Activation of GABAA and GABAB receptors in the lateral septum increases sucrose intake by differential stimulation of sucrose licking activity

Mitra, Arojit; Lenglos, Christophe; Timofeeva, Elena

doi:10.1016/j.bbr.2014.07.035

Cited by 15 publications

(17 citation statements)

References 78 publications

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“…Administration of baclofen into the medial LS significantly increased sucrose intake. This result is in accordance with a previous report showing stimulation of sucrose intake by direct injections of baclofen into the LS (Mitra et al ., ). In addition, the present results revealed the intra‐LS administration of baclofen decreased the anorectic effects of stress.…”

Section: Discussionmentioning

confidence: 99%

Inhibition in the lateral septum increases sucrose intake and decreases anorectic effects of stress

Mitra

Lenglos

Timofeeva

2014

Eur J of Neuroscience

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Sucrose-overeating rats with decreased anorectic response to stress showed lower stress-induced activation of c-fos expression in the lateral septum (LS). The present study tested a hypothesis that neuronal inhibition in the LS is important for the development and maintenance of the sucrose-overeating phenotype. Sucrose overeating was developed with weekly episodes of food restriction (21 h per day, 4 days per week) followed by 1-h access to sucrose. The anorectic effects of stress on 1-h sucrose intake were estimated using weekly foot shock stress sessions. The development of the sucrose-overeating phenotype was accompanied by a decrease in the anorectic effects of stress and by an increase in LS mRNA expression of a γ-aminobutyric acid (GABA) synthesising enzyme, glutamic acid decarboxylase 67 in stressed rats. Direct recordings of neuronal firing in the LS in rats submitted to repeated weekly cycles of food restriction, sucrose refeeding and stress showed that the development of sucrose overeating increased the percentage of LS neurons inhibited during anticipation and at the start of clusters (CS) of sucrose licking. In addition, the CS-excited LS neurons showed a decrease in responsiveness to sucrose during the development of sucrose overeating. Direct injection of baclofen, an agonist of the GABAB receptor, into the LS decreased the anorectic effects of stress and increased sucrose intake. These results suggest that an increase in inhibitory effects in the LS is important for the development of sucrose overeating and the decreased anorectic effects of stress.

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Section: Discussionmentioning

confidence: 99%

Inhibition in the lateral septum increases sucrose intake and decreases anorectic effects of stress

Mitra

Lenglos

Timofeeva

2014

Eur J of Neuroscience

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“…Blockade of CRF 2 Rs in the LS attenuates restraint-stress-induced anorexia [22]. Furthermore, inhibition of LS neurons can reduce the anorectic effects of stress and increase sucrose intake in rats submitted to weekly cycles of stress [23,24]. This area has also been shown to play a role in modulation of HPA axis activity [20].…”

Section: Introductionmentioning

confidence: 99%

Endogenous GLP-1 in lateral septum contributes to stress-induced hypophagia

Terrill

Maske

Williams

2018

Physiology & Behavior

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Glucagon-like peptide 1 (GLP-1) neurons of the caudal brainstem project to many brain areas, including the lateral septum (LS), which has a known role in stress responses. Previously, we showed that endogenous GLP-1 in the LS plays a physiologic role in the control of feeding under non-stressed conditions, however, central GLP-1 is also involved in behavioral and endocrine responses to stress. Here, we asked whether LS GLP-1 receptors (GLP-1R) contribute to stress-induced hypophagia. Male rats were implanted with bilateral cannulas targeting the dorsal subregion of the LS (dLS). In a within-subjects design, shortly before the onset of the dark phase, rats received dLS injections of saline or the GLP-1R antagonist Exendin (9-39) (Ex9) prior to 30 min restraint stress. Food intake was measured continuously for the next 20 h. The stress-induced hypophagia observed within the first 30 min of dark was not influenced by Ex9 pretreatment, but Ex9 tended to blunt the effect of stress as early as 1 and 2 h into the dark phase. By 4-6 h, there were significant stress X drug interactions, and Ex9 pretreatment blocked the stress-induced suppression of feeding. These effects were mediated entirely through changes in average meal size; stress suppressed meal size while dLS Ex9 attenuated this effect. Using a similar design, we examined the role of dLS GLP-1R in the neuroendocrine response to acute restraint stress. As expected, stress potently increased serum corticosterone, but blockade of dLS GLP-1Rs did not affect this response. Together, these data show that endogenous GLP-1 action in the dLS plays a role in some but not all of the physiologic responses to acute stress.

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“…The small- and medium-sized GABAergic neurons of the AHA are particularly dense in the central nucleus of the AHA (cAHA) [ 11 ], and a fraction of the GABAergic neurons in this area induces expression of c-Fos, a molecular marker of neuronal activation, in response to stress [ 12 ]. GABA neurotransmission is involved in food intake regulation [ 13 – 17 ]. Direct administration of the GABA A receptor agonist muscimol into the AHA was found to increase feeding in satiated sheep [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Stress and Sucrose Intake Modulate Neuronal Activity in the Anterior Hypothalamic Area in Rats

2016

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The anterior hypothalamic area (AHA) is an important integrative relay structure for a variety of autonomic, endocrine, and behavioral responses including feeding behavior and response to stress. However, changes in the activity of the AHA neurons during stress and feeding in freely moving rats are not clear. The present study investigated the firing rate and burst activity of neurons in the central nucleus of the AHA (cAHA) during sucrose intake in non-stressful conditions and after acute stress in freely behaving rats. Rats were implanted with micro-electrodes into the cAHA, and extracellular multi-unit activity was recorded during 1-h access to 10% sucrose in non-stressful conditions or after acute foot shock stress. Acute stress significantly reduced sucrose intake, total sucrose lick number, and lick frequency in licking clusters, and increased inter-lick intervals. At the cluster start (CS) of sucrose licking, the cAHA neurons increased (CS-excited, 20% of the recorded neurons), decreased (CS-inhibited, 42% of the neurons) or did not change (CS-nonresponsive, 38% of the neurons) their firing rate. Stress resulted in a significant increase in the firing rate of the CS-inhibited neurons by decreasing inter-spike intervals within the burst firing of these neurons. This increase in the stress-induced firing rate of the CS-inhibited neurons was accompanied by a disruption of the correlation between the firing rate of CS-inhibited and CS-nonresponsive neurons that was observed in non-stressful conditions. Stress did not affect the firing rate of the CS-excited and CS-nonresponsive neurons. However, stress changed the pattern of burst firing of the CS-excited and CS-nonresponsive neurons by decreasing and increasing the burst number in the CS-excited and CS-nonresponsive neurons, respectively. These results suggest that the cAHA neurons integrate the signals related to stress and intake of palatable food and play a role in the stress- and eating-related circuitry.

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Activation of GABAA and GABAB receptors in the lateral septum increases sucrose intake by differential stimulation of sucrose licking activity

Cited by 15 publications

References 78 publications

Inhibition in the lateral septum increases sucrose intake and decreases anorectic effects of stress

Inhibition in the lateral septum increases sucrose intake and decreases anorectic effects of stress

Endogenous GLP-1 in lateral septum contributes to stress-induced hypophagia

Stress and Sucrose Intake Modulate Neuronal Activity in the Anterior Hypothalamic Area in Rats

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