Vulnerabilities of ventral mesencephalic neurons projecting to the nucleus accumbens following infusions of 6-hydroxydopamine into the medial forebrain bundle in the rat

2004 ◽  
Vol 997 (1) ◽  
pp. 119-127
Author(s):  
Andrew J. Lancia ◽  
Evelyn A. Williams ◽  
Lucas V. McKnight ◽  
Daniel S. Zahm
Keyword(s):  
Nucleus Accumbens ◽  
Medial Forebrain Bundle ◽  
Ventral Mesencephalic ◽  
6 Hydroxydopamine

scholarly journals Adeno-Associated Viral Delivery of GDNF Promotes Recovery of Dopaminergic Phenotype following a Unilateral 6-Hydroxydopamine Lesion

2002 ◽  
Vol 11 (3) ◽  
pp. 215-227 ◽  
Author(s):  
John Mcgrath ◽  
Elishia Lintz ◽  
Barry J. Hoffer ◽  
Greg A. Gerhardt ◽  
E. Matthew Quintero ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Viral Vectors ◽  
Medial Forebrain Bundle ◽  
Therapeutic Potential ◽  
Clinical Situation ◽  
Dopamine Neurons ◽  
Nigrostriatal System ◽  
Nigrostriatal Pathway ◽  
Neurotoxic Lesion ◽  
6 Hydroxydopamine

Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for dopamine neurons that has been proposed for use in the treatment of Parkinson's disease (PD). Previous studies using viral vectors to deliver GDNF in rodent models of PD have entailed administering the virus either prior to or immediately after neurotoxin-induced lesions, when the nigrostriatal pathway is largely intact, a paradigm that does not accurately reflect the clinical situation encountered with Parkinson's patients. In this study, recombinant adeno-associated virus carrying the gene encoding GDNF (rAAV-GDNF) was administered to animals bearing a maximal lesion in the nigrostriatal system, more closely resembling fully developed PD. Rats were treated with 6-hydroxydopamine into the medial forebrain bundle and assessed by apomorphine-induced rotational behavior for 5 weeks prior to virus administration. Within 4 weeks of a single intrastriatal injection of rAAV-GDNF, unilaterally lesioned animals exhibited significant behavioral recovery, which correlated with increased expression of dopaminergic markers in the substantia nigra, the medial forebrain bundle, and the striatum. Our findings demonstrate that rAAV-GDNF is capable of rescuing adult dopaminergic neurons from near complete phenotypic loss following a neurotoxic lesion, effectively restoring a functional dopaminergic pathway and diminishing motoric deficits. These data provide further support for the therapeutic potential of rAAV-GDNF-based gene therapy in the treatment of PD.

scholarly journals Comparing the role of the anterior cingulate cortex and 6-hydroxydopamine nucleus accumbens lesions on operant effort-based decision making

2009 ◽  
Vol 29 (8) ◽  
pp. 1678-1691 ◽  
Author(s):  
Mark E. Walton ◽  
James Groves ◽  
Katie A. Jennings ◽  
Paula L. Croxson ◽  
Trevor Sharp ◽  
...  
Keyword(s):  
Decision Making ◽  
Nucleus Accumbens ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
6 Hydroxydopamine

Medial forebrain bundle DBS differentially modulates dopamine release in the nucleus accumbens in a rodent model of depression

2020 ◽  
Vol 327 ◽  
pp. 113224
Author(s):  
Danesh Ashouri Vajari ◽  
Chockalingam Ramanathan ◽  
Yixin Tong ◽  
Thomas Stieglitz ◽  
Volker A. Coenen ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Dopamine Release ◽  
Medial Forebrain Bundle ◽  
Rodent Model

Intranigral Grafts of Fetal Ventral Mesencephalic Tissue in Adult 6-Hydroxydopamine-Lesioned Rats can Induce Behavioral Recovery

1997 ◽  
Vol 6 (3) ◽  
pp. 267-276 ◽  
Author(s):  
R.E. Johnston ◽  
Jill B. Becker
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cyclosporine A ◽  
Ventral Mesencephalon ◽  
Behavioral Recovery ◽  
Treatment Conditions ◽  
Movement Sequence ◽  
Ventral Mesencephalic ◽  
6 Hydroxydopamine ◽  
Disease Specific

Intrastriatal grafts of fetal ventral mesencephalon in rats with unilateral 6-hydroxydopamine lesions can reduce and even reverse rotational behavior in response to direct and indirect dopamine agonists. These grafts can ameliorate deficits on simple spontaneous behaviors, but do not improve complex behaviors that require the skilled integration of the use of both paws. We report here that rats with grafts into the DA-depleted substantia nigra, that receive cyclosporine A, can experience recovery on spontaneous behaviors that mimic those observed in Parkinson's disease. Specific cyclosporine A treatment conditions can differentially affect whether intranigral grafts normalize paw use during initiation or termination of a movement sequence. These findings may have important implications for the treatment of Parkinson's disease.

Mesolimbic dopamine mediates gastric mucosal protection by central neurotensin

1991 ◽  
Vol 260 (1) ◽  
pp. G34-G38 ◽  
Author(s):  
L. P. Xing ◽  
C. Balaban ◽  
J. Seaton ◽  
J. Washington ◽  
G. Kauffman
Keyword(s):  
Nucleus Accumbens ◽  
Substantia Nigra ◽  
Acid Secretion ◽  
Lateral Ventricle ◽  
Cold Water ◽  
Mucosal Injury ◽  
Mucosal Protection ◽  
Minimal Effective Dose ◽  
Gastric Mucosal Protection ◽  
6 Hydroxydopamine

Bilateral microinjection (1.0 microliter/side) of neurotensin (NT; 0.3, 1.5, and 3.0 micrograms/side) into the nucleus accumbens (NACB) and ventral tegmental area (VTA) but not in substantia nigra and striatum reduced gastric mucosal injury produced by 2 h of cold-water restraint (CWR). The minimal effective dose for NT-induced protection was 10-100 times lower when administered directly into NACB than into the lateral ventricle. These effects were blocked by pretreatment with the dopamine (DA) receptor antagonist, haloperidol (Hal; 0.5 microgram/side) given directly into NACB. Injection of 6-hydroxydopamine into VTA depleted endogenous DA and inhibited gastric mucosal protection against CWR-induced injury afforded by NT pretreatment. NT, given into either VTA and NACB, inhibited pentagastrin-stimulated gastric acid secretion. These results suggest that VTA and NACB, which represent the mesolimbic DA system, are important locations for interaction between NT and DA receptors to produce gastric mucosal protection against CWR-induced injury.

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