scholarly journals Vesicular glutamate (VGlut), GABA (VGAT), and acetylcholine (VACht) transporters in basal forebrain axon terminals innervating the lateral hypothalamus

2006 ◽  
Vol 496 (4) ◽  
pp. 453-467 ◽  
Author(s):  
Pablo Henny ◽  
Barbara E. Jones
Keyword(s):  
Lateral Hypothalamus ◽  
Basal Forebrain ◽  
Axon Terminals

scholarly journals A lateral hypothalamus to basal forebrain neurocircuit promotes feeding by suppressing responses to anxiogenic environmental cues

2019 ◽  
Vol 5 (3) ◽  
pp. eaav1640 ◽  
Author(s):  
Ryan M. Cassidy ◽  
Yungang Lu ◽  
Madhavi Jere ◽  
Jin-Bin Tian ◽  
Yuanzhong Xu ◽  
...  
Keyword(s):  
Lateral Hypothalamus ◽  
Basal Forebrain ◽  
Gabaergic Neurons ◽  
Inhibitory Input ◽  
Environmental Cues ◽  
Diagonal Band ◽  
Diagonal Band Of Broca ◽  
External Signals

Animals must consider competing information before deciding to eat: internal signals indicating the desirability of food and external signals indicating the risk involved in eating within a particular environment. The behaviors driven by the former are manifestations of hunger, and the latter, anxiety. The connection between pathologic anxiety and reduced eating in conditions like typical depression and anorexia is well known. Conversely, anti-anxiety drugs such as benzodiazepines increase appetite. Here, we show that GABAergic neurons in the diagonal band of Broca (DBBGABA) are responsive to indications of risk and receive monosynaptic inhibitory input from lateral hypothalamus GABAergic neurons (LHGABA). Activation of this circuit reduces anxiety and causes indiscriminate feeding. We also found that diazepam rapidly reduces DBBGABA activity while inducing indiscriminate feeding. Our study reveals that the LHGABA→DBBGABA neurocircuit overrides anxiogenic environmental cues to allow feeding and that this pathway may underlie the link between eating and anxiety-related disorders.

scholarly journals 0156 Activation of Glutamatergic PPT Neurons and Their Projections Promotes Arousal, and Distinct Wake Behaviors

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A61-A62
Author(s):  
D Kroeger ◽  
J A Thundercliffe ◽  
A Phung ◽  
C Geraci ◽  
R DeLuca ◽  
...  
Keyword(s):  
Substantia Nigra ◽  
Optical Fibers ◽  
Lateral Hypothalamus ◽  
Rem Sleep ◽  
Basal Forebrain ◽  
Viral Vector ◽  
Nrem Sleep ◽  
Blue Laser ◽  
Dependent Manner ◽  
Glutamatergic Neurons

Abstract Introduction The pedunculopontine tegmental (PPT) region in the brainstem is crucial for the regulation of sleep/wake states. We recently showed that chemogenetic activation of glutamatergic PPT neurons promotes wakefulness for several hours. Here we used optogenetic activation of these neurons to further investigate the mechanisms and pathways through which PPT glutamatergic neurons produce wakefulness. Methods Using vGlut2-cre mice, we transfected neurons in the PPT region with a viral vector coding for cre-dependent ChR2 tagged with fluorescent mCherry and implanted bilateral optical fibers above the PPT nuclei as well as EEG/EMG leads. Two weeks later, we administered blue laser light to activate ChR2-expressing neurons and recorded sleep/wake states. Results Activation of ChR2-expressing glutamatergic neurons during NREM sleep rapidly elicited wakefulness in a stimulation-frequency dependent manner, with higher frequencies producing wake more quickly and with longer duration. Random, automated stimulation for 10 s at 5 Hz over 24 h revealed that activation of glutamatergic PPT neurons produces rapid arousals form NREM sleep. Importantly, stimulation did not wake mice from REM sleep, suggesting that glutamatergic PPT signaling does not interfere with REM sleep. To map the target areas through which PPT glut neurons produce wakefulness, we used a viral tracer to visualize PPT glutamatergic projections, and then optogenetically stimulated terminals in 1) basal forebrain, 2) lateral hypothalamus, 3) thalamus, and 4) substantia nigra. We found that stimulating terminals in all of these regions woke mice from NREM sleep, and stimulating terminals in the basal forebrain and lateral hypothalamus produced a number of active wake behaviors such as locomotion. In contrast, stimulation of PPT glut soma and terminals in the thalamus and substantia nigra results mainly in quiet wakefulness. Conclusion Glutamatergic PPT neurons potently promote arousal from NREM sleep but not REM sleep, and the resulting wake behavior is modulated by different projection targets. Support NIH grant P01 - HL095491

scholarly journals Basal forebrain mediates prosocial behavior via disinhibition of midbrain dopamine neurons

2021 ◽  
Vol 118 (7) ◽  
pp. e2019295118
Author(s):  
Jun Wang ◽  
Jie Li ◽  
Qian Yang ◽  
Ya-Kai Xie ◽  
Ya-Lan Wen ◽  
...  
Keyword(s):  
Social Interaction ◽  
Prosocial Behavior ◽  
Basal Forebrain ◽  
Social Preference ◽  
Dopamine Neurons ◽  
Inhibitory Neurons ◽  
Axon Terminals ◽  
Midbrain Dopamine ◽  
Da Release

Sociability is fundamental for our daily life and is compromised in major neuropsychiatric disorders. However, the neuronal circuit mechanisms underlying prosocial behavior are still elusive. Here we identify a causal role of the basal forebrain (BF) in the control of prosocial behavior via inhibitory projections that disinhibit the midbrain ventral tegmental area (VTA) dopamine (DA) neurons. Specifically, BF somatostatin-positive (SST) inhibitory neurons were robustly activated during social interaction. Optogenetic inhibition of these neurons in BF or their axon terminals in the VTA largely abolished social preference. Electrophysiological examinations further revealed that SST neurons predominantly targeted VTA GABA neurons rather than DA neurons. Consistently, optical inhibition of SST neuron axon terminals in the VTA decreased DA release in the nucleus accumbens during social interaction, confirming a disinhibitory action. These data reveal a previously unappreciated function of the BF in prosocial behavior through a disinhibitory circuitry connected to the brain’s reward system.

scholarly journals Adenosine Inhibits Activity of Hypocretin/Orexin Neurons by the A1 Receptor in the Lateral Hypothalamus: A Possible Sleep-Promoting Effect

2007 ◽  
Vol 97 (1) ◽  
pp. 837-848 ◽  
Author(s):  
Zhong-Wu Liu ◽  
Xiao-Bing Gao
Keyword(s):  
Lateral Hypothalamus ◽  
Basal Forebrain ◽  
Fluorescent Protein ◽  
Brain Slices ◽  
Inhibitory Effect ◽  
Calcium Currents ◽  
Excitatory Postsynaptic Potential ◽  
Sleep Regulation ◽  
Promoting Effect ◽  
Frequency Of Action Potentials

Neurons in the lateral hypothalamus (LH) that contain hypocretin/orexin have been established as important promoters of arousal. Deficiencies in the hypocretin/orexin system lead to narcolepsy. The inhibition of hypocretin/orexin neurons by sleep-promoting neurotransmitters has been suggested as one part of the sleep regulation machinery. Adenosine has been identified as a sleep promoter and its role in sleep regulation in the basal forebrain has been well documented. However, the effect of adenosine on arousal-promoting hypocretin/orexin neurons has not been addressed, despite recent evidence that immunocytochemical visualization of adenosine receptors was detected in these neurons. In this study, we examined the hypothesis that adenosine inhibits the activity of hypocretin/orexin neurons by using electrophysiological methods in brain slices from mice expressing green fluorescent protein in hypocretin/orexin neurons. We found that adenosine significantly attenuated the frequency of action potentials without a change in membrane potential in hypocretin/orexin neurons. The adenosine-mediated inhibition arises from depression of excitatory synaptic transmission to hypocretin/orexin neurons because adenosine depresses the amplitude of evoked excitatory postsynaptic potential and the frequency of spontaneous and miniature excitatory postsynaptic currents in these neurons. At the cell body of the hypocretin/orexin neurons, adenosine inhibits voltage-dependent calcium currents without the induction of GIRK current. The inhibitory effect of adenosine is dose dependent, pertussis toxin sensitive, and mediated by A1 receptors. In summary, our data suggest that in addition to its effect in the basal forebrain, adenosine exerts its sleep-promoting effect in the LH by inhibition of hypocretin/orexin neurons.

scholarly journals Medial Parabrachial Nucleus Is Essential in Controlling Wakefulness in Rats

2021 ◽  
Vol 15 ◽  
Author(s):  
Qi Xu ◽  
Dian-Ru Wang ◽  
Hui Dong ◽  
Li Chen ◽  
Jun Lu ◽  
...  
Keyword(s):  
Lateral Hypothalamus ◽  
Basal Forebrain ◽  
Power Spectra ◽  
Parabrachial Nucleus ◽  
Lateral Part ◽  
Medial Part ◽  
Neuronal Circuits ◽  
Medial Thalamus ◽  
Sleep Amount

Activation of the parabrachial nucleus (PB) in the brainstem induced wakefulness in rats, suggesting which is an important nucleus that controls arousal. However, the sub-regions of PB in regulating sleep-wake cycle is still unclear. Here, we employ chemogenetics and optogenetics strategies and find that activation of the medial part of PB (MPB), but not the lateral part, induces continuous wakefulness for 10 h without sleep rebound in neither sleep amount nor the power spectra. Optogenetic activation of glutamatergic MPB neurons in sleeping rats immediately wake rats mediated by the basal forebrain (BF) and lateral hypothalamus (LH), but not the ventral medial thalamus. Most importantly, chemogenetic inhibition of PB neurons decreases wakefulness for 10 h. Conclusively, these findings indicate that the glutamatergic MPB neurons are essential in controlling wakefulness, and that MPB-BF and MPB-LH pathways are the major neuronal circuits.

Effects of aging on axon terminals in the dentate molecular layer

1987 ◽  
Vol 45 ◽  
pp. 928-929
Author(s):  
K. Cullen-Dockstader ◽  
E. Fifkova
Keyword(s):  
Granule Cells ◽  
Molecular Layer ◽  
Age Groups ◽  
Long Term Potentiation ◽  
Male Rats ◽  
Perforant Path ◽  
Axon Terminals ◽  
Fischer 344 ◽  
Spatial Memory Deficit ◽  
Effects Of Aging

Normal aging results in a pronounced spatial memory deficit associated with a rapid decay of long-term potentiation at the synapses between the perforant path and spines in the medial and distal thirds of the dentate molecular layer (DML), suggesting the alteration of synaptic transmission in the dentate fascia. While the number of dentate granule cells remains unchanged, and there are no obvious pathological changes in these cells associated with increasing age, the density of their axospinous contacts has been shown to decrease. There are indications that the presynaptic element is affected by senescence before the postsynaptic element, yet little attention has been given to the fine structure of the remaining axon terminals. Therefore, we studied the axon terminals of the perforant path in the DML across three age groups.5 Male rats (Fischer 344) of each age group (3, 24 and 30 months), were perfused through the aorta.

Basal Forebrain Cholinergic Lesions Produce A Dissociation of Impairment In Delay And Trace Conditioning In Rats

2006 ◽  
Author(s):  
Erica K. Torner ◽  
M. Melissa Flesher ◽  
Anthony M. Cortez ◽  
Dennis Amodeo ◽  
Allen E. Butt
Keyword(s):  
Basal Forebrain ◽  
Trace Conditioning ◽  
Cholinergic Lesions
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