“Light stimulation during postnatal development is not determinant for glutamatergic neurotransmission from the retinohypothalamic tract to the suprachiasmatic nucleus in rats”

2021 ◽  
Author(s):  
Miriam E. Reyes‐Méndez ◽  
J. Manuel Herrera‐Zamora ◽  
Fernando Osuna‐López ◽  
Ricardo A. Navarro‐Polanco ◽  
Néstor Mendoza‐Munoz ◽  
...  
Keyword(s):  
Postnatal Development ◽  
Suprachiasmatic Nucleus ◽  
Glutamatergic Neurotransmission ◽  
Light Stimulation ◽  
Retinohypothalamic Tract

Functional Pre- and Postsynaptic Changes between the Retinohypothalamic Tract and Suprachiasmatic Nucleus during Rat Postnatal Development

2019 ◽  
Vol 35 (1) ◽  
pp. 28-44
Author(s):  
Miriam E. Reyes-Mendez ◽  
Fernando Osuna-López ◽  
J. Manuel Herrera-Zamora ◽  
Ricardo A. Navarro-Polanco ◽  
Eloy G. Moreno-Galindo ◽  
...  
Keyword(s):  
Postnatal Development ◽  
Suprachiasmatic Nucleus ◽  
Communication Systems ◽  
Developmental Changes ◽  
Signaling Cascades ◽  
Resting Potential ◽  
Postsynaptic Receptors ◽  
Initial Release ◽  
Retinohypothalamic Tract ◽  
Membrane Resting Potential

The suprachiasmatic nucleus (SCN) is the main brain clock in mammals. The SCN synchronizes to the light-dark cycle through the retinohypothalamic tract (RHT). RHT axons release glutamate to activate AMPA-kainate and N-methyl-D-aspartate (NMDA) postsynaptic receptors in ventral SCN neurons. Stimulation of SCN NMDA receptors is necessary for the activation of the signaling cascades that govern the advances and delays of phase. To our knowledge, no research has been performed to analyze the functional synaptic modifications occurring during postnatal development that prepare the circadian system for a proper synchronization to light at adult ages. Here, we studied the pre- and postsynaptic developmental changes between the unmyelinated RHT-SCN connections. Spontaneous NMDA excitatory postsynaptic currents (EPSCs) were greater in amplitude and frequency at postnatal day 34 (P34) than at P8. Similarly, both quantal EPSCs (miniature NMDA and evoked quantal AMPA-kainate) showed a development-dependent increase at analyzed stages, P3-5, P7-9, and P13-18. Moreover, the electrically evoked NMDA and AMPA-kainate components were augmented with age, although the increment was larger for the latter, and the membrane resting potential was more depolarized at early postnatal ages. Finally, the short-term synaptic plasticity was significantly modified during postnatal development as was the estimated number of quanta released and the initial release probability. All of these synaptic modifications in the unmyelinated RHT-SCN synapses suggest that synchronization to light at adult ages requires developmental changes similar to those that occur in myelinated fast communication systems.

Expression of Clock and Clock-Driven Genes in the Rat Suprachiasmatic Nucleus during Late Fetal and Early Postnatal Development

2006 ◽  
Vol 21 (2) ◽  
pp. 140-148 ◽  
Author(s):  
Zuzana Kováčiková ◽  
Martin Sládek ◽  
Zdenka Bendová ◽  
Helena Illnerová ◽  
Alena Sumová
Keyword(s):  
Postnatal Development ◽  
Suprachiasmatic Nucleus ◽  
Early Postnatal Development

scholarly journals Light exposure induces short- and long-term changes in the excitability of retinorecipient neurons in suprachiasmatic nucleus

2011 ◽  
Vol 106 (2) ◽  
pp. 576-588 ◽  
Author(s):  
Joseph LeSauter ◽  
Rae Silver ◽  
Robin Cloues ◽  
Paul Witkovsky
Keyword(s):  
Leakage Current ◽  
Suprachiasmatic Nucleus ◽  
Fluorescent Protein ◽  
Light Exposure ◽  
Brain Slices ◽  
Membrane Hyperpolarization ◽  
Retinohypothalamic Tract ◽  
Green Fluorescent ◽  
Spike Firing

The suprachiasmatic nucleus (SCN) is the locus of a hypothalamic circadian clock that synchronizes physiological and behavioral responses to the daily light-dark cycle. The nucleus is composed of functionally and peptidergically diverse populations of cells for which distinct electrochemical properties are largely unstudied. SCN neurons containing gastrin-releasing peptide (GRP) receive direct retinal input via the retinohypothalamic tract. We targeted GRP neurons with a green fluorescent protein (GFP) marker for whole cell patch-clamping. In these neurons, we studied short (0.5–1.5 h)- and long-term (2–6 h) effects of a 1-h light pulse (LP) given 2 h after lights off [Zeitgeber time (ZT) 14:00–15:00] on membrane potential and spike firing. In brain slices taken from light-exposed animals, cells were depolarized, and spike firing rate increased between ZT 15:30 and 16:30. During a subsequent 4-h period beginning around ZT 17:00, GRP neurons from light-exposed animals were hyperpolarized by ∼15 mV. None of these effects was observed in GRP neurons from animals not exposed to light or in immediately adjacent non-GRP neurons whether or not exposed to light. Depolarization of GRP neurons was associated with a reduction in GABAA-dependent synaptic noise, whereas hyperpolarization was accompanied both by a loss of GABAA drive and suppression of a TTX-resistant leakage current carried primarily by Na. This suggests that, in the SCN, exposure to light may induce a short-term increase in GRP neuron excitability mediated by retinal neurotransmitters and neuropeptides, followed by long-term membrane hyperpolarization resulting from suppression of a leakage current, possibly resulting from genomic signals.

Serotonin Modulates Glutamate Responses in Isolated Suprachiasmatic Nucleus Neurons

1999 ◽  
Vol 82 (2) ◽  
pp. 533-539 ◽  
Author(s):  
Jorge E. Quintero ◽  
Douglas G. McMahon
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Cell Communication ◽  
Suppressive Effect ◽  
Cellular Level ◽  
Free Calcium ◽  
Acetoxymethyl Ester ◽  
Calcium Indicator ◽  
Camp Analogue ◽  
Retinohypothalamic Tract ◽  
Serotonergic Modulation

Two input pathways to the suprachiasmatic nucleus (SCN) of the hypothalamus are the glutamatergic retinohypothalamic tract and the serotonergic afferent from the midbrain raphe nucleus. To determine whether these two temporal signaling pathways can converge at the cellular level, we have investigated the effects of serotonin on glutamate-induced calcium responses of individual SCN neurons isolated in cell culture. Dispersed cultures were formed from the SCN of neonatal rats. The calcium indicator Fura-2 acetoxymethyl ester was used to assess the changes in [Ca2+]i by recording the 340-nm/380-nm excitation ratio. Application of glutamate (5 μM) to the culture caused a rapid (within 10 s) increase in the fluorescence ratio of neurons indicating a marked increase in the concentration of intracellular free calcium. However, when 5-hydroxytryptamine (5-HT; 5 μM) was coapplied with glutamate, 31% of neurons showed an overall 61% reduction in the peak of the glutamate-induced calcium increase. Application of the 5-HT7/1A receptor agonist, (±)-8-hydroxy-2-(di- n-propylamino)tetralin [(±)-8-OH-DPAT] (1 μM), also reduced the calcium elevation this time by 80% in 18% of the neurons tested. When the 5-HT7/2/1C receptor antagonist, ritanserin (800 nM), was coapplied with serotonin, it blocked modulation of the glutamate responses. Further support for the involvement of the 5-HT7receptor was provided by the ability of the adenylate cyclase activator, forskolin (10 μM), and the cAMP analogue, 8-Br cAMP (0.5 mM), to mimic the suppressive effect of serotonin. Blocking spike-mediated cell communication with tetrodotoxin (1 μM) did not prevent the serotonergic suppression of glutamate-induced responses. These results support the hypothesis that the serotonergic modulation of photic entraining signals can occur in SCN neurons.

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