Effect of Trimethadione on the Self-Stimulation Phenomenon

1971 ◽  
Vol 49 (9) ◽  
pp. 850-853
Author(s):  
J. St-Laurent
Keyword(s):  
Motor Activity ◽  
Medial Forebrain Bundle ◽  
Epileptiform Activity ◽  
Anticonvulsant Drug ◽  
The Self ◽  
High Drive ◽  
Self Stimulation

The effects of the anticonvulsant drug trimethadione on the self-stimulation (S.S.) phenomenon are studied on rats. S.S. is elicited via electrodes implanted in the posterior medial forebrain bundle (M.F.B.). Following administration of trimethadione (325 mg/kg i.p.) a tendency toward improvement of S.S. is found; this trend is not statistically significant. The fact that no change of S.S. is observed in the areas of the posterior M.F.B. where seizures rarely occur is discussed in the light that the high rates of S.S. obtained from these areas might be related to the absence of disruptive epileptiform activity. It is concluded that the high rates of S.S. usually obtained from the posterior areas of the M.F.B. may be due to properties such as the involvement of these areas in high-drive behavior and facilitation of motor activity.

Response : On the Directionality of Medial Forebrain Bundle Fibers Mediating Self-Stimulation

Science ◽  
1974 ◽  
Vol 183 (4120) ◽  
pp. 102-103
Author(s):  
Dwight C. German ◽  
Frank A. Holloway
Keyword(s):  
Medial Forebrain Bundle ◽  
Self Stimulation

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.

Approach-avoidance dissociations in rat brain

1960 ◽  
Vol 199 (6) ◽  
pp. 965-968 ◽  
Author(s):  
James Olds
Keyword(s):  
Rat Brain ◽  
Lateral Hypothalamus ◽  
Medial Forebrain Bundle ◽  
Sequential Tests ◽  
Medial Hypothalamus ◽  
Approach Avoidance ◽  
Skinner Box ◽  
Self Stimulation

Two electrode pairs were implanted in each rat, one in dorso-medial tegmentum or medial hypothalamus and one in lateral hypothalamus. Four sequential tests were repeatedly administered in a two-pedal Skinner box: hypothalamic self-stimulation, tegmental self-stimulation, hypothalamic escape, and tegmental escape. Results indicate that with electrodes in medial forebrain bundle regions of hypothalamus, there is self-stimulation but no escape; with electrodes in dorso-medial tegmentum, there is escape but no self-stimulation. In both cases, this holds for all suprathreshold stimulus levels. With electrodes placed more medially in hypothalamus, or lower in tegmentum, the same electrode may yield both self-stimulation and escape depending on the nature of the test.

scholarly journals Intracranial Self-stimulation of the Paraventricular Nucleus of the Hypothalamus

2012 ◽  
Vol 116 (5) ◽  
pp. 1116-1123 ◽  
Author(s):  
Eric E. Ewan ◽  
Thomas J. Martin
Keyword(s):  
Neuropathic Pain ◽  
Paraventricular Nucleus ◽  
Medial Forebrain Bundle ◽  
Spinal Nerve ◽  
Maximal Effect ◽  
Direct Stimulation ◽  
And Control ◽  
Self Stimulation ◽  
Dopaminergic Pathways ◽  
Stimulation Of

Background Neuropathic pain attenuates opioid facilitation of rewarding electrical stimulation of limbic dopaminergic pathways originating from the ventral tegmental area. Whether neuropathic pain alters opioid effects of other brain-reward systems is unknown. Methods Control and spinal nerve-ligated (SNL) rats had electrodes implanted into the paraventricular nucleus (PVN) of the hypothalamus or medial forebrain bundle. Control and SNL rats were trained to lever-press for intracranial self-stimulation (ICSS), and modulation by morphine or cocaine was assessed. Results Control and SNL rats lever-pressed for stimulation of the PVN and medial forebrain bundle. Morphine produced greater reductions in the frequency at which rats emitted 50% of maximal responding for PVN ICSS (maximal effect 24.67 ± 4.60 [mean ± SEM] and 24.11 ± 5.96 in SNL [n = 6] and control [n = 8] rats, respectively, compared with medial forebrain bundle ICSS (12.38 ± 6.77 [n = 8] and 12.69 ± 1.55 [n = 7]). In contrast, cocaine was less efficacious in potentiating PVN ICSS (maximal effect 11.76 ± 2.86 and 12.38 ± 4.01 in SNL [n = 12] and control [n = 8] rats, respectively) compared with medial forebrain bundle ICSS (30.58 ± 3.40 [n = 9] and 27.55 ± 4.51 [n = 7]). Conclusions PVN ICSS is facilitated to a greater extent by morphine than cocaine, and the effects of each drug on this behavior are unaltered after spinal nerve ligation. These effects contrast those observed with direct stimulation of limbic dopamine pathways, suggesting that the PVN may have a greater role in the reinforcing effects of opioids than classic limbic regions, particularly in the presence of chronic pain.

Sign in / Sign up

Export Citation Format

Share Document