Hypothalamic inhibition of neurones in the nucleus tractus solitarius of the cat is GABA mediated.

Jordan, David L.; Mifflin, Steve; Spyer, K. M.

doi:10.1113/jphysiol.1988.sp017087

Cited by 127 publications

(101 citation statements)

References 24 publications

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“…However, increased c-Fos responses in the DMM were not occurring in parasympathetic preganglionic acetylcholinergic neurons (DMV and Amb), or other regions involved in the baroreflex-mediated sympathetic inhibition (eg CVLM) (Chan and Sawchenko, 1998). The DMH directly innervates the nTS (Fontes et al, 2001), and electrical or chemical (see review (McDowall et al, 2006)) stimulation of the DMH decreases the sensitivity of the baroreflex through a GABAergic mechanism in the nTS/DMV (Jordan et al, 1988). This circuit represents an adaptive means of inhibiting the baroreflex during 'fight or flight' responses and exercise (Potts et al, 2003).…”

Section: Pathways For Lactate-induced Panic-like Responsesmentioning

confidence: 99%

Neural Pathways Underlying Lactate-Induced Panic

Johnson

Truitt

Fitz

et al. 2007

Neuropsychopharmacol

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Panic disorder is a severe anxiety disorder characterized by susceptibility to induction of panic attacks by subthreshold interoceptive stimuli such as 0.5 M sodium lactate infusions. Although studied for four decades, the mechanism of lactate sensitivity in panic disorder has not been understood. The dorsomedial hypothalamus/perifornical region (DMH/PeF) coordinates rapid mobilization of behavioral, autonomic, respiratory and endocrine responses to stress, and rats with disrupted GABA inhibition in the DMH/PeF exhibit panic-like responses to lactate, similar to panic disorder patients. Utilizing a variety of anatomical and pharmacological methods, we provide evidence that lactate, via osmosensitive periventricular pathways, activates neurons in the compromised DMH/PeF, which relays this signal to forebrain limbic structures such as the bed nucleus of the stria terminalis to mediate anxiety responses, and specific brainstem sympathetic and parasympathetic pathways to mediate the respiratory and cardiovascular components of the panic-like response. Acutely restoring local GABAergic tone in the DMH/PeF blocked lactate-induced panic-like responses. Autonomic panic-like responses appear to be a result of DMH/PeF-mediated mobilization of sympathetic responses (verified with atenolol) and resetting of the parasympathetically mediated baroreflex. Based on our findings, DMH/PeF efferent targets such as the C1 adrenergic neurons, paraventricular hypothalamus, and the central amygdala are implicated in sympathetic mobilization; the nucleus of the solitary tract is implicated in baroreflex resetting; and the parabrachial nucleus is implicated in respiratory responses. These results elucidate neural circuits underlying lactate-induced panic-like responses and the involvement of both sympathetic and parasympathetic systems.

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Section: Pathways For Lactate-induced Panic-like Responsesmentioning

confidence: 99%

Neural Pathways Underlying Lactate-Induced Panic

Johnson

Truitt

Fitz

et al. 2007

Neuropsychopharmacol

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“…To date there is good evidence to suggest that descending control of the cardiac baroreflex by the dorsal PAG, as well as other defense regions of the brain, involves activation of both GABA-A and 5-HT3 receptors in the nucleus of the solitary tract (NTS) (7,21,38). Interestingly blockade of these receptor subtypes in the NTS does not evoke a parallel change in baseline baroreflex function or dorsal PAG evoked increases in baseline MAP or HR (38).…”

Section: Pag Modulation Of the Arterial Baroreflex Controlmentioning

confidence: 99%

Midbrain modulation of the cardiac baroreflex involves excitation of lateral parabrachial neurons in the rat

Hayward

2007

Brain Research

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Activation of the dorsal periaqueductal gray (PAG) evokes defense-like behavior including a marked increase in sympathetic drive and resetting of baroreflex function. The goal of this study was to investigate the role of the lateral parabrachial nucleus (LPBN) in mediating dorsal PAG modulation of the arterial baroreflex. Reflex responses were elicited by electrical stimulation of the aortic depressor nerve (ADN) at 5 Hz or 15 Hz in urethane anesthetized rats (n=18). Electrical stimulation of the dorsal PAG at 10 Hz did not alter baseline mean arterial pressure (MAP) but did significantly attenuate baroreflex control of heart rate (HR) evoked by low frequency ADN stimulation. Alternatively, 40 Hz dorsal PAG stimulation increased baseline MAP (43±3 mmHg) and HR (33±3 bpm) and attenuated baroreflex control of HR at both ADN stimulation frequencies. Reflex control of MAP was generally unchanged by dorsal PAG stimulation. Bilateral inhibition of neurons in LPBN area (n=6) with muscimol (0.45 nmol per side) reduced dorsal PAG evoked increases in MAP and HR by 50±4% and 95±4%, respectively, and significantly reduced, but did not completely eliminate dorsal PAG attenuation of the cardiac baroreflex. Bilateral blockade of glutamate receptors in the LPBN area (n=6) with kynurenic acid (1.8 nmol) had a similar effect on dorsal PAG evoked increases in MAP, HR and cardiac baroreflex function. Reflex control of MAP was unchanged with either treatment. These findings suggest that the LPBN area is one of several brainstem regions involved in descending modulation of the cardiac baroreflex function during defensive behavior.

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“…Some GABA terminals likely originate from local interneurons, whereas others may well arise from outside NTS (Jordan et al, 1988). Shortlatency, afferent-synched IPSCs (Mifflin and Felder, 1988;Andresen and Yang, 1995) appear to reflect local feedback circuits onto second-order NTS neurons.…”

Section: Heterogeneous Group-specific Mglur Modulation Of Gaba Transmentioning

confidence: 99%

Cranial Afferent Glutamate Heterosynaptically Modulates GABA Release onto Second-Order Neurons via Distinctly Segregated Metabotropic Glutamate Receptors

Jin¹,

Bailey²,

Andresen³

2004

J. Neurosci.

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The balance between excitation and inhibition dictates central integration. Glutamatergic and GABAergic neurotransmission dominate this process. Cranial primary afferents enter the brainstem to release glutamate (Glu) onto second-order neurons within the caudal nucleus tractus solitarius (NTS) to initiate autonomic reflexes. The simplest pathways for these reflexes contain as few as two central neurons, but display robust frequency-dependent behavior. Within NTS, multiple metabotropic Glu receptors (mGluRs) are present, but their roles are poorly understood. Using synaptically discriminated second-order NTS neurons in brainstem slices and mechanically dissociated NTS neurons with intact boutons, we show that Glu differentially controls GABA release via distinct presynaptic mGluRs. In second-order NTS neurons recorded in slices, activation of primary afferents at frequencies as low as 10 shocks per second released sufficient Glu to alter rates of spontaneous IPSCs (sIPSCs). In both approaches, group I mGluRs increased GABA release in some neurons, but, on different neurons, group II and group III mGluRs decreased the sIPSC rate. mGluR actions were remarkably rapid, with onset and reversal beginning within 100 msec. In all cases, mGluR actions were exclusively presynaptic, and mGluRs did not alter postsynaptic properties in second-order neurons in either slices or isolated neurons. Tests with capsaicin and ␣␤-methylene ATP suggest that myelinated and unmyelinated afferent pathways engage both mGluR-GABA mechanisms. Afferent Glu spillover provides heterosynaptic cross talk with GABAergic inhibition in NTS. This process may critically shape the dynamic character and use dependence for cranial afferent transmission at the first stage of autonomic reflexes.

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Hypothalamic inhibition of neurones in the nucleus tractus solitarius of the cat is GABA mediated.

Cited by 127 publications

References 24 publications

Neural Pathways Underlying Lactate-Induced Panic

Neural Pathways Underlying Lactate-Induced Panic

Midbrain modulation of the cardiac baroreflex involves excitation of lateral parabrachial neurons in the rat

Cranial Afferent Glutamate Heterosynaptically Modulates GABA Release onto Second-Order Neurons via Distinctly Segregated Metabotropic Glutamate Receptors

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