Disease relevance of Medial Forebrain Bundle

• Hyperprolactinemia was, however, associated with decreased glucose utilization in the medial forebrain bundle and the CA subfield of the dorsal hippocampus [1].
• The efficacy of this compound was assessed in rats with unilateral 6-hydroxydopamine lesions of the medial forebrain bundle, a standard rat model of Parkinson's disease [2].
• Changes in corticotrophin (ACTH) and corticosterone (CS) serum levels, were examined in rats in which either 6-hydroxydopamine or vehicle were injected into the medial forebrain bundle (MFB) and which were sacrificed by decapitation 14 days later [3].
• However, parasagittal cuts which separated the AV3V region from the medial forebrain bundle attenuated the hypertension following 5 weeks of DOCA-salt treatment [4].
• These effects are produced by deprenyl potentiation of dopamine actions since dopamine depletion produced by previous injection of the dopaminergic toxin 6-hydroxydopamine within the medial forebrain bundle overcomes deprenyl effects and the involvement of dopamine in the quinolinic acid-induced toxicity in striatum [5].

Psychiatry related information on Medial Forebrain Bundle

• Two substrates for medial forebrain bundle self-stimulation: myelinated axons and dopamine axons [6].
• Effect of bilateral 6-hydroxydopamine lesions of the medial forebrain bundle on reaction time [7].
• When 2,4-D was injected into one medial forebrain bundle (MFB, 50 microg/rat), animals presented ipsilateral circling, while locomotor activity was unchanged at 3 and 7 days post-injection [8].

High impact information on Medial Forebrain Bundle

• Cocaine, mu and delta opiates, nicotine, phencyclidine, and cannabis each have actions that summate with rewarding electrical stimulation of the medial forebrain bundle (MFB) [9].
• Nigral basal adenylate cyclase and dopamine-sensitive adenylate cyclase, glutamate decarboxylase, choline acetyltransferase, and tyrosine hydroxylase activities were measured in rats with hemitransections at various levels or with electrolytic lesions of the medial forebrain bundle or the crus cerebri [10].
• Nevertheless, mice lacking Pax6 display an altered pathfinding of SN-VTA projections: instead of following the route of the medial forebrain bundle ventrally, most of the SN-VTA projections are deflected dorsorostrally at the pretectal-dorsal thalamic transition zone and in the dorsal thalamic alar plate [11].
• GDNF reduces drug-induced rotational behavior after medial forebrain bundle transection by a mechanism not involving striatal dopamine [12].
• Regional distribution of DAT coincided with established dopaminergic innervation of several regions, including ventral mesencephalon, medial forebrain bundle, and dorsal and ventral striatum [13].

Chemical compound and disease context of Medial Forebrain Bundle

• The hypothesis that ethanol would reduce the threshold for self-stimulation of the medial forebrain bundle was not supported [14].
• Brain stem self-stimulation attenuated by lesions of medial forebrain bundle but not by lesions of locus coeruleus or the caudal ventral norepinephrine bundle [15].
• (+)-Amphetamine significantly decreased frequency threshold measures in an intracranial self-stimulation (ICSS) procedure using medial forebrain bundle electrodes, while 4-methoxyamphetamine and 4-ethoxyamphetamine increased these ICSS frequency thresholds [16].
• Experiments were performed to examine the effects of intracerebroventricularly administered cholecystokinin octapeptide sulfate ester (CCK-8-SE) and unsulfated cholecystokinin octapeptide (CCK-8-NS) on electrical self-stimulation behavior elicited from the medial forebrain bundle [17].
• Low doses of haloperidol (3--18 micrograms/kg) caused dose related increases in reinforcing thresholds for self-stimulation to the medial forebrain bundle in rats [18].

Biological context of Medial Forebrain Bundle

• Moderate levels of ANF binding sites were observed in the thalamus and throughout the mesencephalon, whereas low levels were detected in the lateral and medial pallium, the medial forebrain bundle, and the nucleus rotondus [19].
• Upregulation of BDNF mRNA and trkB mRNA in the nigrostriatal system and in the lesion site following unilateral transection of the medial forebrain bundle [20].
• Axonal transport of proteins to telencephalic structures is greatly diminished by selective lesions of catecholamine terminals with 6-hydroxydopamine (6-OHDA) and following destruction of the medial forebrain bundle [21].
• Transection of the medial forebrain bundle caused apoptosis of dopamine neurons in the rat substantia nigra [22].

Anatomical context of Medial Forebrain Bundle

• Rats received unilateral 6-hydroxydopamine lesions of the medial forebrain bundle and substantia nigra pars compacta that were confirmed by apomorphine-induced rotation and 3H-GBR-12935 binding [23].
• Forebrain origins and terminations of the medial forebrain bundle metabolically activated by rewarding stimulation or by reward-blocking doses of pimozide [24].
• Extracellular dopamine and neurotensin in rat prefrontal cortex in vivo: effects of median forebrain bundle stimulation frequency, stimulation pattern, and dopamine autoreceptors [25].
• Stimulation of the medial forebrain bundle resulted in synaptic overflow of dopamine in the caudate nucleus [26].
• 6-Hydroxydopamine lesions of the median forebrain bundle resulted in a total loss of NT2 sites in the caudate-putamen but did not affect NT2 sites in the nucleus accumbens and the olfactory tubercle [27].

Associations of Medial Forebrain Bundle with chemical compounds

• Intracellular injection in fixed slices and neuronal reconstruction were used to analyze the dendritic trees of 62 neurons in the shell and core of animals that received a unilateral, chronic 6-hydroxydopamine lesion of the medial forebrain bundle [28].
• The ultrastructural localization of serotonin immunoreactivity in myelinated and unmyelinated axons within the medial forebrain bundle of rat and monkey [29].
• The authors suggest a decreased central norepinephrine activity, which may be secondary to the interruption of norepinephrine fibers in the medial forebrain bundle [30].
• Injection of 5,7-DHT into the medial forebrain bundle at the hypothalamic level slightly potentiated LSD, attenuated DOM, and did not affect the pausing produced by mescaline [31].
• Infusion of tetrodotoxin into the medial forebrain bundle or the striatum did not alter the voltammetric response to the intrastriatal kynurenate infusions, suggesting that glutamate receptors control a non-vesicular release process that contributes to the basal extracellular dopamine level [32].

Gene context of Medial Forebrain Bundle

• Following extensive unilateral 6-hydroxydopamine lesions of the medial forebrain bundle, ret immunoreactivity in the substantia nigra and striatum was reduced significantly, to a similar extent as tyrosine hydroxylase immunoreactivity [33].
• Following transection of the medial forebrain bundle, however, JNK3 ko conferred persisting neuroprotection of axotomised SNC neurons [34].
• TH immunoreactive nerve fibres were seen to enter the globus pallidus from the medial forebrain bundle [35].
• Colchicine injections into the medial forebrain bundle to specifically disrupt neuronal trafficking between SN and striatum induced BDNF mRNA levels in the ipsilateral SNPC, thus demonstrating that nigral expression of BDNF mRNA is dependent of striatal target tissue [36].
• To test whether amyloid precursor protein (APP) could serve as such a signal, we evaluated microglial activation in SN after unilateral transection of the medial forebrain bundle (MFB) in mice either wild-type (WT) or null (KO) for APP [37].

Analytical, diagnostic and therapeutic context of Medial Forebrain Bundle

• Stereotaxic injections of 6-hydroxydopamine (6-OHDA), a selective neurotoxin, into either the medial forebrain bundle or the substantia nigra result in a massive DA denervation of the nigrostriatal pathway [38].
• This allowed voltammetry and microdialysis to be used under identical in vivo experimental conditions to monitor extracellular dopamine levels during electrical stimulation of the medial forebrain bundle both before and after uptake inhibition with nomifensine [39].
• By quantitative in situ hybridization, we examined in vivo in the rat caudate-putamen the effects on levels of cannabinoid receptor mRNA of an interruption of dopamine neurotransmission for up to 1 month, by either 6-hydroxydopamine lesioning of the medial forebrain bundle or dopamine receptor blockade [40].
• Although caspase-3-like proteolysis was induced in the SNc dopamine neurons of juvenile rats lesioned with 6-OHDA and in adult rats following axotomy of the medial forebrain bundle, caspase-3 is not induced in the dopamine neurons of adult 6-OHDA-lesioned animals [41].
• Mesencephalic tissue was suspended in solutions containing either growth/differentiation factor 5 or glial cell line-derived neurotrophic factor prior to transplantation into the left striatum of rats with 6-hydroxydopamine lesions of the left medial forebrain bundle [42].

References