Dopamine D1 and opioid receptor antagonist-induced reductions of fructose and saccharin intake in BALB/c and SWR inbred mice

Kraft, Tamar T.; Huang, Donald; Natanova, Elona; Lolier, Melanie; Yakubov, Yakov; Magna, S.; Warshaw, Deena; Sclafani, Anthony; Bodnar, Richard J.

doi:10.1016/j.pbb.2015.01.010

Cited by 16 publications

(7 citation statements)

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“…In contrast, NTX BALB/c mice trained with sucrose failed to show a CS+ preference in Test 1 (54%) although a weak preference emerged in the second test (66%; Table 2D; Dym et al, 2012). The different NTX effects on fructose- and sucrose-CFP in BALB/c mice cannot be explained by any differential inhibitory actions of NTX on sucrose and fructose intake, per se (Dym et al, 2007; Kraft et al, 2015). Conceivably, the stronger NTX inhibitory effect on sucrose-CFP than fructose-CFP may be related to sucrose, but not fructose having a post-ingestive conditioning action in this strain.…”

Section: Discussionmentioning

confidence: 97%

“…Raclopride inhibited sucrose intake in these and other murine strains only at very high doses, and was not examined in further studies (Dym et al, 2009). With respect to fructose, SCH and NTX were more effective in reducing intake in SWR than BALB/c mice (Table 1: Kraft et al, 2015). Both DA D1 and opioid receptor antagonists were very effective in reducing saccharin intake in both strains (Table 1: Kraft et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

“…With respect to fructose, SCH and NTX were more effective in reducing intake in SWR than BALB/c mice (Table 1: Kraft et al, 2015). Both DA D1 and opioid receptor antagonists were very effective in reducing saccharin intake in both strains (Table 1: Kraft et al, 2015). Thus, selective strain differences were observed in the abilities of DA D1 and opioid antagonists to reduce nutritive and non-nutritive sweetener intakes in mice.…”

Section: Introductionmentioning

confidence: 99%

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Dopamine D1 and opioid receptor antagonists differentially reduce the acquisition and expression of fructose-conditioned flavor preferences in BALB/c and SWR mice

Kraft

Yakubov

Huang

et al. 2015

Physiology & Behavior

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Sugar appetite is influenced by unlearned and learned preferences in rodents. The present study examined whether dopamine (DA) D1 (SCH23390: SCH) and opioid (naltrexone: NTX) receptor antagonists differentially altered the expression and acquisition of fructose-conditioned flavor preferences (CFP) in BALB/c and SWR mice. In expression experiments, food-restricted mice alternately (10 sessions, 1 h) consumed a flavored (e.g., cherry) 8% fructose + 0.2% saccharin solution (CS+) and a differently-flavored (e.g., grape) 0.2% saccharin solution (CS−). Two-bottle CS choice tests (1 h) occurred 0.5 h following vehicle, SCH (200 or 800 nmol/kg) or NTX (1 or 5 mg/kg). SCH, but not NTX significantly reduced CS+ preference in both strains. In acquisition experiments, 0.5 h prior to 10 acquisition training sessions, vehicle, SCH (50 nmol/kg), NTX (1 mg/kg) or Limited Control vehicle treatments were administered, followed by two-bottle CS choice tests without injections. SCH and NTX reduced training intakes in both strains. BALB/c mice displayed hastened extinction of the fructose-CFP following training with SCH, but not NTX. SCH eliminated fructose-CFP acquisition in SWR mice, whereas NTX hastened extinction of the CFP. These results are compared to previous drug findings obtained with sucrose-CFP in SWR and BALB/c mice, and are discussed in terms of differential effects of these sugars on oral and post-oral conditioning.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dopamine D1 and opioid receptor antagonists differentially reduce the acquisition and expression of fructose-conditioned flavor preferences in BALB/c and SWR mice

Kraft

Yakubov

Huang

et al. 2015

Physiology & Behavior

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“…Both of these behaviors depend on an intact dopaminergic pleasure/reward system. 25 , 26 , 27 , 28 , 29 , 30 , 31 The dopaminergic reward system is not fully mature until the 3rd postnatal week in rodents 35 and is sensitive to the influence of early-life experiences. 34 , 36 Importantly, predictable sequences of events have been reported to engage the reward system.…”

Section: Discussionmentioning

confidence: 99%

“…Adolescent males reared in the LBN cages had a reduced capacity to experience pleasure (anhedonia) 24 and this was evident in two independent tests. Preference for sucrose and playing with peers, both dependent on normal function of the dopaminergic pleasure/reward system, 25 , 26 , 27 , 28 , 29 , 30 , 31 were diminished in LBN-reared vs CTL adolescents. Unexpectedly, these anhedonic characteristics could not be explained by differences in the quantity of maternal contact or by several typical qualitative measures of maternal-nurturing behaviors, because these did not differ between the two groups of dams.…”

Section: Introductionmentioning

confidence: 94%

Fragmentation and high entropy of neonatal experience predict adolescent emotional outcome

et al. 2016

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Vulnerability to emotional disorders including depression derives from interactions between genes and environment, especially during sensitive developmental periods. Across evolution, maternal care is a key source of environmental sensory signals to the developing brain, and a vast body of work has linked quantitative and qualitative aspects of maternal care to emotional outcome in children and animals. However, the fundamental properties of maternal signals, that promote advantageous vs pathological outcomes in the offspring, are unknown and have been a topic of intense study. We studied emotional outcomes of adolescent rats reared under routine or impoverished environments, and used mathematical approaches to analyze the nurturing behaviors of the dams. Unexpectedly, whereas the quantity and typical qualities of maternal care behaviors were indistinguishable in the two environments, their patterns and rhythms differed drastically and influenced emotional outcomes. Specifically, unpredictable, fragmented maternal care patterns translated into high-entropy rates of sensory signals to the offspring in the impoverished cages. During adolescence, these offspring had significant reductions in sucrose preference and in peer-play, two independent measures of the ability to experience pleasure. This adolescent anhedonia, often a harbinger of later depression, was not accompanied by measures of anxiety or helplessness. Dopaminergic pleasure circuits underlying anhedonia are engaged by predictable sequences of events, and predictable sensory signals during neonatal periods may be critical for their maturation. Conversely, unpredictability maternal-derived signals may disrupt these developmental processes, provoking anhedonia. In sum, high-entropy and fragmented patterns of maternal-derived sensory input to the developing brain predicts, and might promote, the development of anhedonia in rodents, with potential clinical implications.

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Does Anhedonia Presage Increased Risk of Posttraumatic Stress Disorder?

Risbrough

Glynn

Davis

et al. 2018

Behavioral Neurobiology of PTSD

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Anhedonia, the reduced ability to experience pleasure, is a dimensional entity linked to multiple neuropsychiatric disorders, where it is associated with diminished treatment response, reduced global function, and increased suicidality. It has been suggested that anhedonia and the related disruption in reward processing may be critical precursors to development of psychiatric symptoms later in life. Here, we examine cross-species evidence supporting the hypothesis that early life experiences modulate development of reward processing, which if disrupted, result in anhedonia. Importantly, we find that anhedonia may confer risk for later neuropsychiatric disorders, especially posttraumatic stress disorder (PTSD). Whereas childhood trauma has long been associated with increased anhedonia and increased subsequent risk for trauma-related disorders in adulthood, here we focus on an additional novel, emerging direct contributor to anhedonia in rodents and humans: fragmented, chaotic environmental signals ("FRAG") during critical periods of development. In rodents, recent data suggest that adolescent anhedonia may derive from aberrant pleasure/reward circuit maturation. In humans, recent longitudinal studies support that FRAG is associated with increased anhedonia in adolescence. Both human and rodent FRAG exposure also leads to aberrant hippocampal function. Prospective studies are underway to examine if anhedonia is also a marker of PTSD risk. These preliminary cross-species studies provide a critical construct for future examination of the etiology of trauma-related symptoms in adults and for and development of prophylactic and therapeutic interventions. In addition, longitudinal studies of reward circuit development with and without FRAG will be critical to test the mechanistic hypothesis that early life FRAG modifies reward circuitry with subsequent consequences for adolescent-emergent anhedonia and contributes to risk and resilience to trauma and stress in adulthood.

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Dopamine D1 and opioid receptor antagonist-induced reductions of fructose and saccharin intake in BALB/c and SWR inbred mice

Cited by 16 publications

References 58 publications

Dopamine D1 and opioid receptor antagonists differentially reduce the acquisition and expression of fructose-conditioned flavor preferences in BALB/c and SWR mice

Dopamine D1 and opioid receptor antagonists differentially reduce the acquisition and expression of fructose-conditioned flavor preferences in BALB/c and SWR mice

Fragmentation and high entropy of neonatal experience predict adolescent emotional outcome

Does Anhedonia Presage Increased Risk of Posttraumatic Stress Disorder?

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