Localization of glutamatergic/aspartatergic neurons projecting to the hypothalamic paraventricular nucleus studied by retrograde transport of [3H]d-aspartate autoradiography

Csáki, Ágnes; Kocsis, Krisztián; Halász, Béla; Kiss, József Zoltán

doi:10.1016/s0306-4522(00)00411-5

Cited by 159 publications

(103 citation statements)

References 72 publications

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“…The specificity of NBQX infused into this area on fear-potentiated startle compared with baseline startle suggests that amygdala terminals may release glutamate into the deep SC/DpMe when activated by a CS. It is currently not clear, however, whether there is a direct glutamatergic projection from the amygdala to the deep SC/DpMe, although it has been reported of glutamatergic projections from the central nucleus of the amygdala to other brain regions that have connections with the midbrain (Csaki et al, 2000;Takayama and Miura, 1991). Additional labeling studies using retrograde tracers in the PnC, anterograde tracers in the central nucleus of the amygdala, and immunocytochemistry for glutamate transporters might help clarify this picture.…”

Section: Discussionmentioning

confidence: 99%

Fear-Potentiated Startle in Rats Is Mediated by Neurons in the Deep Layers of the Superior Colliculus/Deep Mesencephalic Nucleus of the Rostral Midbrain through the Glutamate Non-NMDA Receptors

Zhao¹,

Davis²

2004

J. Neurosci.

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The amygdala sends heavy and broad projections to the rostral midbrain including the periaqueductal gray (PAG), the deep layers of the superior colliculus/deep mesencephalic nucleus (deep SC/DpMe), and the lateral mesencephalic reticular formation (MRF) that in turn project to the nucleus reticularis pontis caudalis (PnC), an obligatory relay in the primary acoustic startle circuit. Chemical lesions or inactivation of these areas blocked fear-potentiated startle, suggesting that these areas serve as a relay between the amygdala and the PnC. In the present study, we tried to determine more precisely which of these sites were critical for fear-potentiated startle and the role of glutamate receptors in this site in mediating fear-potentiated startle. Local infusion of the non-NMDA receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(F)-quinoxaline (NBQX) dose-dependently blocked fear-potentiated startle when infused into the deep SC/ DpMe before testing but had no effect on baseline startle amplitude. NBQX did not block fear-potentiated startle when infused before training. The same dose of NBQX infused into the dorsal/lateral PAG, the lateral MRF, or the superficial layers of the SC did not affect fear-potentiated startle. However, NBQX tended to reduce contextual freezing when infused into the dorsal/lateral PAG. These findings suggest that the deep SC/DpMe is the site that serves as a critical output relay between the amygdala and the PnC in mediating fearpotentiated startle and that glutamatergic transmission is required for this action.

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Section: Discussionmentioning

confidence: 99%

Fear-Potentiated Startle in Rats Is Mediated by Neurons in the Deep Layers of the Superior Colliculus/Deep Mesencephalic Nucleus of the Rostral Midbrain through the Glutamate Non-NMDA Receptors

Zhao¹,

Davis²

2004

J. Neurosci.

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“…The glutamatergic synaptic input to the PVN presympathetic neurons originates mostly from interneurons within the PVN, the medial and lateral preoptic area, the suprachiasmatic nucleus, the anterior and lateral hypothalamus, the thalamic PVN, and some telencephalic regions (including the lateral septum, the bed nucleus of the stria terminalis, and the amygdala). 14,22,26 It should be noted that stimulation of the dorsomedial hypothalamus with bicuculline or NMDA can increase sympathetic vasomotor tone in normotensive rats. 40,41 Although our study is focused on the PVN, we do not exclude the possibility that increased glutamatergic input may occur in the dorsomedial hypothalamus or other brain nuclei in SHRs.…”

Section: Discussionmentioning

confidence: 99%

“…20,21 The glutamatergic synaptic inputs to the PVN neurons are from glutamatergic interneurons within the PVN, subnuclei of the hypothalamus, and telencephalic regions. 14,22,23 Microinjection of glutamate or NMDA into the PVN increases arterial blood pressure, sympathetic nerve activity, and plasma norepinephrine concentration in anesthetized and conscious rats. 24,25 Furthermore, electrophysiological studies using the hypothalamic slice preparation have shown that glutamatergic stimulation can excite PVN neurons and that blockade of glutamatergic transmission reduces spontaneous and evoked postsynaptic activity.…”

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confidence: 99%

Glutamatergic Inputs in the Hypothalamic Paraventricular Nucleus Maintain Sympathetic Vasomotor Tone in Hypertension

2007

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Abstract-The paraventricular nucleus (PVN) of the hypothalamus is critical to the regulation of sympathetic output. The PVN hyperactivity is known to cause increased sympathetic nerve activity in spontaneously hypertensive rats (SHRs). The purpose of this study was to determine whether glutamatergic input to the PVN contributes to heightened sympathetic outflow in hypertension. Lumbar sympathetic nerve activity, mean arterial blood pressure, and heart rate were recorded from anesthetized SHRs and Wistar-Kyoto (WKY) rats. Bilateral microinjection of an N-methyl-Daspartate receptor antagonist, 2-amino-5-phosphonopentanoic acid, or a non-N-methyl-D-aspartate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione, into the PVN dose-dependently decreased lumbar sympathetic nerve activity, mean arterial blood pressure, and heart rate in SHRs but not in WKY rats. Bilateral microinjection of kynurenic acid into the PVN also significantly decreased lumbar sympathetic nerve activity, mean arterial blood pressure, and heart rate in SHRs but not in WKY rats. Furthermore, microinjection of gabazine, a specific GABA A receptor antagonist, into the PVN increased lumbar sympathetic nerve activity, mean arterial blood pressure, and heart rate in both SHRs and WKY rats. Notably, this response was significantly attenuated in SHRs compared with that in WKY rats. In addition, kynurenic acid abolished the sympathoexcitatory and pressor responses to microinjection of gabazine into the PVN in both SHRs and WKY rats. Thus, this study provides new functional evidence that resting sympathetic vasomotor tone is maintained by tonic glutamatergic input in the PVN in SHRs. Removal of GABAergic inhibition results in augmented glutamatergic input in the PVN, which probably constitutes an important source of excitatory drive to the brain stem vasomotor neurons in hypertension. Key Words: excitatory amino acids Ⅲ hypothalamus Ⅲ sympathetic nervous system Ⅲ synaptic transmission Ⅲ autonomic nervous system Ⅲ NMDA receptors H ypertension is a significant risk factor for cardiovascular, renal, and cerebrovascular disorders. Increased sympathetic activity is often associated with hypertension and may contribute to the pathogenesis and maintenance of hypertension. 1,2 Previous studies suggested that altered central mechanisms are responsible for the elevated sympathetic outflow and arterial blood pressure in hypertension. In this regard, transection of the brain caudal to the hypothalamus reduces arterial blood pressure in spontaneously hypertensive rats (SHRs) but not in Wistar-Kyoto (WKY) rats. 3 The paraventricular nucleus (PVN) of the hypothalamus is an important region for the regulation of sympathetic output and arterial blood pressure. 4 -7 Lesions of the PVN in hypertensive rats, such as SHRs, Dahl salt-sensitive rats, and rats with renal hypertension, decrease blood pressure. 8 -11 Furthermore, inhibition of the PVN with muscimol reduces the blood pressure and sympathetic nerve activity in SHRs. 12 Thus, hyperactivity of PVN neurons may d...

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“…Future studies will have to show how the SCN (via the sympathetic and parasympathetic branches of the ANS) controls the balance between glycogenolysis and glycogenesis. In this regard, glutamatergic SCN outputs might also be important (Csaki et al, 2000;Chen et al, 2003;Perreau-Lenz et al, 2004). Indeed, apart from GABA, glutamatergic (SCN) inputs to the PVN may also show a daily variation.…”

Section: Discussionmentioning

confidence: 99%

Suprachiasmatic GABAergic Inputs to the Paraventricular Nucleus Control Plasma Glucose Concentrations in the Rat via Sympathetic Innervation of the Liver

Kalsbeek¹,

Fleur²,

Heijningen³

et al. 2004

J. Neurosci.

212

216

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Daily peak plasma glucose concentrations are attained shortly before awakening. Previous experiments indicated an important role for the biological clock, located in the suprachiasmatic nuclei (SCN), in the genesis of this anticipatory rise in plasma glucose concentrations by controlling hepatic glucose production. Here, we show that stimulation of NMDA receptors, or blockade of GABA receptors in the paraventricular nucleus of the hypothalamus (PVN) of conscious rats, caused a pronounced increase in plasma glucose concentrations. The local administration of TTX in brain areas afferent to the PVN revealed that an important part of the inhibitory inputs to the PVN was derived from the SCN. Using a transneuronal viral-tracing technique, we showed that the SCN is connected to the liver via both branches of the autonomic nervous system (ANS). The combination of a blockade of GABA receptors in the PVN with selective removal of either the sympathetic or parasympathetic branch of the hepatic ANS innervation showed that hyperglycemia produced by PVN stimulation was primarily attributable to an activation of the sympathetic input to the liver. We propose that the daily rise in plasma glucose concentrations is caused by an SCN-mediated withdrawal of GABAergic inputs to sympathetic preautonomic neurons in the PVN, resulting in an increased hepatic glucose production. The remarkable resemblance of the presently proposed control mechanism to that described previously for the control of daily melatonin rhythm suggests that the GABAergic control of sympathetic preautonomic neurons in the PVN is an important pathway for the SCN to control peripheral physiology.

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Localization of glutamatergic/aspartatergic neurons projecting to the hypothalamic paraventricular nucleus studied by retrograde transport of [3H]d-aspartate autoradiography

Cited by 159 publications

References 72 publications

Fear-Potentiated Startle in Rats Is Mediated by Neurons in the Deep Layers of the Superior Colliculus/Deep Mesencephalic Nucleus of the Rostral Midbrain through the Glutamate Non-NMDA Receptors

Fear-Potentiated Startle in Rats Is Mediated by Neurons in the Deep Layers of the Superior Colliculus/Deep Mesencephalic Nucleus of the Rostral Midbrain through the Glutamate Non-NMDA Receptors

Glutamatergic Inputs in the Hypothalamic Paraventricular Nucleus Maintain Sympathetic Vasomotor Tone in Hypertension

Suprachiasmatic GABAergic Inputs to the Paraventricular Nucleus Control Plasma Glucose Concentrations in the Rat via Sympathetic Innervation of the Liver

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