Basal forebrain grafts in the rat neocortex restore in vivo acetylcholine release and respond to behavioural activation

Rosenblad, Carl; Nilsson, Ola

doi:10.1016/0306-4522(93)90504-9

Cited by 32 publications

(11 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As might be expected, the increase in ACh release after the combined treatment in lesioned animals was lower than in control animals (Diez-Ariza et al, 2002). However, it should be noted that the releasing effect of the combined treatment was similar to the effect of a high depolarizing stimulus, such as KCl (100 mM), known to produce a maximal ACh release both in young or aged rats (Herzog et al, 2003) or after a cholinergic lesion (Rosenblad and Nilsson, 1993).…”

Section: Discussionsupporting

confidence: 55%

See 1 more Smart Citation

Facilitation of cholinergic transmission by combined treatment of ondansetron with flumazenil after cortical cholinergic deafferentation

et al. 2004

View full text Add to dashboard Cite

We have studied the effects of concomitant blockade of 5-HT 3 and GABA A receptors on acetylcholine (ACh) release in the frontal cortex of rats with a selective cholinergic lesion. Lesions were performed by microinjection of the cholinergic toxin 192 IgG-saporin into the nucleus basalis magnocellularis. Single treatment with either the 5-HT 3 receptor antagonist ondansetron, 0.1 lg/kg, or the GABA A receptor benzodiazepine site antagonist flumazenil, 10 mg/kg, did not affect ACh release. However, the combined ondansetron þ flumazenil administration significantly increased ACh release to a similar extent as a depolarising stimulus with K + , 100 mM, at both 7 and 30 days post-lesion. Cortical perfusion with the combined ondansetron þ flumazenil treatment also increased [ 3 H]ACh efflux ''in vitro'' 30 days after lesion, suggesting that local events within the frontal cortex may participate in the interaction of ondansetron with GABAergic neurons, modulating ACh release in situations of cholinergic hypoactivity. No differences in the expression of 5-HT 3 and GABA A receptors in the frontal cortex were found after the cholinergic lesion. These results suggest that a combined ondansetron þ flumazenil treatment would contribute to restoring a diminished cholinergic function and may provide a basis for using this treatment in the therapy of cognitive disorders associated with degeneration of the cholinergic system. #

show abstract

Section: Discussionsupporting

confidence: 55%

“…ACh content in the dialysis samples was determined using high-performance liquid chromatography (HPLC) with electrochemical detection as previously reported (Rosenblad and Nilsson, 1993). ACh content was calculated by comparing with a 1 pmol standard.…”

Section: Acetylcholine Release ''In Vivo''mentioning

confidence: 99%

Facilitation of cholinergic transmission by combined treatment of ondansetron with flumazenil after cortical cholinergic deafferentation

et al. 2004

View full text Add to dashboard Cite

show abstract

“…It has been reported that ACh is released in the rat neocortex in response to a variety of behavioral and environmental conditions, including wakefulness (7), motor activity (8), restraint, or handlinginduced stress (9) and by exposure to auditory, visual, and gustatory stimulation (10)(11)(12). In addition to these findings, which demonstrate differences in ACh release related to different states of arousal, other evidence suggests that associative conditioning (13)(14)(15)(16)) also may modify ACh release in the neocortex.…”

mentioning

confidence: 74%

“…Our results show that the release of cortical ACh, immediately after saccharin consumption during the acquisition trial, could be directly related to the possibility of recognition of the novel gustatory stimulus. The TTX dose used in the present experiment was based on previous work (9,24) and preliminary experiments of ACh release in the cortex after TTX blockage and simultaneous KCI stimulation of NBM, where the results showed a significantly TTX-blocked cortical ACh release. TTX did not affect other behavioral parameters that have been related to cholinergic afferents, for example, attention or motivation, given that both the control and TTX-treated groups show similar saccharin consumption during the acquisition trial.…”

Section: Discussionmentioning

confidence: 99%

Reversible inactivation of the nucleus basalis magnocellularis induces disruption of cortical acetylcholine release and acquisition, but not retrieval, of aversive memories

Miranda

Bermúdez‐Rattoni

1999

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

The basal forebrain complex, which includes the nucleus basalis magnocellularis (NBM), provides widespread cholinergic and ␥-aminobutyric acid-containing projections throughout the brain, including the insular and pyriform cortices. A number of studies have implicated the cholinergic neurons in the mediation of learning and memory processes. However, the role of basal forebrain activity in information retrieval mechanisms is less known. The aim of the present study is to evaluate the effects of reversible inactivation of the NBM by tetrodotoxin (TTX, a voltagesensitive sodium channel blocker) during the acquisition and retrieval of conditioned taste aversion (CTA) and to measure acetylcholine (ACh) release during TTX inactivation in the insular cortex, by means of the microdialysis technique in free-moving rats. Bilateral infusion of TTX in the NBM was performed 30 min before the presentation of gustative stimuli, in either the CTA acquisition trial or retrieval trial. At the same time, levels of extracellular ACh release were measured in the insular cortex. The behavioral results showed significant impairment in CTA acquisition when the TTX was infused in the NBM, whereas retrieval was not affected when the treatment was given during the test trial. Biochemical results showed that TTX infusion into the NBM produced a marked decrease in cortical ACh release as compared with the controls during consumption of saccharin in the acquisition trial. Depleted ACh levels were found during the test trial in all groups except in the group that received TTX during acquisition. These results suggest a cholinergic-dependent process during acquisition, but not during memory retrieval, and that NBM-mediated cholinergic cortical release may play an important role in early stages of learning, but not during recall of aversive memories.The cerebral cortex has been considered as the ubiquitous place for the storage of long-term memory. In this regard, a great deal of investigation into brain health has focused on a particular central nervous system disorder, Alzheimer's disease. This disease results, at least in part, from a deficit in acetylcholine (ACh) neurotransmission caused by a degeneration of large basal forebrain (BF) cholinergic neurons and a deficit in choline acetyltransferase, the enzyme that synthesizes ACh (1).Accumulative evidence supports the role of cholinergic neurons in the BF in processes such as arousal, attention, learning, and memory. Behavioral deficits associated with lesions produced by injections of excitatory amino acid agonists into the nucleus basalis magnocellularis (NBM) have been demonstrated in a variety of tasks (2, 3). However, the behavioral deficits of these lesions might be caused not only by the resulting cholinergic deafferentation, because 30-35% of the population of BF projections neurons to the cortex are ␥-aminobutyric acid-containing neurons (4-6).In this regard, there are several experiments trying to study more directly the modulatory role of ACh in the activity of cortical ...

show abstract

“…Corticolimbic areas, including the PFC, are central to processing complex aspects of stress in humans (Shin et al, 2005) and rats (Amat et al, 2005;Jinks and McGregor, 1997). Several groups have reported that various psychogenic stressors elicit PFC ACh release (Laplante et al, 2004;Mark et al, 1996;Rosenblad and Nilsson, 1993;Thiel et al, 1998). Thus, we hypothesized that MCHR1 blockade would attenuate the effects of a POS on PFC ACh release.…”

Section: Discussionmentioning

confidence: 99%

Melanin-Concentrating Hormone-1 Receptor Modulates Neuroendocrine, Behavioral, and Corticolimbic Neurochemical Stress Responses in Mice

Smith

Davis

Rorick-Kehn

et al. 2005

Neuropsychopharmacol

View full text Add to dashboard Cite

Repeated exposure to stressful conditions is linked to the etiology of affective disorders. The melanin-concentrating hormone-1 receptor (MCHR1) may be a novel mechanism that is involved in the modulation of stress responses and affective states. The role of MCHR1 in neuroendocrine, behavioral, and neurochemical stress, and anxiety-related responses was examined by monitoring the effects of melanin-concentrating hormone (MCH) and the selective MCHR1 antagonist, GW3430, in inbred C57Bl/6NTac and MCHR1-knockout (KO) and wild-type (WT) mice. Intracerebroventricular injection of MCH increased plasma corticosterone, and produced anxiety-related responses in the elevated plus maze. The selective MCHR1 antagonist, GW3430, blocked the neuroendocrine and behavioral effects of MCH and produced anxiolytic-like effects by itself in animal models of anxiety. Moreover, KO mice had an anxiolytic-like phenotype in behavioral models of anxiety, and GW3430 had anxiolytic-like effects in WT, but not KO mice. Lastly, stressor-evoked acetylcholine release within the prefrontal cortex of inbred and WT mice, but not KO mice, was blocked by GW3430. We show that MCH elicits anxiety-like responses and that the effects of a selective MCHR1 antagonist and the phenotype of KO mice are consistent with anxiolyticlike action. Distinct behavioral, physiological, and neurochemical stress, and anxiety-related responses were selectively modulated by the MCHR1, and these actions may involve corticolimbic regulation of stress responsivity and anxiety.

show abstract

Basal forebrain grafts in the rat neocortex restore in vivo acetylcholine release and respond to behavioural activation

Cited by 32 publications

References 42 publications

Facilitation of cholinergic transmission by combined treatment of ondansetron with flumazenil after cortical cholinergic deafferentation

Facilitation of cholinergic transmission by combined treatment of ondansetron with flumazenil after cortical cholinergic deafferentation

Reversible inactivation of the nucleus basalis magnocellularis induces disruption of cortical acetylcholine release and acquisition, but not retrieval, of aversive memories

Melanin-Concentrating Hormone-1 Receptor Modulates Neuroendocrine, Behavioral, and Corticolimbic Neurochemical Stress Responses in Mice

Contact Info

Product

Resources

About