Table 1.

Overview of studies showing effects of discussed peptides and hormones on food, alcohol, drug, and social behavior.

Peptide	Brain area		Manipulation	Behavioral effect	Citation
α-MSH	VTA		Intraparenchymal MCR agonist injection	Reduced the intake of chow and sucrose	(Roseberry, 2013; Yen and Roseberry, 2014)
				Decreased sucrose self-administration	(Shanmugarajah et al., 2017)
			Intraparenchymal MC3R agonist injection	Increased sucrose self-administration but not free feeding on sucrose.	(Pandit et al., 2016)
			Chemogenetic activation of MC3R-expressing neurons	Decreased feeding in female mice	(Dunigan et al., 2021)
	NAcc		Intraparenchymal MC4-R agonist injection	Decreased feeding	(Lerma-Cabrera et al., 2012)
			Intraparenchymal α-MSH injection	Decreased motivation for sucrose	(Pandit et al., 2015)
AgRP	VTA		Intraparenchymal MCR antagonist injection	Increased chow intake	(Roseberry, 2013)
				Increased sucrose self-administration	(Shanmugarajah et al., 2017)
			Chemogenetic inhibition of MC3R-expressing neurons	Decreased feeding in male mice	(Dunigan et al., 2021)
	NAcc		Intraparenchymal MC4-R antagonist injection	Increased feeding	(Lerma-Cabrera et al., 2012)
			Intraparenchymal AgRP or MCR antagonist injection	Increased motivation for sucrose	(Pandit et al., 2015)
				Blocked reinforcing, motivational and sensitizing effects of cocaine	(Hsu et al., 2005)
	Global		MC3R knockout and re-expression	Sex-dependently altered sucrose preference and DA turnover.	(Lippert et al., 2014).
				Altered food self-administration under FR1 and PR conditions in food-restricted mice with a reversal in PR responding following MC3R re-expression in DA neurons.	(Mavrikaki et al., 2016)
NPY	NAcc		Constitutive activation of NAcc NPY2R	Reduced expression of ethanol-induced behavioral sensitization	(Hayes et al., 2012)
			Intraparenchymal NPY or NPY1R agonist injection	Increased ethanol self-administration directly into the posterior VTA.	(Borkar et al., 2016)
					(Desai et al., 2013)
				Potentiated the rewarding effect of morphine.	(Wang et al., 2020)
				Prolonged the extinction period following chronic morphine exposure
			Intraparenchymal NPY5R antagonist injection	Reduced morphine extinction period	(Wang et al., 2020)
CRF	VTA		Intraparenchymal CRF injection	Reduced motivation for food reward	(Wanat et al., 2013)
				Reinstated lever pressing for cocaine	(Wang et al., 2005; Wang et al., 2007)
			Intraparenchymal CRF antagonist injection	Blocked foot shock-induced reinstatement of cocaine seeking.	(Wang et al., 2005)
					(Boyson et al., 2014).
				Prevented dopaminergic cross-sensitizations and escalated cocaine self-administration.
			Intraparenchymal CRFR1 antagonist or CRFR2 agonist injection	Decreased binge-like ethanol drinking (drinking in the dark)	(Rinker et al., 2017; Sparta et al., 2013)
			Intraparenchymal CRFR1 antagonist	Reduce alcohol consumption in an intermittent access two-bottle choice paradigm.	(Hwa et al., 2013)
					(Hwa et al., 2016)
					(Grieder et al., 2014).
				Reduced social defeat stress-enhanced ethanol drinking.
				Prevented anxiety-like behavior during nicotine withdrawal.
			ShRNA-mediated knockdown of CRFR1	Reduced cue-induced cocaine seeking but not cue-induced sucrose seeking	(Chen et al., 2014)
	NAcc		Intraparenchymal CRF injection	Enhanced the ability of Pavlovian reward cues to trigger instrumental performance for sucrose reward	(Peciña et al., 2006)
			CRF overexpression	Increased operant responding to nicotine and increased food intake (females> males)	(Uribe et al., 2020).
MCH	NAcc		Intraparenchymal MCH injection	Increased feeding (only in males) Restored feeding in Pmch null mice to wild-type levels	(Georgescu et al., 2005; Terrill et al., 2020)
					(Mul et al., 2011).
			Intraparenchymal MCHR1 antagonist injection	Decreased feeding	(Georgescu et al., 2005)
Orexin	VTA		Intraparenchymal OX-A injection	Increased chow, HFD and sucrose intake.	(Terrill et al., 2016)
				Attenuated intragastric nutrient-induced hypophagia.	(España et al., 2011)
					(Harris et al., 2005; Wang et al., 2009)
				Promoted cocaine self-administration. Reinstated previously extinguished morphine and cocaine preference.
			Intraparenchymal OX-1R antagonist injection	Attenuated orexigenic effects of ICV ghrelin.	(Cone et al., 2014)
					(Olney et al., 2017)
				Blunted binge-like ethanol intake.	(Borgland et al., 2009; España et al., 2010)
				Reduced cocaine self-administration.
				Prevented acquisition of locomotor sensitization to cocaine.	(Borgland et al., 2006)
					(James et al., 2011)
				Attenuated cue-induced cocaine reinstatement.
			Intraparenchymal OX-1R/OX-2R antagonist injection	Attenuated alcohol self-administration	(Srinivasan et al., 2012)
		NAcc	Intraparenchymal OX-A injection	Increased feeding	(Thorpe and Kotz, 2005)
				Increased the hedonic impact of sucrose taste and increased palatable food intake	(Castro et al., 2016)
			Intraparenchymal OX-1R antagonist injection	Decreased alcohol intake in excessive but not moderate drinkers	(Lei et al., 2019; Lei et al., 2016)
					(Qi et al., 2013)
				Attenuated stress-induced morphine reinstatement
Oxytocin		VTA	Intraparenchymal OT injection	Decreased chow intake at acute time points.	(Wald et al., 2020)
					(Mullis et al., 2013)
				Decreased sucrose intake.	(Wald et al., 2020)
				Reduced food motivation and food seeking. (Mullis et al., 2013; Wald et al., 2020)	(Song et al., 2016).
					(Borland et al., 2018)
				Reduced place avoidance for the social interaction chamber.
				Decreased the frequency of seeking social interaction in Operant Social Preference task.
			Optogenetic stimulation of PVN OT axon terminals	Promoted sociability.	(Hung et al., 2017)
			Intraparenchymal OTR antagonist injection	Increased sucrose intake.	(Mullis et al., 2013)
				Increased the frequency of entering social interaction chambers in Operant Social Preference task.	(Borland et al., 2018)
		NAcc	Intraparenchymal OT injection	Decreased chow intake in deprived conditions and the consumption of palatable nutritive and non-nutritive sweet solutions.	(Herisson et al., 2016)
					(Baracz et al., 2012; Cox et al., 2017)
					(Ibragimov et al., 1987; Weber et al., 2018)
				Attenuated METH-induced CPP, drug seeking and demand.
				Inhibited cocaine seeking and heroin self-administration.
			OTR overexpression	Reduced ethanol preference, ethanol intake, and reinstatement of ethanol conditioned place preference.	(Bahi, 2015; Bahi et al., 2016)
			Intraparenchymal OTR antagonist injection	Prevented social CPP.	(Dolen et al., 2013)
Amylin		VTA	Intraparenchymal AmyR agonist injection	Decreased the intake of chow, sucrose, and HFD primarily through a reduction in meal size.	(Mietlicki-Baase et al., 2015; Mietlicki-Baase et al., 2013b)
					(Mietlicki-Baase et al., 2017)
				Decreased the intake of palatable, non-nutritive sweetener.	(Mietlicki-Baase et al., 2013b)
					(Kalafateli et al., 2021b)
				Decreased the motivation to work for sucrose reward.	(Kalafateli et al., 2021a)
				Blocked alcohol-induced locomotor stimulation and decreased alcohol-induced DA release in the NAcc shell in mice and decreased alcohol intake in rats.
				Decreased cocaine-evoked locomotor stimulation.
			Intraparenchymal AmyR antagonist injection	Increased food intake.	(Mietlicki-Baase et al., 2013b)
			VTA CTR knockdown	Produced hyperphagia in HFD-fed animals.	(Mietlicki-Baase et al., 2015)
		NAcc	Intraparenchymal AmyR agonist injection	Blocked alcohol-induced locomotor stimulation.	(Kalafateli et al., 2021b)
					(Kalafateli et al., 2021a)
				Decreased cocaine-induced locomotor stimulation.
Neurotensin		VTA	Intraparenchymal NT injection	Increased latency to eat and reduced food intake in fasted animals.	(Cador et al., 1986; Hawkins, 1986)
					(Kelley et al., 1989)
				Reduced operant responding for food.
			NTS1R-expressing neuron ablation	Increased the intake of chow, sucrose, and HFD.	(Woodworth et al., 2017).
GLP-1		VTA	Intraparenchymal GLP-1R agonist injection	Reduced the intake of palatable food.	(Alhadeff et al., 2012)
				Reduced chow intake in fasted animals or when chow was the only caloric source.	(Dickson et al., 2012).
					(Alhadeff et al., 2012; Mietlicki-Baase et al., 2014; Mietlicki-Baase et al., 2013a)
				Decreased HFD intake while increasing chow intake in animals fed both diets simultaneously.	(Alhadeff et al., 2012).
					(Dickson et al., 2012).
				Decreased 1hr sucrose intake.	(Shirazi et al., 2013)
				Decreased the motivation to obtain sucrose reward.	(Vallöf et al., 2019).
					(Schmidt et al., 2016)
				Decreased alcohol intake.	(Hernandez et al., 2018)
				Decreased alcohol-induced locomotor behavior.
				Reduced cocaine self-administration.
				Reduced cocaine-primed reinstatement.
			Chemogenetic induction of GLP-1 release from NTS terminals	Reduced HFD intake.	(Wang et al., 2015)
		NAcc	Intraparenchymal GLP-1R agonist injection	Decreased HFD intake while increasing chow intake in animals fed both diets simultaneously.	(Alhadeff et al., 2012; Mietlicki-Baase et al., 2014; Mietlicki-Baase et al., 2013a)
					(Alhadeff et al., 2012).
				Decreased 1hr sucrose intake.	(Dickson et al., 2012).
				Decreased the motivation to obtain sucrose reward.	(Vallöf et al., 2019)
					(Hernandez et al., 2019).
				Decreased alcohol consumption in alcohol-preferring animals only.
				Decreased alcohol-induced locomotor response and alcohol CPP.
				Reduced cocaine-primed reinstatement.
			Intraparenchymal GLP-1R antagonist injection	Increased sucrose meal size and sucrose palatability.	(Dossat et al., 2013)