Immunohistochemical characterisation of Fos‐positive cells in brainstem monoaminergic nuclei following intracranial self‐stimulation of the medial forebrain bundle in the rat

Ishida, Yoshiteru; Nakamura, Masato; Ebihara, Kosuke; Hoshino, Kaeko; Hashiguchi, Hiroyuki; Mitsuyama, Yoshio; Nishimori, Toshikazu; Nakahara, Daiichiro

doi:10.1046/j.0953-816x.2001.01520.x

Cited by 24 publications

(15 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In contrast, blockade of the norepinephrine transporter could well have contributed to the observed influence of cocaine. Neurons in the locus coeruleus and lateral tegmental A7 cluster show increased double labeling for tyrosine hydroxylase and the immediate early-gene product, Fos, following self-stimulation of MFB sites [60], suggesting that the activated neurons are noradrenergic. Injection of the α 1 antagonist, terazosin, into the locus coeruleus produces rightward shifts in rate-frequency curves obtained from rats working for MFB stimulation [61].…”

Section: Discussionmentioning

confidence: 99%

At What Stage of Neural Processing Does Cocaine Act to Boost Pursuit of Rewards?

et al. 2010

View full text Add to dashboard Cite

Dopamine-containing neurons have been implicated in reward and decision making. One element of the supporting evidence is that cocaine, like other drugs that increase dopaminergic neurotransmission, powerfully potentiates reward seeking. We analyze this phenomenon from a novel perspective, introducing a new conceptual framework and new methodology for determining the stage(s) of neural processing at which drugs, lesions and physiological manipulations act to influence reward-seeking behavior. Cocaine strongly boosts the proclivity of rats to work for rewarding electrical brain stimulation. We show that the conventional conceptual framework and methods do not distinguish between three conflicting accounts of how the drug produces this effect: increased sensitivity of brain reward circuitry, increased gain, or decreased subjective reward costs. Sensitivity determines the stimulation strength required to produce a reward of a given intensity (a measure analogous to the KM of an enzyme) whereas gain determines the maximum intensity attainable (a measure analogous to the vmax of an enzyme-catalyzed reaction). To distinguish sensitivity changes from the other determinants, we measured and modeled reward seeking as a function of both stimulation strength and opportunity cost. The principal effect of cocaine was a two-fourfold increase in willingness to pay for the electrical reward, an effect consistent with increased gain or decreased subjective cost. This finding challenges the long-standing view that cocaine increases the sensitivity of brain reward circuitry. We discuss the implications of the results and the analytic approach for theories of how dopaminergic neurons and other diffuse modulatory brain systems contribute to reward pursuit, and we explore the implications of the conceptual framework for the study of natural rewards, drug reward, and mood.

show abstract

Section: Discussionmentioning

confidence: 99%

At What Stage of Neural Processing Does Cocaine Act to Boost Pursuit of Rewards?

et al. 2010

View full text Add to dashboard Cite

show abstract

“…On one hand, it has been shown that basal forebrain neurons, including the ones in the amygdala, are antidromically driven by LH stimulation (Murray & Shizgal 1996), suggesting that many of the labelled cells could be directly activated by the electrical stimulation delivered at the tip of the electrode. On the other hand, LH ICSS induces a significant increase in the number of Fos‐immunopositive cells in several brainstem monoaminergic nuclei, such as the locus coeruleus (Arvanitogiannis et al 1997; Ishida et al 2001), that in turn activate the amygdala (Samuels & Szabadi 2008). Thus, these data indicate that some amygdalar neurons also can be trans‐synaptically activated by ICSS.…”

Section: Discussionmentioning

confidence: 99%

Intracranial self-stimulation induces expression of learning and memory-related genes in rat amygdala

Kádár

Aldavert-Vera

Huguet

et al. 2010

Genes, Brain and Behavior

View full text Add to dashboard Cite

Intracranial self-stimulation (ICSS) in the lateral hypothalamus improves memory when administered immediately after a training session. In our laboratory, ICSS has been shown as a very reliable way to increase two-way active avoidance (TWAA) conditioning, an amygdaladependent task. The aim of this work was to study, in the rat amygdala, anatomical and molecular aspects of ICSS, using the same parameters facilitating TWAA. First, we examined the activation of ipsilateral and contralateral lateral (LA) and basolateral (BLA) amygdala, the main amygdalar regions involved in the TWAA, by the immunohistochemical determination of c-Fos protein expression. Second, we tested the effects of the ICSS treatment on the expression of 14 genes related to learning and memory processes using real-time polymerase chain reaction. Results showed a bilateral increase in c-Fos protein expression in LA and BLA nuclei after ICSS treatment. We also found that Fos, brain-derived nerve growth factor (BDNF ), Arc, inducible cAMP early repressor (ICER), COX-2, Dnajb1, FKpb5 and Ret genes were upregulated in the amygdala 90 min and 4.5 h post ICSS. From this set of genes, BDNF, Arc and ICER are functionally associated with the cAMP-responsive element-mediated gene transcription molecular pathway that plays a pivotal role in memory, whereas Dnajb1 and Ret are associated with protein folding required for plasticity or neuroprotection. Our results suggest that ICSS induces expression of genes related with synaptic plasticity and protein folding functions in the rat amygdaloid area, which may be involved in the molecular mechanisms by which ICSS may improve or restore memory functions related to this brain structure.

show abstract

“…Interestingly, the VTA receives an NT input exclusively from structures in which brain self‐stimulations have been shown to be rewarding (Olds & Olds, 1963). The parabrachial nucleus, dorsal raphe, PPTg, lateral hypothalamic area, lateral and medial preoptic area, lateral septum and nucleus accumbens have been shown to either elicit rewarding brain stimulation or be activated after brain stimulation reward of the medial forebrain bundle (Olds & Milner, 1954; Olds & Olds, 1963; Arvanitogiannis et al ., 1997; Ishida et al ., 2001; Nakahara et al ., 2001). On the other hand, structures that provide a strong input to the VTA but are neutral or aversive (paraventricular thalamic nucleus, lateral habenula, deep mesencephalic field of reticular formation) to self‐stimulation (Olds & Olds, 1963; but see Vachon & Miliaressis, 1992) do not contain NT neurons innervating the VTA.…”

Section: Discussionmentioning

confidence: 99%

Neurotensin afferents of the ventral tegmental area in the rat: [1] re‐examination of their origins and [2] responses to acute psychostimulant and antipsychotic drug administration

Geisler

Zahm

2006

Eur J of Neuroscience

View full text Add to dashboard Cite

The ventral tegmental area (VTA) is involved in reward-related behaviours and the actions of psychostimulant drugs. It is influenced by afferents expressing a variety of neurotransmitters and neuromodulators; the innervation containing neurotensin is among the densest of these. Intra-VTA neurotensin activates dopaminergic neurons and plays an important role in the development of behavioural sensitization to psychostimulant drugs and possibly in schizophrenia. Using gold-coupled wheatgerm agglutinin as retrograde tracer in combination with nonisotopic in situ hybridization for neurotensin mRNA or neurotensin antibodies after colchicine treatment, the present study was undertaken to demonstrate the neurotensinergic neurons projecting to the VTA and determine whether (and in which subpopulations) neurotensin expression is regulated in VTA-projecting neurons after administrations of the psychostimulant drug methamphetamine or the antipsychotic haloperidol. This study reveals the lateral preoptico-rostral lateral hypothalamic continuum and the medial preoptic area as main sources for the neurotensin afferents of the VTA. Fewer neurotensinergic, VTA-projecting neurons are situated in the dorsal raphe, pedunculopontine and laterodorsal tegmental nuclei, lateral hypothalamic area, ventral endopiriform area, lateral septum, accumbens shell, parabrachial nucleus and different parts of the extended amygdala. The number of neurotensinergic VTA-projecting neurons increased significantly only after methamphetamine administration and exclusively in the accumbens shell. It is concluded that the widespread neurotensinergic VTA-projecting neurons, situated in areas involved in different reward-related behaviours, are well suited to convey distinct reward information to the VTA. The up-regulation of neurotensin expression selectively in VTA-projecting neurons in the accumbens shell following methamphetamine administration may be an important factor in the development of behavioural sensitization.

show abstract

Immunohistochemical characterisation of Fos‐positive cells in brainstem monoaminergic nuclei following intracranial self‐stimulation of the medial forebrain bundle in the rat

Cited by 24 publications

References 47 publications

At What Stage of Neural Processing Does Cocaine Act to Boost Pursuit of Rewards?

At What Stage of Neural Processing Does Cocaine Act to Boost Pursuit of Rewards?

Intracranial self-stimulation induces expression of learning and memory-related genes in rat amygdala

Neurotensin afferents of the ventral tegmental area in the rat: [1] re‐examination of their origins and [2] responses to acute psychostimulant and antipsychotic drug administration

Contact Info

Product

Resources

About