Effects of ibotenic acid lesion in the basal forebrain on electrical self-stimulation in the middle part of the lateral hypothalamus

Rats with bilateral lesions of the lateral hypothalamus (LH) fail to exhibit sodium appetite. Lesions of the parabrachial nuclei (PBN) also block salt appetite. The PBN projection to the LH is largely ipsilateral. If these deficits are functionally dependent, damaging the PBN on one side and the LH on the other should also block Na appetite. First, bilateral ibotenic acid lesions of the LH were needed because the electrolytic damage used previously destroyed both cells and axons. The ibotenic LH lesions produced substantial weight loss and eliminated Na appetite. Controls with ipsilateral PBN and LH lesions gained weight and displayed robust sodium appetite. The rats with asymmetric PBN-LH lesions also gained weight, but after sodium depletion consistently failed to increase intake of 0.5 M NaCl. These results dissociate loss of sodium appetite from the classic weight loss after LH damage and prove that Na appetite requires communication between neurons in the LH and the PBN.

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Neurons controlling cardiovascular responses to emotion are located in lateral hypothalamus-perifornical region

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1990.259.5.r943 ◽

1990 ◽

Vol 259 (5) ◽

pp. R943-R954 ◽

Cited By ~ 7

Author(s):

O. A. Smith ◽

J. L. DeVito ◽

C. A. Astley

Keyword(s):

Electrical Stimulation ◽

Lateral Hypothalamus ◽

Axonal Degeneration ◽

Neuronal Cell ◽

Cardiovascular Responses ◽

Ibotenic Acid ◽

Defense Reaction ◽

Autonomic Responses ◽

Neuronal Cell Bodies ◽

Thoracic Cord

We did four experiments to determine whether the lateral hypothalamus-perifornical (LH/PF) region is the source of neuronal cell bodies responsible for producing the cardiovascular (CV) responses associated with emotion or the defense reaction. Of particular concern was whether the paraventricular nucleus (PVN) plays a role in the generation of these CV responses. Mapping the hypothalamus with electrical stimulation showed that the CV pattern of responses was never produced by stimulating the PVN and was invariably produced by stimulating the LH/PF region. Complete electrolytic destruction of the PVN and subsequent axonal degeneration did not change the CV pattern of responses elicited by LH/PF stimulation, whereas any encroachment of the lesion on the LH/PF region decreased the magnitude of the CV responses. Injection of the neuroexcitotoxin ibotenic acid (Ibo) into the PVN did not affect responses to LH/PF stimulation, whereas Ibo injection into the LH/PF region eliminated or severely attenuated the CV responses. Retrograde labeling of cells from the thoracic cord and the ventrolateral reticular formation revealed a scattered group of cells in the LH/PF region that may be the cells controlling the CV responses. These results point directly to the LH/PF region as the source of the cell bodies responsible for the autonomic responses associated with emotion or defense reactions.

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Neuroanatomical aspects of the memory-improving effect of intracranial self-stimulation at the lateral hypothalamus: a c-Fos study

Frontiers in Behavioral Neuroscience ◽

10.3389/conf.neuro.08.2009.09.080 ◽

2009 ◽

Vol 3 ◽

Author(s):

Segura-Torres Pilar

Keyword(s):

Lateral Hypothalamus ◽

Self Stimulation

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

Science Advances ◽

10.1126/sciadv.aav1640 ◽

2019 ◽

Vol 5 (3) ◽

pp. eaav1640 ◽

Cited By ~ 9

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.

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