The effect of 6-OHDA lesions of the nucleus accumbens septum on schedule-induced drinking, wheelrunning and corticosterone levels in the rat
References (31)
- et al.
The pituitary-adrenal response to “minimized” scheduled-induced drinking
Physiol. Behav.
(1981) - et al.
Pituitary-adrenal consequences of adjunctive activities in pigs
Hormones Behav.
(1981) - et al.
Effects of intraventricular 6-hydroxydopamine injections on serum prolactin and LH levels: absence of stress-induced pituitary prolactin release
Brain Res.
(1976) - et al.
The role of the medial forebrain bundle in the mediation of the hypothalamic-hypophyseal-adrenal responses to acute neurogenic stress
Brain Res. Bull.
(1981) - et al.
Effect of norepinephrine applied to the lateral hypothalamus on schedule-induced polydipsia
Pharmac. Biochem. Behav.
(1975) - et al.
Schedule-induced behavior: A review of its generality, determinants and pharmacological data
Pharmac. Biochem. Behav.
(1976) Motor control functions of the lateral hypothalamus and adjunctive behavior
Physiol. Behav.
(1970)Specificity of behavioral regulation
Physiol. Behav.
(1974)- et al.
Effects of lateral hypothalamic lesions on schedule dependent and schedule-induced behavior
Physiol. Behav.
(1977) - et al.
Effects of VMH lesions on schedule induced and schedule dependent behaviors
Physiol. Behav.
(1978)
Adrenal demedullation suppresses schedule-induced polydipsia in rats
Physiol. Behav.
Plasma corticosterone response to environmental stimulation: effects of duration of stimulation and the 24-hour adrenocortical rhythm
Neuroendocrinology
Neurochemical changes elicited by stress
Depletion of brain noradrenaline and dopamine by 6-hydroxydopamine
Br. J. Pharmac.
Schedule-induced polydipsia suppresses pituitary-adrenal activity in rats
J. comp. physiol. Psychol.
Cited by (83)
Socioemotional deficit and HPA axis time response in high compulsive rats selected by schedule-induced polydipsia
2022, Hormones and BehaviorCitation Excerpt :Moreover, there was a negative significant correlation between the amount of water consumed and CORT levels after the 10th SIP session (Mittleman et al., 1988). A classic explanation of this phenomenon is that excessive drinking may be a coping response to stress caused by intermittent food delivery (Brett and Levine, 1979; Brett and Levine, 1981; Wallace et al., 1983; Tazi et al., 1986; Dantzer et al., 1988; Mittleman et al., 1988; López-Grancha et al., 2006). In accordance with this hypothesis, animals with a proactive coping style exhibit low CORT production compared to animals with a reactive coping style that reacts passively to stress (Bowen et al., 2014).
Behavioral and biological markers for predicting compulsive-like drinking in schedule-induced polydipsia
2019, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :The hypothesis of SIP drinking as coping and anxiolytic behavior (Brett and Levine, 1981; Brett and Levine, 1979) is based on studies reporting lower plasma CORT levels immediately after a SIP session in rats exhibiting excessive drinking than in animals with lower drinking rates or without a bottle in the operant chamber (Brett and Levine, 1981; Brett and Levine, 1979; Dantzer et al., 1988). Contrary, other studies reported similar or higher CORT levels in rats acquiring SIP than in rats under conditions without a water bottle or without a schedule of intermittent reinforcement (Mittleman et al., 1988; Tazi et al., 1986; Wallace et al., 1983). Moreover, the intracerebroventricular administration of corticotropin-releasing hormone decreased SIP drinking instead of increasing it (Cole and Koob, 1994).
Parsing the Role of Mesolimbic Dopamine in Specific Aspects of Motivation: Behavioral Activation, Invigoration, and Effort-Based Decision Making
2018, Advances in Motivation ScienceNeural substrates underlying effort, time, and risk-based decision making in motivated behavior
2016, Neurobiology of Learning and MemoryCitation Excerpt :The effects of dopamine antagonist within the NAcc also impacts goal-directed locomotion as intra-NAcc dopamine antagonists lead to both increased latency to run down a runway maze and reach a goal box containing food reward (slowing of reward approach) as well as reductions in spontaneous locomotion in the start box (Ikemoto & Panksepp, 1996). Moreover, the readily observed increases in numerous different types of activity which develop following the scheduled presentation of food (excessive drinking, voluntary wheel running, and locomotion) are all correlated with increases in mesolimbic dopamine signaling (McCullough & Salamone, 1992), and NAcc dopamine depletions suppress these behaviors (McCullough & Salamone, 1992; Robbins & Koob, 1980; Wallace, Singer, Finlay, & Gibson, 1983). These observations resulted in the development of a number of different genetic models which alter dopamine signaling.
The pharmacology of effort-related choice behavior: Dopamine, depression, and individual differences
2016, Behavioural ProcessesCitation Excerpt :Although food intake is generally preserved after administration of low doses of DA antagonists or accumbens DA depletion, considerable evidence indicates that interference with DA transmission in this manner can alter the behavioral activation induced by scheduled presentation of food reinforcement. Scheduled delivery of food pellets to food restricted animals can have activating properties (Killeen, 1975; Killeen et al., 1978; Salamone, 1988), and considerable evidence indicates that DA antagonism and accumbens DA depletions can reduce schedule-induced activities such as wheel running, polydipsia, and increased locomotor activity (Robbins and Koob, 1980; Robbins et al., 1983; Wallace et al., 1983; Salamone, 1988; McCullough and Salamone, 1992; Robbins and Everitt, 2007). Moreover, it is has been suggested that reductions in behavioral activation underlie the effects of DA antagonism or accumbens DA depletions on the performance of operant schedules, including progressive ratios (Salamone 1986, 1987, 1988; Hamill et al., 1999; Salamone and Correa, 2002, 2012; Olarte-Sánchez et al., 2013; see also Section 4).
Brain circuit dysfunction in a distinct subset of chronic psychotic patients
2014, Schizophrenia Research