Basal forebrain knife cuts and medial forebrain bundle self-stimulation

Waraczynski, Meg

doi:10.1016/0006-8993(88)91319-4

Cited by 38 publications

(27 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…5, 6). The ranges of lesion size and location in these experiments were comparable to those in previous studies (Stellar and Neely, 1982;Waraczynski, 1988;Shizgal, 1991, 1996b;Gallistel et al, 1996).…”

Section: Lh Lesionssupporting

confidence: 89%

“…In previously published experiments, animals with elevations of threshold pps tended to have smaller lesions than did animals without threshold elevations. It has been suggested that this effect may be caused by a cancellation phenomenon, whereby larger lesions damage two reciprocal or mutually inhibitory systems and produce a net functional balance (Irle, 1987;Waraczynski, 1988;Murray and Shizgal, 1991). Although small lesions often caused (MPO and LPO).…”

Section: Lesion Sizementioning

confidence: 99%

“…Identification of the specific MFB projections mediating BSR has been hampered by the inability of MFB lesions to consistently reduce the rewarding efficacy of brain stimulation (Huston and Borbely, 1974;Carey, 1982;Huston, 1982;Stellar and Neely, 1982;Colle and Wise, 1987;Janas and Stellar, 1987;Waraczynski, 1988;Murray and Shizgal, 1991;Johnson and Stellar, 1994). Lesions made through the stimulating electrode itself consistently produce large, enduring, and size-dependent decreases in rewarding efficacy (Gallistel et al, 1996).…”

mentioning

confidence: 99%

“…By contrast, lesions in the MFB rostral to the site of stimulation have produced variable effects on rewarding efficacy. Moreover, there has been a puzzling overlap between the size and location of lesions that caused significant reductions in rewarding efficacy and those that failed to affect reward thresholds (Stellar and Neely, 1982;Colle and Wise, 1987;Janas and Stellar, 1987;Waraczynski, 1988;Murray and Shizgal, 1991;Johnson and Stellar, 1994;Arvanitogiannis et al, 1996b;Gallistel et al, 1996;Murray and Shizgal, 1996b).…”

mentioning

confidence: 99%

See 3 more Smart Citations

Medial Forebrain Bundle Lesions Fail to Structurally and Functionally Disconnect the Ventral Tegmental Area from Many Ipsilateral Forebrain Nuclei: Implications for the Neural Substrate of Brain Stimulation Reward

1998

View full text Add to dashboard Cite

Lesions in the medial forebrain bundle rostral to a stimulating electrode have variable effects on the rewarding efficacy of self-stimulation. We attempted to account for this variability by measuring the anatomical and functional effects of electrolytic lesions at the level of the lateral hypothalamus (LH) and by correlating these effects to postlesion changes in threshold pulse frequency (pps) for self-stimulation in the ventral tegmental area (VTA). We implanted True Blue in the VTA and compared cell labeling patterns in forebrain regions of intact and lesioned animals. We also compared stimulation-induced regional [14C]deoxyglucose (DG) accumulation patterns in the forebrains of intact and lesioned animals. As expected, postlesion threshold shifts varied: threshold pps remained the same or decreased in eight animals, increased by small but significant amounts in three rats, and increased substantially in six subjects. Unexpectedly, LH lesions did not anatomically or functionally disconnect all forebrain nuclei from the VTA. Most septal and preoptic regions contained equivalent levels of True Blue label in intact and lesioned animals. In both intact and lesioned groups, VTA stimulation increased metabolic activity in the fundus of the striatum (FS), the nucleus of the diagonal band, and the medial preoptic area. On the other hand, True Blue labeling demonstrated anatomical disconnection of the accumbens, FS, substantia innominata/magnocellular preoptic nucleus (SI/MA), and bed nucleus of the stria terminalis. [14C]DG autoradiography indicated functional disconnection of the lateral preoptic area and SI/MA. Correlations between patterns of True Blue labeling or [14C]deoxyglucose accumulation and postlesion shifts in threshold pulse frequency were weak and generally negative. These direct measures of connectivity concord with the behavioral measures in suggesting a diffuse net-like connection between forebrain nuclei and the VTA.

show abstract

Section: Lh Lesionssupporting

confidence: 89%

Section: Lesion Sizementioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Medial Forebrain Bundle Lesions Fail to Structurally and Functionally Disconnect the Ventral Tegmental Area from Many Ipsilateral Forebrain Nuclei: Implications for the Neural Substrate of Brain Stimulation Reward

1998

View full text Add to dashboard Cite

show abstract

“…Attempting to separate the axons arising from these hypothesized sources from anterior MFB stimulation sites, Waraczynski (1988) made unilateral coronal plane knife cuts throughout the basal forebrain, ranging from the septum back to the anterior hypothalamus. If the descending path hypothesis were correct, these transections should have induced orthograde degeneration along the severed axons, removing them from beneath the stimulation electrode and thereby compromising the stimulation's reward value.…”

Section: Forebrain Lesionsmentioning

confidence: 99%

The central extended amygdala network as a proposed circuit underlying reward valuation

Waraczynski

2006

Neuroscience & Biobehavioral Reviews

Self Cite

View full text Add to dashboard Cite

Alcohol‐induced reinforcement: Dopamine and 5‐HT₃ receptor interactions in animals and humans

Johnson

Cowen

1993

Drug Development Research

View full text Add to dashboard Cite

Alcohol abuse i s a major health problem worldwide. Whatever the treatment goal, be it abstinence or "controlled" drinking, the outcome from both pharmacological and nonbiological treatments remains disappointing. Behavioural experiments in animals have suggested that the reinforcing properties of alcohol, like other drugs of abuse, are critical to drug-seeking behaviour. Dopaminergic fibres running from the ventral tegmental area to the nucleus accumbens may play a central role in mediating the reinforcing effects of drugs of abuse including alcohol. Thus, alcohol increases extracellular levels of dopamine in the nucleus accumbens and dopamine receptor antagonists decrease alcohol consumption in a number of behavioural paradigms. A recently described subtype of serotonin (5-HT) receptor, the 5-HT3 receptor, appears to modulate the effects of alcohol on dopamine release in the nucleus accumbens. In rodents, 5-HT3 receptor antagonists inhibit alcohol-induced doparnine release in the nucleus accumbens. Further, in behavioural studies, 5-HT3 receptor blockade decreases alcohol consumption in a free-choice paradigm. In humans, reinforcement i s difficult to measure directly. Nevertheless, the pleasurable subjective effects of alcohol are important behavioural correlates of the reinforcement process. Our preliminary findings in humans suggest that the 5-HT3 receptor antagonist, ondansetron, can attenuate some of the pleasurable effects of a small dose of alcohol including the subjective desire to drink. We speculate, although we have no direct evidence for this at present, that in humans this effect could also be due to a blockade of alcohol-induced dopamine release in the nucleus accumbens as has been demonstrated in animals. Further studies with clinical populations are required to assess the effects of 5-HT3 receptor antagonists on drinking behaviour and to explore their potential in the management of alcohol abuse.

show abstract

Basal forebrain knife cuts and medial forebrain bundle self-stimulation

Cited by 38 publications

References 35 publications

Medial Forebrain Bundle Lesions Fail to Structurally and Functionally Disconnect the Ventral Tegmental Area from Many Ipsilateral Forebrain Nuclei: Implications for the Neural Substrate of Brain Stimulation Reward

Medial Forebrain Bundle Lesions Fail to Structurally and Functionally Disconnect the Ventral Tegmental Area from Many Ipsilateral Forebrain Nuclei: Implications for the Neural Substrate of Brain Stimulation Reward

The central extended amygdala network as a proposed circuit underlying reward valuation

Alcohol‐induced reinforcement: Dopamine and 5‐HT₃ receptor interactions in animals and humans

Contact Info

Product

Resources

About

Basal forebrain knife cuts and medial forebrain bundle self-stimulation

Cited by 38 publications

References 35 publications

Medial Forebrain Bundle Lesions Fail to Structurally and Functionally Disconnect the Ventral Tegmental Area from Many Ipsilateral Forebrain Nuclei: Implications for the Neural Substrate of Brain Stimulation Reward

Medial Forebrain Bundle Lesions Fail to Structurally and Functionally Disconnect the Ventral Tegmental Area from Many Ipsilateral Forebrain Nuclei: Implications for the Neural Substrate of Brain Stimulation Reward

The central extended amygdala network as a proposed circuit underlying reward valuation

Alcohol‐induced reinforcement: Dopamine and 5‐HT3 receptor interactions in animals and humans

Contact Info

Product

Resources

About

Alcohol‐induced reinforcement: Dopamine and 5‐HT₃ receptor interactions in animals and humans