Injection of muscimol, a GABA receptor agonist, into the lateral parabrachial nucleus (LPBN) induces 0.3 M NaCl intake in rats. In the present work, we investigated whether such an effect applies to hypertonic (0.3 M) mineral solutions in general or is selective to sodium solutions in a 240 min intake test. Muscimol injection (0.5 nmol/0.2 μL) compared to vehicle injection into the LPBN of adult hydrated rats produced a preferential ingestion of 0.3 M NaCl (25.3 ± 10.2 mL) followed by a 0.3 M NaHCO intake (11.7 ± 5.6 mL), with no significant effect on water, KCl and CaCl intake. Only the effect of muscimol on NaCl intake (19.0 ± 10.4 mL) persisted in cell-dehydrated rats, with hardly any effect on water or other mineral solutions. The results suggest that the LPBN controls the ingestion of hypertonic NaCl and NaHCO. They also suggest a selective mechanisms involving the LPBN to check hypertonic sodium intake.
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http://dx.doi.org/10.1016/j.neulet.2020.134989 | DOI Listing |
J Comp Neurol
January 2025
Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.
The parabrachial nucleus (PB), located in the dorsolateral pons, contains primarily glutamatergic neurons that regulate responses to a variety of interoceptive and cutaneous sensory signals. One lateral PB subpopulation expresses the Calca gene, which codes for the neuropeptide calcitonin gene-related peptide (CGRP). These PB neurons relay signals related to threatening stimuli such as hypercarbia, pain, and nausea, yet their inputs and their neurochemical identity are only partially understood.
View Article and Find Full Text PDFNeuroscience
January 2025
Center for Neuroscience, Indian Institute of Science, Bengaluru 560012, India. Electronic address:
Pain and itch are unpleasant and distinct sensations that give rise to behaviors such as reflexive withdrawal and scratching in humans and mice. Interestingly, it has been observed that pain modulates itch through the neural circuits housed in the brain and spinal cord. However, we have yet to fully understand the identities and mechanisms by which specific neural circuits mediate pain-induced modulation of itch.
View Article and Find Full Text PDFbioRxiv
December 2024
Department of Neurology, Division of Sleep Medicine, and Program in Neuroscience, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, 02215, USA.
Pain therapies that alleviate both pain and sleep disturbances may be the most effective for pain relief, as both chronic pain and sleep loss render the opioidergic system, targeted by opioids, less sensitive and effective for analgesia. Therefore, we first studied the link between sleep disturbances and the activation of nociceptors in two acute pain models. Activation of nociceptors in both acute inflammatory (AIP) and opto-pain models led to sleep loss, decreased sleep spindle density, and increased sleep fragmentation that lasted 3 to 6 hours.
View Article and Find Full Text PDFNeuron
December 2024
Department of Anesthesiology, Huashan Hospital, State Key Laboratory of Medical Neurobiology, Institute for Translational Brain Research, MOE Frontiers Center for Brain Science, Fudan University, Shanghai 200032, China. Electronic address:
The lateral parabrachial nucleus (PBN) is critically involved in neuropathic pain modulation. However, the cellular and molecular mechanisms underlying this process remain largely unknown. Here, we report that in mice, the right-sided, but not the left-sided, PBN plays an essential role in the development of hyperalgesia following nerve injury, irrespective of the injury side.
View Article and Find Full Text PDFPain
November 2024
Center for Neuroscience, Indian Institute of Science, Bengaluru, Karnataka, India.
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