Monosynaptic inhibition of thalamic neurons produced by stimulation of the substantia nigra

1977 ◽  
Vol 33 (11) ◽  
pp. 1480-1482 ◽  
Author(s):  
Akira Ueki ◽  
Masatake Uno ◽  
Marjorie Anderson ◽  
Mitsuo Yoshida
Keyword(s):  
Substantia Nigra ◽  
Thalamic Neurons ◽  
Monosynaptic Inhibition ◽  
Stimulation Of

Effect of stimulation of the putamen on the substantia nigra in the cat

1981 ◽  
Vol 217 (1) ◽  
pp. 169-174 ◽  
Author(s):  
Mitsuo Yoshida ◽  
Nobue Nakajima ◽  
Kenji Niijima
Keyword(s):  
Substantia Nigra ◽  
Stimulation Of

Properties of a T-Type Ca2+Channel–Activated Slow Afterhyperpolarization in Thalamic Paraventricular Nucleus and Other Thalamic Midline Neurons

2009 ◽  
Vol 101 (6) ◽  
pp. 2741-2750 ◽  
Author(s):  
Li Zhang ◽  
Leo P. Renaud ◽  
Miloslav Kolaj
Keyword(s):  
Information Transfer ◽  
Brain Slice ◽  
Calcium Concentration ◽  
Channel Blockers ◽  
Thalamic Neurons ◽  
Adrenoceptor Agonist ◽  
Report Data ◽  
Low Threshold ◽  
Rat Brain Slice ◽  
Stimulation Of

Burst firing mediated by a low-threshold spike (LTS) is the hallmark of many thalamic neurons. However, postburst afterhyperpolarizations (AHPs) are relatively uncommon in thalamus. We now report data from patch-clamp recordings in rat brain slice preparations that reveal an LTS-induced slow AHP (sAHP) in thalamic paraventricular (PVT) and other midline neurons, but not in ventrobasal or reticular thalamic neurons. The LTS-induced sAHP lasts 8.9 ± 0.4 s and has a novel pharmacology, with resistance to tetrodotoxin and cadmium and reduction by Ni2+ or nominally zero extracellular calcium concentration, which also attenuate both the LTS and sAHP. The sAHP is inhibited by 10 mM intracellular EGTA or by equimolar replacement of extracellular Ca2+ with Sr2+, consistent with select activation of LVA T-type Ca2+ channels and subsequent Ca2+ influx. In control media, the sAHP reverses near EK+, shifting to −78 mV in 10.1 mM [K+]o and is reduced by Ba2+ or tetraethylammonium. Although these data are consistent with opening of Ca2+-activated K+ channels, this sAHP lacks sensitivity to specific Ca2+-activated K+ channel blockers apamin, iberiotoxin, charybdotoxin, and UCL-2077. The LTS-induced sAHP is suppressed by a β-adrenoceptor agonist isoproterenol, a serotonin 5-HT7 receptor agonist 5-CT, a neuropeptide orexin-A, and by stimulation of the cAMP/protein kinase A pathway with 8-Br-cAMP and forskolin. The data suggest that PVT and certain midline thalamic neurons possess an LTS-induced sAHP that is pharmacologically distinct and may be important for information transfer in thalamic–limbic circuitry during states of attentiveness and motivation.

Cardiovascular depressor responses to stimulation of substantia nigra and ventral tegmental area

1997 ◽  
Vol 273 (6) ◽  
pp. H2549-H2557 ◽  
Author(s):  
Gilbert J. Kirouac ◽  
John Ciriello
Keyword(s):  
Substantia Nigra ◽  
Ventral Tegmental Area ◽  
Intravenous Administration ◽  
Dopaminergic Neurons ◽  
Cardiovascular Responses ◽  
Receptor Blocker ◽  
Transitional Region ◽  
Pars Lateralis ◽  
Ventral Tegmental ◽  
Stimulation Of

Experiments were done in α-chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect ofl-glutamate (Glu) stimulation of the substantia nigra (SN) and ventral tegmental area (VTA) on arterial pressure (AP) and heart rate (HR). Glu stimulation of the SN pars compacta (SNC) elicited decreases in both mean AP (MAP; −18.9 ± 1.3 mmHg; n = 52) and HR (−26.1 ± 1.6 beats/min; n = 46) at 81% of the sites stimulated. On the other hand, stimulation of the SN pars lateralis or pars reticulata did not elicit cardiovascular responses. Stimulation of the adjacent VTA region elicited similar decreases in MAP (−18.0 ± 2.6 mmHg; n = 20) and HR (−25.4 ± 3.8 beats/min; n = 17) at ∼74% of the sites stimulated. Intravenous administration of the dopamine D2-receptor antagonist raclopride significantly attenuated both the MAP (70%) and the HR (54%) responses elicited by stimulation of the transitional region where the SNC merges with the lateral VTA (SNC-VTA region). Intravenous administration of the muscarinic receptor blocker atropine methyl bromide had no effect on the magnitude of the MAP and HR responses to stimulation of the SNC-VTA region, whereas administration of the nicotinic receptor blocker hexamethonium bromide significantly attenuated both the depressor and the bradycardic responses. These data suggest that dopaminergic neurons in the SNC-VTA region activate a central pathway that exerts cardiovascular depressor effects that are mediated by the inhibition of sympathetic vasoconstrictor fibers to the vasculature and cardioacceleratory fibers to the heart.

Role of the Subthalamic Nucleus in Cannabinoid Actions in the Substantia Nigra of the Rat

1997 ◽  
Vol 77 (3) ◽  
pp. 1635-1638 ◽  
Author(s):  
M. Clara Sañudo-Peña ◽  
J. Michael Walker
Keyword(s):  
Substantia Nigra ◽  
Subthalamic Nucleus ◽  
Cannabinoid Receptors ◽  
Excitatory Input ◽  
Physiological Regulation ◽  
Cannabinoid Antagonist ◽  
Substantia Nigra Reticulata ◽  
Cannabinoid Agonist ◽  
Stimulation Of

Sañudo-Peña, M. Clara and J. Michael Walker. Role of the subthalamic nucleus in cannabinoid actions in the substantia nigra of the rat. J. Neurophysiol. 77: 1635–1638, 1997. The effect of cannabinoids on the excitatory input to the substantia nigra reticulata (SNr) from the subthalamic nucleus was explored. For this purpose a knife cut was performed rostral to the subthalamic nucleus to isolate the subthalamic nucleus and the SNr from the striatum, a major source of cannabinoid receptors to the SNr. The data showed that the cannabinoid agonist WIN55,212-2 blocked the increase in the firing rate of SNr neurons induced by stimulation of the subthalamic nucleus with bicuculline. Furthermore, the cannabinoid antagonist SR141716A antagonized the effect of the cannabinoid agonist. This study showed that cannabinoids regulate not only the striatonigral pathway, as previously reported, but also the subthalamonigral pathway. The opposite influences of these two inputs to the SNr, inhibitory and excitatory respectively, suggest that endogenous cannabinoids play a major role in the physiological regulation of the SNr.

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