Lateral hypothalamic stimulation: Stimulus-bound eating and self-deprivation☆

Frank, Robert; Preshaw, Randolph L.; Stutz, Robert M.; Valenstein, Elliot S.

doi:10.1016/0031-9384(82)90359-6

Cited by 13 publications

(12 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…behavior and lesions of the LH reduce food intake (Arase et al 1987;Frank et al 1982;Grossman and Grossman 1982;Morgane 1961), and these effects have been shown to interact with taste-guided behavior (Conover and Shizgal 1994;Murzi et al 1986;Touzani and Sclafani 2001;Touzani and Velley 1990;Vasudev et al 1985). Whereas previous experiments in the rat have shown that LH stimulation activates NST neurons known to receive input from tongue afferent neurons (Bereiter et al 1980;Matsuo et al 1984;Murzi et al 1986), the present investigation physiologically confirms a bilateral influence of the LH on the responses of NST neurons to gustatory stimulation of the tongue.…”

Section: Discussionsupporting

confidence: 78%

“…Electrical stimulation of the LH enhances the responses of rat NST neurons evoked by chorda tympani (CT) nerve stimulation (Bereiter et al 1980) or by electrical stimulation of the anterior tongue (Matsuo et al 1984). Stimulation of the LH induces feeding behavior (Frank et al 1982;Shiraishi 1991;Sweet et al 1999) and alters taste preference behavior (Vasudev et al 1985) in rats. Lesions of the LH reduce food intake and alter plasma glucose levels and taste preferences (Arase et al 1987;Bernardis et al 1990;Grossman and Grossman 1982;Touzani and Velley 1990).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Taste Responses of Neurons of the Hamster Solitary Nucleus Are Enhanced by Lateral Hypothalamic Stimulation

Cho

Smith

2002

Journal of Neurophysiology

View full text Add to dashboard Cite

. Taste responses of neurons of the hamster solitary nucleus are enhanced by lateral hypothalamic stimulation. J Neurophysiol 87: 1981-1992, 2002; 10.1152/jn.00765.2001. Gustatory responses in the brain stem are modifiable by several physiological factors, including blood insulin and glucose, intraduodenal lipids, gastric distension, and learning, although the neural substrates for these modulatory effects are not known. Stimulation of the lateral hypothalamus (LH) produces increases in food intake and alterations in taste preference behavior, whereas damage to this area has opposite effects. In the present study, we investigated the effects of LH stimulation on the neural activity of taste-responsive cells in the nucleus of the solitary tract (NST) of the hamster. Bipolar stimulating electrodes were bilaterally implanted in the LH, and the responses of 99 neurons in the NST, which were first characterized for their taste sensitivities, were tested for their response to both ipsilateral and contralateral LH stimulation. Half of the tasteresponsive cells in the NST (49/99) were modulated by LH stimulation. Contralateral stimulation was more often effective (41 cells) than ipsilateral (13 cells) and always excitatory; 10 cells were excited bilaterally. Six cells were inhibited by ipsilateral stimulation. A subset of these cells (n ϭ 13) was examined for the effects of microinjection of DL-homocysteic acid (DLH), a glutamate receptor agonist, into the LH. The effects of electrical stimulation were completely mimicked by DLH, indicating that cell somata in and around the LH are responsible for these effects. Other cells (n ϭ 14) were tested for the effects of electrical stimulation of the LH on the responses to stimulation of the tongue with 0.032 M sucrose, NaCl, and quinine hydrochloride, and 0.0032 M citric acid. Responses to taste stimuli were more than doubled by the excitatory influence of the LH. These data show that the LH, in addition to its role in feeding and metabolism, exerts descending control over the processing of gustatory information through the brain stem.

show abstract

Section: Discussionsupporting

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Taste Responses of Neurons of the Hamster Solitary Nucleus Are Enhanced by Lateral Hypothalamic Stimulation

Cho

Smith

2002

Journal of Neurophysiology

View full text Add to dashboard Cite

show abstract

“…Stimulation of the LH produces increases in food intake and alterations in taste preference behavior (Frank et al, 1982;Vasudev et al, 1985), whereas damage to this area has opposite effects (Grossman et al, 1978;Touzani and Velley, 1990). Half of the taste-responsive cells in the NST (49/99) were modulated by LH stimulation (Cho et al, 2002).…”

Section: Lateral Hypothalamusmentioning

confidence: 96%

Neurochemistry of the Gustatory System

Smith

Boughter²

2006

Handbook of Neurochemistry and Molecular Neurobiology

View full text Add to dashboard Cite

“…However, access to palatable food dampens the increasing rate of level pressing for stimuli (Routtenberg and Lindy, 1965; Spies, 1965). These classical experiments suggest that 1) Activation of the LHA initiates food intake; 2) LHA stimulation is reinforcing and ‘rewarding’ (Hoebel and Teitelbaum, 1962; Frank et al, 1982); and 3) Pleasure derived from eating palatable foods is more intense than direct activation of the LHA, potentially due to involvement of additional elements of the reward circuitry (Routtenberg and Lindy, 1965; Spies, 1965; Coons and Cruce, 1968; Wise, 1974). Thus, it is likely that the initiation of food intake and the rewarding aspects of hedonic feeding (as well as direct LHA stimulation) are mediated by distinct pathways that converge in the LHA (Frank et al, 1982).…”

Section: The Lateral Hypothalamus (Lha)— the Linker Between The Hypotmentioning

confidence: 99%

High on food: the interaction between the neural circuits for feeding and for reward

et al. 2015

View full text Add to dashboard Cite

Hunger, mostly initiated by a deficiency in energy, induces food seeking and intake. However, the drive toward food is not only regulated by physiological needs, but is motivated by the pleasure derived from ingestion of food, in particular palatable foods. Therefore, feeding is viewed as an adaptive motivated behavior that involves integrated communication between homeostatic feeding circuits and reward circuits. The initiation and termination of a feeding episode are instructed by a variety of neuronal signals, and maladaptive plasticity in almost any component of the network may lead to the development of pathological eating disorders. In this review we will summarize the latest understanding of how the feeding circuits and reward circuits in the brain interact. We will emphasize communication between the hypothalamus and the mesolimbic dopamine system and highlight complexities, discrepancies, open questions and future directions for the field.

show abstract

Lateral hypothalamic stimulation: Stimulus-bound eating and self-deprivation☆

Cited by 13 publications

References 21 publications

Taste Responses of Neurons of the Hamster Solitary Nucleus Are Enhanced by Lateral Hypothalamic Stimulation

Taste Responses of Neurons of the Hamster Solitary Nucleus Are Enhanced by Lateral Hypothalamic Stimulation

Neurochemistry of the Gustatory System

High on food: the interaction between the neural circuits for feeding and for reward

Contact Info

Product

Resources

About