scholarly journals Expression of Fos during sham sucrose intake in rats with central gustatory lesions

2008 ◽  
Vol 295 (3) ◽  
pp. R751-R763 ◽  
Author(s):  
Suriyaphun S. Mungarndee ◽  
Robert F. Lundy ◽  
Ralph Norgren
Keyword(s):  
Central Nucleus ◽  
Parabrachial Nucleus ◽  
Stria Terminalis ◽  
Sucrose Intake ◽  
Solitary Tract ◽  
Final Test ◽  
Taste System ◽  
Bed Nucleus ◽  
Thalamic Lesions ◽  
Gustatory Neurons

For humans and rodents, ingesting sucrose is rewarding. This experiment tested the prediction that the neural activity produced by sapid sucrose reaches reward systems via projections from the pons through the limbic system. Gastric cannulas drained ingested fluid before absorption. For 10 days, the rats alternated an hour of this sham ingestion between sucrose and water. On the final test day, half of them sham drank water and the other half 0.6 M sucrose. Thirty minutes later, the rats were killed and their brains immunohistochemically stained for Fos. The groups consisted of controls and rats with excitotoxic lesions in the gustatory thalamus (TTA), the medial (gustatory) parabrachial nucleus (PBN), or the lateral (visceral afferent) parabrachial nucleus. In controls, compared with water, sham ingesting sucrose produced significantly more Fos-positive neurons in the nucleus of the solitary tract, PBN, TTA, and gustatory cortex (GC). In the ventral forebrain, sucrose sham licking increased Fos in the bed nucleus of the stria terminalis, central nucleus of amygdala, and the shell of nucleus accumbens. Thalamic lesions blocked the sucrose effect in GC but not in the ventral forebrain. After lateral PBN lesions, the Fos distributions produced by distilled H2O or sucrose intake did not differ from controls. Bilateral medial PBN damage, however, eliminated the sucrose-induced Fos increase not only in the TTA and GC but also in the ventral forebrain. Thus ventral forebrain areas associated with affective responses appear to be activated directly by PBN gustatory neurons rather than via the thalamocortical taste system.

scholarly journals Forebrain neurons that project to the gustatory parabrachial nucleus in rat lack glutamic acid decarboxylase

2008 ◽  
Vol 294 (1) ◽  
pp. R52-R57 ◽  
Author(s):  
Shalini Saggu ◽  
Robert F. Lundy
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Input Resistance ◽  
Central Nucleus ◽  
Parabrachial Nucleus ◽  
Acid Decarboxylase ◽  
Inhibitory Influence ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Forebrain Neurons

Evidence suggests that GABA might mediate the inhibitory influence of centrifugal inputs on taste-evoked responses in the parabrachial nucleus (PBN). Previous studies show that activation of the gustatory cortex (GC), bed nucleus of the stria terminalis (BNST), central nucleus of the amygdala (CeA), and lateral hypothalamus (LH) inhibits PBN taste responses, GABAergic neurons are present in these forebrain regions, and GABA reduces the input resistance of PBN neurons. The present study investigated the expression of glutamic acid decarboxylase immunoreactivity (GAD_67 ir) in GC, BNST, CeA, and LH neurons that project to the PBN in rats. After anesthesia (50 mg/kg ip Nembutal), injections of the retrograde tracer Fluorogold (FG) were made in the physiologically defined gustatory PBN. Brain tissue containing the above forebrain structures was processed and examined for FG and GAD_67 ir. Similar to previous studies, each forebrain site contained retrogradely labeled neurons. Our results suggest further that the major source of input to the PBN taste region is the CeA (608 total cells) followed by GC (257 cells), LH (106 cells), and BNST (92 cells). This suggests a differential contribution to centrifugal control of PBN taste processing. We further show that despite the presence of GAD_67 neurons in each forebrain area, colocalization was extremely rare, occurring only in 3 out of 1,063 FG-labeled cells. If we assume that the influence of centrifugal input is mediated by direct projections to the gustatory region of the PBN, then GABAergic forebrain neurons apparently are not part of this descending pathway.

Efferent projection from the bed nucleus of the stria terminalis suppresses activity of taste-responsive neurons in the hamster parabrachial nuclei

2006 ◽  
Vol 291 (4) ◽  
pp. R914-R926 ◽  
Author(s):  
Cheng-Shu Li ◽  
Young K. Cho
Keyword(s):  
Feeding Behavior ◽  
Electrophysiological Study ◽  
Ingestive Behavior ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Descending Modulation ◽  
Efferent Projection ◽  
Neural Substrate ◽  
Parabrachial Nuclei ◽  
Gustatory Neurons

Although the reciprocal projections between the bed nucleus of the stria terminalis (BNST) and the gustatory parabrachial nuclei (PbN) have been demonstrated neuroanatomically, there is no direct evidence showing that the projections from the PbN to the BNST carry taste information or that descending inputs from the BNST to the PbN modulate the activity of PbN gustatory neurons. A recent electrophysiological study has demonstrated that the BNST exerts modulatory influence on taste neurons in the nucleus of the solitary tract (NST), suggesting that the BNST may also modulate the activity of taste neurons in the PbN. In the present study, we recorded from 117 taste-responsive neurons in the PbN and examined their responsiveness to electrical stimulation of the BNST bilaterally. Thirteen neurons (11.1%) were antidromically invaded from the BNST, mostly from the ipsilateral side (12 cells), indicating that a subset of taste neurons in the PbN project their axons to the BNST. The BNST stimulation induced orthodromic responses on most of the PbN neurons: 115 out of 117 (98.3%), including all BNST projection units. This descending modulation on the PbN gustatory neurons was exclusively inhibitory. We also confirmed that activation of this efferent inhibitory projection from the BNST reduces taste responses of PbN neurons in all units tested. The BNST is part of the neural circuits that involve stress-associated feeding behavior. It is also known that brain stem gustatory nuclei, including the PbN, are associated with feeding behavior. Therefore, this neural substrate may be important in the stress-elicited alteration in ingestive behavior.

Anxiety Reduction and Maternal Aggression in Postpartum Nonhuman Mammals

2020 ◽  
pp. 164-193
Author(s):  
Michael Numan
Keyword(s):  
Neural Circuitry ◽  
Corticotropin Releasing Factor ◽  
Anxiety Reduction ◽  
Central Nucleus ◽  
Ventromedial Nucleus ◽  
Stria Terminalis ◽  
Maternal Aggression ◽  
Postpartum Anxiety ◽  
Bed Nucleus ◽  
Crf Neurons

Chapter 6 explores the neural mechanisms that regulate the decrease in anxiety and increase in maternal aggression that co-occur in postpartum mammals. Too much anxiety antagonizes maternal aggression. Therefore, postpartum anxiety reduction promotes maternal aggression. The neural circuitry of maternal aggression includes projections from the ventromedial nucleus of the hypothalamus to the periaqueductal gray and to other brainstem sites. Anxiety-related behaviors are mediated by corticotropin-releasing factor (CRF) neurons, and the projection of central nucleus of amygdala (CeA) CRF neurons to the dorsal bed nucleus of the stria terminalis is involved. Neural circuits are described to show how enhanced CRF release can depress maternal aggression. These circuits are typically downregulated in postpartum females, and oxytocin (OT) is involved. OT exerts anxiolytic effects and one mechanism of OT action is to depress the output of CeA.

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