Involvement of the ventral tegmental area in the inhibitory avoidance memory in rats

Mahmoodi, Minoo; Shahidi, Siamak; Hasanein, Parisa

doi:10.1016/j.physbeh.2011.01.011

Cited by 18 publications

(6 citation statements)

References 43 publications

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“…Temporary blockade of the VTA activity by unilateral microinjection of procaine caused bilateral loss of sensory stimulation‐elicited theta in urethanized rat (Orzeł‐Gryglewska et al, ). Likewise, bilateral intra‐VTA infusions of lidocaine‐affected theta in rats trained in an inhibitory avoidance task (Mahmoodi et al, ). Irreversible abolition of the VTA activity by electrolytic lesions was related to partial desynchronization of tail pinch‐elicited theta, with a reduction in maximum of power in the 3–6‐Hz band and an increase in the maximum power in the range of 6–12 Hz.…”

Section: Participation Of the Vta In The Regulation Of Thetamentioning

confidence: 99%

Brainstem system of hippocampal theta induction: The role of the ventral tegmental area

Orzeł-Gryglewska

Matulewicz

Jurkowlaniec

2015

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This article summarizes the results of studies concerning the influence of the ventral tegmental area (VTA) on the hippocampal theta rhythm. Temporary VTA inactivation resulted in transient loss of the hippocampal theta. Permanent destruction of the VTA caused a long-lasting depression of the power of the theta and it also had some influence on the frequency of the rhythm. Activation of glutamate (GLU) receptors or decrease of GABAergic tonus in the VTA led to enhancement of dopamine release and increased hippocampal theta power. High time and frequency cross-correlation was detected for the theta band between the VTA and hippocampus during paradoxical sleep and active waking. Thus, the VTA may belong to the broad network involved in theta rhythm regulation. This article also presents a model of brainstem-VTA-hippocampal interactions in the induction of the hippocampal theta rhythm. The projections from the VTA which enhance theta rhythm are incorporated into the main theta generation pathway, in which the septum acts as the central node. The neuronal activity that may be responsible for the ability of the VTA to regulate theta probably derives from the structures associated with rapid eye movement (sleep) (REM) sleep or with sensorimotor activity (i.e., mainly from the pedunculopontine and laterodorsal tegmental nuclei and also from the raphe).

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Section: Participation Of the Vta In The Regulation Of Thetamentioning

confidence: 99%

Brainstem system of hippocampal theta induction: The role of the ventral tegmental area

Orzeł-Gryglewska

Matulewicz

Jurkowlaniec

2015

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“…Rats either received bilateral injections of bupivacaine hydrochloride (2.5% dissolved in 0.9% saline solution) or vehicle (0.9% saline solution) only once, on their shock day, immediately before shock (Figure 1bD). This type of reversible local anesthetic has been previously used in the inactivation of VTA neurons (Mahmoodi et al, 2011;Moaddab et al, 2009;Seip and Morrell, 2009). All injections were done in awake rats with the internal cannulae extending 1 mm beyond the tip of the guide cannula and were performed using a microliter Hamilton syringe (Hamilton, Reno, NV) attached to flexible polyethylene tubing.…”

Section: Intracerebral Cannulation and Injectionsmentioning

confidence: 99%

Involvement of the Ventral Tegmental Area in a Rodent Model of Post-Traumatic Stress Disorder

Corral-Frías

Lahood

Edelman-Vogelsang

et al. 2012

Neuropsychopharmacol

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Post-traumatic stress disorder (PTSD) is an anxiety disorder of considerable prevalence in individuals who have experienced a traumatic event. Studies of the neural substrate of this disorder have focused on the role of areas such as the hippocampus, the amygdala and the medial prefrontal cortex. We show that the ventral tegmental area (VTA), which directly modulates these areas, is part of this circuitry. Using a rat model of PTSD, we show that a brief but intense foot shock followed by three brief reminders can cause long-term behavioral changes as shown by anxiety-like, nociception, and touch-sensitivity tests. We show that an intraperitoneal injection of a dopamine (DA) antagonist or a bilateral inactivation of the VTA administered immediately before the traumatic event decrease the occurrence or intensity of these behavioral changes. Furthermore, we show that there is a significant decrease of baseline VTA dopaminergic but not GABAergic cell firing rates 2 weeks after trauma. Our data suggest that VTA DA neurons undergo long-term physiological changes after trauma and that this brain area is a crucial part of the circuits involved in PTSD symptomatology.

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“…Taken together, three independent results point towards a hippocampus-related phenotype in the TH-Cre-mediated cKO mice; the slower acquisition and the accentuated error rate in the radial arm maze, a spatial memory test designed to assay hippocampus function (Meck et al 1984 ); the significantly lower DA tissue levels observed by electrochemical detection in homogenates prepared from the hippocampus (while no other region containing either DA cell bodies or projection terminals showed similar alterations); and the increased sensitivity to the ionotropic glutamate receptor agonist kainate, leading to seizure-like activity in slice preparations obtained from cKO brains. In recent studies, it was shown in rats that severing of the signalling from the VTA to the hippocampus via the local administration of lidocaine (Mahmoodi et al 2011 ) or baclofen (Martig and Mizumori 2011 ), resulted in a decreased performance in memory tests. Neither study showed motivational or movement disruptions, but an increase in errors and an elevated number of trials required to reach the acquisition criterion in memory tasks (Mahmoodi et al 2011 ; Martig and Mizumori 2011 ).…”

Section: Discussionmentioning

confidence: 99%

Increased hippocampal excitability and impaired spatial memory function in mice lacking VGLUT2 selectively in neurons defined by tyrosine hydroxylase promoter activity

et al. 2014

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Three populations of neurons expressing the vesicular glutamate transporter 2 (Vglut2) were recently described in the A10 area of the mouse midbrain, of which two populations were shown to express the gene encoding, the rate-limiting enzyme for catecholamine synthesis, tyrosine hydroxylase (TH).One of these populations (“TH–Vglut2 Class1”) also expressed the dopamine transporter (DAT) gene while one did not (“TH–Vglut2 Class2”), and the remaining population did not express TH at all (“Vglut2-only”). TH is known to be expressed by a promoter which shows two phases of activation, a transient one early during embryonal development, and a later one which gives rise to stable endogenous expression of the TH gene. The transient phase is, however, not specific to catecholaminergic neurons, a feature taken to advantage here as it enabled Vglut2 gene targeting within all three A10 populations expressing this gene, thus creating a new conditional knockout. These knockout mice showed impairment in spatial memory function. Electrophysiological analyses revealed a profound alteration of oscillatory activity in the CA3 region of the hippocampus. In addition to identifying a novel role for Vglut2 in hippocampus function, this study points to the need for improved genetic tools for targeting of the diversity of subpopulations of the A10 area.Electronic supplementary materialThe online version of this article (doi:10.1007/s00429-014-0778-9) contains supplementary material, which is available to authorized users.

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Involvement of the ventral tegmental area in the inhibitory avoidance memory in rats

Cited by 18 publications

References 43 publications

Brainstem system of hippocampal theta induction: The role of the ventral tegmental area

Brainstem system of hippocampal theta induction: The role of the ventral tegmental area

Involvement of the Ventral Tegmental Area in a Rodent Model of Post-Traumatic Stress Disorder

Increased hippocampal excitability and impaired spatial memory function in mice lacking VGLUT2 selectively in neurons defined by tyrosine hydroxylase promoter activity

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