can also demonstrate a dissociation in the neural basis of recollection and familiarity in nonhumans.