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D Corbett

Publications and source records attributed to D Corbett.

At least 73 records · Page 4Linked to original sources
PubMed1989

Prefrontal cortex lesions attenuate substantia nigra self-stimulation: a reward summation analysis.

A curve-shift paradigm was used to assess the effects of lesions of the prefrontal cortex on self-stimulation from electrode sites in the substantia nigra. Combined lesions of the medial and sulcal cortical regions severely attenuated substantia nigra self-stimulation. These results are discussed in the context of the frontal cortex and the substantia nigra as belonging to a reinforcement system that is largely independent of the medial forebrain bundle system.

Animals↗
PubMed1989

Regional neuroleptic microinjections indicate a role for nucleus accumbens in lateral hypothalamic self-stimulation reward.

Bilateral microinjections of the neuroleptic, cis-flupenthixol, were made into 56 forebrain targets distributed across various dopamine (DA) terminal fields in the forebrain. Drug effects on medial forebrain bundle (MFB) stimulation-produced reward were assessed with a rate-frequency procedure implemented in a runway paradigm in a discrete-trial fashion. This method generated independent measures of drug-induced changes in the MFB stimulation reward and operant motor/performance capacity. Control experiments were run with the inactive isomer, trans-flupenthixol. Results indicate a major role for accumbens DA in MFB reward, but not for the DA in caudate and medial frontal cortex. Few drug-induced motor/performance deficits were found at any site. In 14 selected subjects, 6-OHDA-induced chronic DA lesions were made at the same site as neuroleptic microinjection. These results confirmed the reward effects of acute DA receptor blockade, but produced a greater associated motor/performance impairment. Both behavioral effects of the lesion recovered within 2 weeks in many, but not all subjects.

Animals↗
PubMed1985

An investigation of the factors affecting development of frontal cortex self-stimulation.

Intracranial self-stimulation (ICSS) of the medial prefrontal cortex (MFC) is acquired gradually, taking 4 or more days to establish. One explanation for this finding is that the stimulation becomes more rewarding with repetition. Four experiments were conducted to test this hypotheses. In Experiment 1, the MFC ICSS frequency thresholds remained constant over the first 3 weeks of testing while the rate of lever pressing response increased. In Experiment 2, it was found that acquisition of MFC ICSS was much more rapid when a motorically simpler response (nose-poking) was employed. Similarly, Experiments 3 and 4 further demonstrated that response factors such as task complexity may ultimately determine the rate of development of frontal cortex ICSS. Overall, these data suggest that independent of the rewarding effects of MFC stimulation there are other effects that initially interfere with learning of complex operant responses.

Animals↗
PubMed1984

Axonal branching of ventral tegmental and raphe projections to the frontal cortex in the rat.

Axonal collateralization of neurons whose divergent branches innervate the medial prefrontal cortex (MFC) and the sulcal cortex was studied in the rat by using the retrograde double-labeling technique. Injections of bisbenzimide and propidium iodide into the MFC and sulcal cortex resulted in double-labeling of a small population of cells within the ventral tegmental area (VTA) and pars compacta of the substantia nigra (SNC). More extensive double-labeling was evident in the midbrain raphe nuclei. Collateralization++ therefore does not appear to be an important property of the dopamine innervation of the prefrontal cortex.

Animals↗
PubMed1983

Neurological reactivity during medial prefrontal cortex stimulation: effects of self-stimulation experience.

Electrical stimulation of the medial prefrontal cortex (MFC) induced a moderate behavioral suppression in a series of neurological tests that included measures of (1) open field activity (2) righting and climbing reflexes (3) somatosensory reactivity and (4) approach-withdrawal responsiveness to positive and negative stimuli. The same animals were trained to lever press for medial prefrontal cortex stimulation and after several days of self-stimulation were again tested for neurological reactivity during MFC stimulation. No habituation or lessening of behavioral suppression was evident as a result of self-stimulation experience. Therefore behavioral suppression, by itself, cannot account for the slow acquisition of MFC self-stimulation. Other data suggest that the stimulation interferes with the learning of complex operant responses and/or that the reward value of the stimulation is increased as a result of repetition.

Animals↗
PubMed1983

Effects of peripheral and central dopamine blockade on lateral hypothalamic self-stimulation: evidence for both reward and motor deficits.

The effects of dopamine receptor antagonists on lateral hypothalamic self-stimulation were analyzed using a reward summation function (RSF) technique. This paradigm relates running speed in a runway to the number of stimulation pulses received as a reward, and it is able to separately characterize changes in reward pulse effectiveness and motor performance. Pimozide, administered peripherally (0.125, 0.25, 0.5 mg/kg, IP), dose-dependently shifted the RSF toward higher values of number of pulses indicating reduced reward. Pimozide also reduced the asymptotic running speed of the RSF, indicating a deficit in motor performance. In a second experiment, alpha-flupenthixol infused directly into the nucleus accumbens (0.5 micrograms-0.5 micrograms, bilaterally) induced changes in the RSF similar to those obtained with peripheral neuroleptic treatment. These findings are discussed from the perspective that dopamine is involved both in the perception of reward value and in the performance of the response to obtain reward.

Animals↗
PubMed1982

Plasticity of the medial prefrontal cortex: facilitated acquisition of intracranial self-stimulation by pretraining stimulation.

Prior electrical stimulation of the medial prefrontal cortex MFC facilitated the subsequent acquisition of intracranial self-stimulation (ICSS) from the same MFC electrode site. Stimulations that were spaced over a period of six days were more effective in producing this facilitation than the same number of stimulations delivered over a two day period. These data suggest that the rewarding effects of MFC stimulation may involve some process akin to the kindling phenomenon and as such may provide insights in the neuronal modifications thought to underlie learning and memory.

Animals↗
PubMed1982

Elimination of medial prefrontal cortex self-stimulation following transection of efferents to the sulcal cortex in the rat.

Intracranial self-stimulation (ICSS) of the medial prefrontal cortex (MFC) was not affected by lesions of the medial forebrain bundle, the nucleus accumbens or medialis dorsalis. However, bilateral, parasagittal knife cuts that transected fibers interconnecting the medial and sulcal cortices eliminated ICSS from the MFC with no apparent recovery over a 21 day test period. Similar knife cuts produced only transient effects on lateral hypothalamic ICSS. These data suggest that the neural substrates of frontal cortex ICSS are very different than those that subserve ICSS along the medial forebrain bundle.

Animals↗
PubMed1982

Fiber pathways associated with cerebellar self-stimulation in the rat: a retrograde and anterograde tracing study.

Intracranial self-stimulation (ICSS) was obtained from an area of cerebellum just rostro-ventral to the fastigial nucleus. The acquisition of cerebellar ICSS was slow, although this depended in part on the type of operant task required. The afferent and efferent fiber connections of the region of cerebellum supporting ICSS were identified using silver-degeneration and horseradish peroxidase tracing techniques. Two major pathways, one ascending to the ventromedial thalamus and one descending to the paramedian reticular formation and the region of the solitary nucleus, are discussed as possible substrates of ICSS at sites in the cerebellum as well as from other pontine and medullary regions.

Animals↗
PubMed1980

Intracranial self-stimulation in relation to the ascending dopaminergic systems of the midbrain: a moveable electrode mapping study.

Chronically implanted moveable electrodes were used to map the midbrain and caudal diencephalon for intracranial self-stimulation in relation to the ascendindg dopamine systems as revealed by fluorescence histochemistry. In the diencephalon the lowest self-stimulation thresholds and the highest response rates were in the areas traversed by the dopamine fiber bundles. In the midbrain, self-stimulation was restricted to the layer of dopamine containing cell bodies. Self-stimulation current thresholds and responses rates were proportional to the density of dopaminergic elements surrounding the electrode tip; the lowest thresholds and highest response rates were associated with the densest packing of dopaminergic neurons. However, not all portions of the dopamine cell groups supported self-stimulation. Self-stimulation was not obtained from the caudal poles of the A9 and A10 groups, nor from the A8 cell group. These findings suggest that a certain population of dopaminergic neurons directly participates in what is probably a multiple-link circuitry subserving positive reinforcement.

Animals↗
PubMed1980

Behavioral methods for inferring anatomical linkage between rewarding brain stimulation sites.

Rats lever pressed for concurrent electrical stimulation of the lateral hypothalamus and ventral tegmentum. The pulse-pair stimulation technique was used, with the first pulse of each pair applied to one electrode and the second to the other electrode; the intrapair interval was varied. The effectiveness of stimulation, measured behaviorally, increased abruptly (within .4 msec) as the intrapair interval was increased in the range from 1.0 to 2.0 msec. These results, which do not resemble single-electrode refractory period results, are interpreted as evidence of collision in the directly stimulated, reward-related neurons linking the two sites. We conclude that self-stimulation of the medial forebrain bundle involves the direct activation of long-axon, longitudinal pathways. Estimates of the conduction velocity in the fibers subserving the collision-like effects are consistent with the properties of small myelinated axons but not central monoaminergic fibers.

Animals↗
PubMed1979

Intracranial self-stimulation in relation to the ascending noradrenergic fiber systems of the pontine tegmentum and caudal midbrain: a moveable electrode mapping study.

Chronically implanted moveable electrodes were used to map the pontine tegmentum and caudal midbrain for intracranial self-stimulation in relation to the ascending noradrenergic systems as revealed by fluorescence histochemistry. In no area tested was there a consistent correlation between the quality or the presence of self-stimulation and the degree of noradrenergic fiber density or cellular aggregation. Of particular importance was the failure to obtain self-stimulation from the locus coeruleus, despite repeated testing and extensive attempts at behavioral shaping. Those areas supporting self-stimulation included the dorsal raphe nucleus, the superior cerebellar peduncle and the mesencephalic and motor nuclei of the trigeminal nerve. These data appear to rule out activation of the ascending noradrenergic systems as an explanation of the rewarding effects of stimulation in these areas. A gustatory-visceral fiber system is suggested as an alternative possible substrate.

Adrenergic Fibers↗
PubMed1977

Dorsal noradrenergic bundle lesions fail to disrupt self-stimulation from the region of locus coeruleus.

Intracranial self-stimulation (ICSS) from the region of the locus coeruleus (LC) was not attenuated by ipsilateral dorsal noradrenergic bundle (DNB) lesions. Bilateral DNB lesions also failed to affect LC ICSS, whereas the same lesions, in the same animals, resulted in a marked enhancement of lateral hypothalamic (LHA) ICSS responding. Behavioral, neuroanatomical and fluorescent histochemical data confirmed destruction of the DNB, thus suggesting that the dorsal noradrenergic system is not necessary for ICSS from the region of the LC.

Animals↗
PubMedDate not supplied

Cortical and ventral tegmental systems exert opposing influences on self-stimulation from the prefrontal cortex.

Intracranial self-stimulation (ICSS) was obtained from 3 areas of anteromedial cortex: the prelimbic area (Brodman's area 32), the anterior cingulate area and the posterior cingulate area. Electrical stimulation in the prelimbic and anterior cingulate areas also produces a behavioral inhibition which is most pronounced at anterior sites (i.e. prelimbic) and declines at increasingly more posterior sites. It was found that the acquisition of responding for ICSS and the magnitude of amphetamine's facilitation of ICSS were inversely related to the degree of behavioral inhibition. These data and the ability of amphetamine to reverse prefrontal stimulation-induced inhibition suggest an important interaction between the prefrontal cortex and the mesolimbic dopamine systems in the control of goal-directed behavior. A model involving cortical suppression of mesolimbic dopamine function is discussed.

Animals↗
PubMedDate not supplied

Long term potentiation of lateral hypothalamic self-stimulation following parabrachial lesions in the rat.

Two neural systems in the pontine tegmentum have been implicated in reward processes. One is the visceral afferent-column arising from the nucleus of the solitary tract and the pontine tegmental taste area (PTA), the other being the dorsal noradrenergic system that has its origin in the locus coeruleus (LC). Lesions of the LC had no effect on lateral hypothalamic (LH) intracranial self-stimulation (ICSS) whereas lesions of the PTA produce a dramatic and seemingly permanent increase in LH ICSS response rates. These results are discussed in the context of noradrenergic/dopaminergic interactions in the control of goal-directed behaviors.

Afferent Pathways↗