Blockade of nicotinic acetylcholine or dopamine D1-like receptors in the central nucleus of the amygdala or the bed nucleus of the stria terminalis does not precipitate nicotine withdrawal in nicotine-dependent rats

2006 ◽  
Vol 400 (1-2) ◽  
pp. 140-145 ◽  
Author(s):  
Sietse Jonkman ◽  
Athina Markou
Keyword(s):  
Nicotine Withdrawal ◽  
Central Nucleus ◽  
Stria Terminalis ◽  
Nicotinic Acetylcholine ◽  
Bed Nucleus

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.

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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