Effects of catecholamine-depleting drugs and amphetamine on self-stimulation of brain following various 6-hydroxydopamine treatments

1974 ◽  
Vol 37 (3) ◽  
pp. 235-248 ◽  
Author(s):  
Barrett R. Cooper ◽  
Jerry M. Cott ◽  
George R. Breese
Keyword(s):  
6 Hydroxydopamine ◽  
Self Stimulation ◽  
Stimulation Of

scholarly journals Effect of 6-hydroxydopamine on electrical self stimulation of the brain

1971 ◽  
Vol 43 (1) ◽  
pp. 255-257 ◽  
Author(s):  
G. R. BREESE ◽  
J. L. HOWARD ◽  
J. P. LEAHY
Keyword(s):  
6 Hydroxydopamine ◽  
Self Stimulation ◽  
The Brain ◽  
Stimulation Of

Effect of β-phenylethylamine and d-amphetamine on electrical self-stimulation of brain

1976 ◽  
Vol 5 (6) ◽  
pp. 661-664 ◽  
Author(s):  
J.L. Howard ◽  
G.T. Pollard ◽  
K.W. Rohrbach ◽  
N.E. Harto
Keyword(s):  
Self Stimulation ◽  
Stimulation Of

Monopolar and bipolar stimulation of the brain

1962 ◽  
Vol 203 (2) ◽  
pp. 371-373 ◽  
Author(s):  
Paul Stark ◽  
Giovanni Fazio ◽  
Eugene S. Boyd
Keyword(s):  
Current Density ◽  
Bipolar Electrode ◽  
Wire Electrode ◽  
Bipolar Stimulation ◽  
Monopolar Stimulation ◽  
Stimulation Experiments ◽  
Self Stimulation ◽  
The Brain ◽  
Rate Of Response ◽  
Stimulation Of

Intracranial self-stimulation experiments in the dog using a two-wire electrode, with each wire used as a monopolar electrode and the combination as a bipolar electrode, show that monopolar stimulation may produce either a higher or a lower rate of response than that produced by bipolar stimulation. A theoretical consideration of the changes in current density around the electrode when it is changed from a monopolar to a bipolar electrode shows that such differences are to be expected. The exact location of the structure being stimulated with reference to the two electrode tips will determine whether the structure is subjected to a higher current density on monopolar or on bipolar stimulation.

Stimulation of the nigrostriatal dopamine system produces hypertension and tachycardia in rats

1994 ◽  
Vol 266 (6) ◽  
pp. H2489-H2496 ◽  
Author(s):  
M. T. Lin ◽  
J. J. Yang
Keyword(s):  
Corpus Striatum ◽  
Substantia Nigra Pars Compacta ◽  
Dopamine System ◽  
Arterial Blood ◽  
Nigrostriatal Dopamine ◽  
Induced Hypertension ◽  
Bilateral Vagotomy ◽  
6 Hydroxydopamine ◽  
Da Release ◽  
Stimulation Of

To test for the ability of the nigrostriatal dopamine (DA) system to influence cardiovascular function, experiments were carried out to assess the effects of electrical or chemical stimulation of the nigrostriatal DA system on arterial blood pressure, heart rate, and striatal DA release in anesthetized rats. Electrical stimulation of the substantia nigra pars compacta (SNC), in addition to enhancing the DA release in the corpus striatum (CS), elicited proportional hypertension and tachycardia. This could be mimicked by microinjection of two excitatory amino acids, kainic acid and glutamate, into the SNC area of rat brain. The SNC stimulation-induced hypertension, tachycardia, and increased striatal DA release were attenuated by prior destruction of the nigrostriatal DA system produced by intramedial forebrain bundle injection of 6-hydroxydopamine and by prior blockade of postsynaptic DA receptors produced by intra-CS injection of DA receptor antagonists, haloperidol or pimozide. The SNC stimulation-induced hypertension was attenuated by spinal transection, whereas the SNC stimulation-induced tachycardia was attenuated by bilateral vagotomy. The data suggest that stimulation of the nigrostriatal DA system produces both hypertension and tachycardia in rats.

scholarly journals Dopamine neurons projecting to medial shell of the nucleus accumbens drive heroin reinforcement

2018 ◽  
Author(s):  
Julie Corre ◽  
Ruud van Zessen ◽  
Michaël Loureiro ◽  
Tommaso Patriarchi ◽  
Lin Tian ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Causal Link ◽  
The Self ◽  
Dopamine Neurons ◽  
Self Administration ◽  
Gaba Neurons ◽  
Calcium Indicators ◽  
Compulsive Consumption ◽  
Self Stimulation ◽  
Stimulation Of

AbstractThe dopamine (DA) hypothesis posits the increase of mesolimbic dopamine levels as a defining commonality of addictive drugs, initially causing reinforcement, eventually leading to compulsive consumption. While much experimental evidence from psychostimulants supports this hypothesis, it has been challenged for opioid reinforcement. Here, we use genetically encoded DA and calcium indicators as well as cFos to reveal that heroin activates DA neurons located in the medial part of the VTA, preferentially projecting to the medial shell of the nucleus accumbens (NAc). Chemogenetic and optogenetic manipulations of VTA DA or GABA neurons establish a causal link to heroin reinforcement. Inhibition of DA neurons blocked heroin self-administration, while heroin inhibited optogenetic self-stimulation of DA neurons. Likewise, heroin occluded the self-inhibition of VTA GABA neurons. Together, these experiments support a model of disinhibition of a subset of VTA DA neurons in opioid reinforcement.

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