Activation of dopamine D1 receptors in the medial septum improves scopolamine-induced amnesia in the dorsal hippocampus

Zarrindast, Mohammad Reza; Ardjmand, Alireza; Ahmadi, Shamseddin; Rezayof, Ameneh

doi:10.1016/j.bbr.2011.12.033

Cited by 21 publications

(9 citation statements)

References 62 publications

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“…As described, EEEP ameliorated cognitive dysfunction induced by scopolamine, and scopolamine blocked the effect of EEEP on LTP (unpublished data). Therefore, the changes of Akt/GSK-3β signaling in the present study may be resulted from activation of cholinergic muscarinic receptor (Li et al, 2001) or from a compensatory activation of other neurotransmitter receptors, as observed in previous reports (Chen et al, 2007;Zarrindast et al, 2012). GSK-3β is also known to be a crucial regulator of neurogenesis in the hippocampus (Esfandiari et al, 2012).…”

Section: Discussionsupporting

confidence: 76%

The ethanolic extract of the Eclipta prostrata L. ameliorates the cognitive impairment in mice induced by scopolamine

Jung

Kim

Park

et al. 2016

Journal of Ethnopharmacology

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Section: Discussionsupporting

confidence: 76%

The ethanolic extract of the Eclipta prostrata L. ameliorates the cognitive impairment in mice induced by scopolamine

Jung

Kim

Park

et al. 2016

Journal of Ethnopharmacology

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“…Disrupting IA by inhibiting MS neural activity is reversed by enhancing ACh release in the dHipp (Degroot and Parent, 2001). MAChR antagonism disrupts acquisition (Khakpai, Nasehi, Haeri-Rohani, Eidi, and Zarrindast, 2012; Nail-Boucherie et al, 1998; Qi and Gold, 2009) and consolidation (Zarrindast, Ardjmand, Ahmadi, and Rezayof, 2012) of IA, as well as long-term contextual fear memory in IA (Parfitt, Campos, Barbosa, Koth, and Barros, 2012). …”

Section: Bf Cholinergic Neurons In Fear and Extinction Memorymentioning

confidence: 99%

The role of basal forebrain cholinergic neurons in fear and extinction memory

Knox

2016

Neurobiology of Learning and Memory

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Cholinergic input to the neocortex, dorsal hippocampus (dHipp), and basolateral amygdala (BLA) is critical for neural function and synaptic plasticity in these brain regions. Synaptic plasticity in the neocortex, dHipp, ventral Hipp (vHipp), and BLA has also been implicated in fear and extinction memory. This finding raises the possibility that basal forebrain (BF) cholinergic neurons, the predominant source of acetylcholine in these brain regions, have an important role in mediating fear and extinction memory. While empirical studies support this hypothesis, there are interesting inconsistencies among these studies that raise questions about how best to define the role of BF cholinergic neurons in fear and extinction memory. Nucleus basalis magnocellularis (NBM) cholinergic neurons that project to the BLA are critical for fear memory and contextual fear extinction memory. NBM cholinergic neurons that project to the neocortex are critical for cued and contextual fear conditioned suppression, but are not critical for fear memory in other behavioral paradigms and in the inhibitory avoidance paradigm may even inhibit contextual fear memory formation. Medial septum and diagonal band of Broca cholinergic neurons are critical for contextual fear memory and acquisition of cued fear extinction. Thus, even though the results of previous studies suggest BF cholinergic neurons modulate fear and extinction memory, inconsistent findings among these studies necessitates more research to better define the neural circuits and molecular processes through which BF cholinergic neurons modulate fear and extinction memory. Furthermore, studies determining if BF cholinergic neurons can be manipulated in such a manner so as to treat excessive fear in anxiety disorders are needed.

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“…Moreover, manipulation of DA transmission in the septal area affects hippocampal theta synchronicity (Miura et al, 1987 ; Fitch et al, 2006 ), and a specific role for MS/VDB cells expressing D1/5 receptor in theta rhythm modulation has been observed (Fitch et al, 2006 ). Additionally, injection of D1 agonists in the MS has been reported to increase acetylcholine levels in the hippocampus (Zarrindast et al, 2012 ).…”

Section: Discussionmentioning

confidence: 99%

“…Studies using DAT knockout mice demonstrated that dopaminergic and norepinephric transmission mediates MPD induction of c-fos expression in a number of brain areas (Trinh et al, 2003 ). Catecholamine projections to septal area have been reported (Sánchez-Camacho et al, 2003 ), moreover injection of D1 receptor agonists in the MS have been demonstrated to induce acetylcholine neurotransmitter increase in hippocampus (Zarrindast et al, 2012 ). Furthermore, D1 and D5 activation enhances the firing rates of medial septal neurons that provides a state with higher probability for hippocampal theta occurrence (Fitch et al, 2006 ), Thus we hypothesized that MPD could exerts its effects improving attention processes via modulating the septo-hippocampal circuitry.…”

Section: Introductionmentioning

confidence: 99%

Acute oral administration of low doses of methylphenidate targets calretinin neurons in the rat septal area

García-Avilés

Albert-Gascó²,

Arnal-Vicente

et al. 2015

Front. Neuroanat.

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Methylphenidate (MPD) is a commonly administered drug to treat children suffering from attention deficit hyperactivity disorder (ADHD). Alterations in septal driven hippocampal theta rhythm may underlie attention deficits observed in these patients. Amongst others, the septo-hippocampal connections have long been acknowledged to be important in preserving hippocampal function. Thus, we wanted to ascertain if MPD administration, which improves attention in patients, could affect septal areas connecting with hippocampus. We used low and orally administered MPD doses (1.3, 2.7 and 5 mg/Kg) to rats what mimics the dosage range in humans. In our model, we observed no effect when using 1.3 mg/Kg MPD; whereas 2.7 and 5 mg/Kg induced a significant increase in c-fos expression specifically in the medial septum (MS), an area intimately connected to the hippocampus. We analyzed dopaminergic areas such as nucleus accumbens and striatum, and found that only 5 mg/Kg induced c-fos levels increase. In these areas tyrosine hydroxylase correlated well with c-fos staining, whereas in the MS the sparse tyrosine hydroxylase fibers did not overlap with c-fos positive neurons. Double immunofluorescence of c-fos with neuronal markers in the septal area revealed that co-localization with choline acethyl transferase, parvalbumin, and calbindin with c-fos did not change with MPD treatment; whereas, calretinin and c-fos double labeled neurons increased after MPD administration. Altogether, these results suggest that low and acute doses of methylphenidate primary target specific populations of caltretinin medial septal neurons.

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Activation of dopamine D1 receptors in the medial septum improves scopolamine-induced amnesia in the dorsal hippocampus

Cited by 21 publications

References 62 publications

The ethanolic extract of the Eclipta prostrata L. ameliorates the cognitive impairment in mice induced by scopolamine

The ethanolic extract of the Eclipta prostrata L. ameliorates the cognitive impairment in mice induced by scopolamine

The role of basal forebrain cholinergic neurons in fear and extinction memory

Acute oral administration of low doses of methylphenidate targets calretinin neurons in the rat septal area

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