scholarly journals Changes in L1 Antigen Expression in the Rat Striatum After Substantia Nigra Lesions

1997 ◽  
Vol 6 (1) ◽  
pp. 59-62 ◽  
Author(s):  
Maciej Poltorak ◽  
Jamesine R. Williams ◽  
Kraig D. Moore ◽  
Willam J. Freed
Keyword(s):  
Tissue Culture ◽  
Substantia Nigra ◽  
Frontal Cortex ◽  
Neurite Outgrowth ◽  
Dopaminergic Neurons ◽  
Antigen Expression ◽  
Rat Striatum ◽  
Complex Regulation ◽  
Lateral Area

L1 antigen promotes neurite outgrowth from dopaminergic neurons in tissue culture. In the present study, we examined the effects of dopaminergic deafferentation of the striatum on L1 expression. In the medial-periventricular part of the striatum, both complete and partial substantia nigra (SN) lesions decreased L1 expression. Complete lesions increased L1 expression in the dorso-medial and ventrolateral parts of the striatum on the lesioned side when compared with that on the non-lesioned side. The decrease in the ventro-lateral area was maintained in animals examined three months after the lesioning. Animals with partial SN lesions showed a different pattern of altered L1 expression. After frontal cortex lesions, changes in L1 expression also occur preferentially in the dorso-medial and periventricular striatum. Therefore, the results indicate a complex regulation of L1 expression after damage of striatal circuitry, manifested by a preferential occurrence of changes in periventricular regions.

The Effects of Fibrillar Forms of α-Synuclein Protein on Neurogenesis in the Hippocampus, Dopaminergic Neurons of the Substantia Nigra, and the Behavior of Ageing Mice

2018 ◽  
Vol 12 (4) ◽  
pp. 359-365
Author(s):  
V. V. Sherstnev ◽  
O. A. Solov’eva ◽  
M. A. Gruden’ ◽  
A. V. Kedrov ◽  
E. V. Konovalova ◽  
...  
Keyword(s):  
Substantia Nigra ◽  
Dopaminergic Neurons

ChemInform Abstract: Synthesis of 2β-Acyl-3β-aryl-8-azabicyclo(3.2.1)octanes and Their Binding Affinities at Dopamine and Serotonin Transport Sites in Rat Striatum and Frontal Cortex.

ChemInform ◽  
2010 ◽  
Vol 25 (36) ◽  
pp. no-no
Author(s):  
H. M. L. DAVIES ◽  
E. SAIKALI ◽  
N. J. S. HUBY ◽  
V. J. GILLIATT ◽  
J. J. MATASI ◽  
...  
Keyword(s):  
Frontal Cortex ◽  
Rat Striatum ◽  
Binding Affinities ◽  
Serotonin Transport

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.

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