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PubMed1999

Biochemical and anatomical characterization of forepaw adjusting steps in rat models of Parkinson's disease: studies on medial forebrain bundle and striatal lesions.

Deficits in forepaw adjusting steps in rats have been proposed as a non-drug-induced model of the akinesia associated with Parkinson's disease. The present study examined the relationship between contralateral forepaw adjusting steps and dopamine depletion after medial forebrain bundle lesions with 6-hydroxydopamine. Depletion of striatal dopamine by >80% resulted in dramatic reductions in the ability of rats to make adjusting steps, but rats with < 80% dopamine depletion had no detectable deficit. The deficit in forepaw adjusting steps was evident by three days after lesions and did not recover for up to 13 weeks. Compared to apomorphine-induced rotation, the deficit in adjusting steps was evident at milder dopamine depletion. Discrete striatal lesions were also utilized to localize the striatal subregions that mediate forepaw adjusting steps. Forepaw adjusting steps were reduced after lesions of dorsolateral, ventrolateral or ventrocentral striatum, but not after lesions of dorsomedial, dorsocentral or ventromedial striatum. The reductions in adjusting steps after the discrete striatal lesions were not as severe as after medial forebrain bundle lesions. Furthermore, none of the discrete striatal lesions resulted in rotation after apomorphine administration, although a few resulted in increase in amphetamine-induced rotation. Administration of L-3,4-dihydroxyphenylalanine partially reversed the reductions of forepaw adjusting steps in both sets of lesion experiments. Together, these results suggest that forepaw adjusting step deficits in the rat provide a good model for the akinesia of Parkinson's disease both in medial forebrain bundle and striatal lesions, and would be a useful tool for investigating the efficacy of various therapeutic strategies.

Adaptation, Physiological↗
PubMed1979

Interactions of septal evoked responses to stimulation of the fornix and medial forebrain bundle.

Gross and single unit septal evoked response to stimulation of the fornix and medial forebrain bundle (MFB) were studied in anesthetized, acutely prepared rats. Stimulation of the fornix and MFB produced short-latency antidromic and synaptic activation of localized groups of septal target cells. In addition, stimulation of either pathway produced inhibition of spontaneous single cell activity. The interactions of these responses were studied by delivering paired stimuli to the fornix and/or MFB. A prior stimulus to the fornix potentiated the responses of cell groups synaptically activated by subsequent fornical stimulation, but briefly depressed the sunaptic activation of septal cells by subsequent MFB stimulation. A prior stimulus to the MFB slightly potentiated the synaptic activation of septal cells by a subsequent MFB stimulus, but depressed the responses of cell groups synaptically activated by a subsequent stimulus to the fornix. These results were discussed in terms of their implications for septal organization and function.

Animals↗
PubMedDate not supplied

Two substrates for medial forebrain bundle self-stimulation: myelinated axons and dopamine axons.

The directly activated substrates for medial forebrain bundle (MFB) self-stimulation are primarily low threshold, myelinated axons with absolute refractory periods of 0.4 to 1.2 msec, conduction velocities of 1 to 8 m/sec and current-distance constants of 1000 to 3000 microA/mm2. When small electrode tips or high currents are used, however, a second population of long refractory period (1.2 to 5 msec) axons is added. The excitability properties of this second population are almost identical with those of dopamine (DA) axons. Furthermore, the long-refractory period effects of MFB self-stimulation are reduced, but not completely blocked, by peripheral injections of alpha-flupenthixol, suggesting that dopamine axons make small contributions to MFB self-stimulation when small tips are used. Collision data, strength-duration data and refractory period data in various self-stimulation experiments are compared. Asymmetric collision effects, recently observed in cortical and striatal sites mediating electrically evoked turning, may help determine where synapses are located in circuits mediating electrically evoked behaviors. A neural model of symmetric, asymmetric and mixed collision is proposed.

Animals↗
PubMed1982

Neuropharmacological and electrophysiological evidence implicating the mesolimbic dopamine system in feeding responses elicited by electrical stimulation of the medial forebrain bundle.

The contribution of the mesolimbic dopamine pathway to feeding behavior was investigated in rats in which feeding responses were elicited by electrical stimulation of the medial forebrain bundle at the level of the lateral hypothalamus. Injections of spiroperidol, a dopamine antagonist, into the nucleus accumbens ipsilateral to the stimulating electrode significantly attenuated the elicited feeding responses whereas injecting spiroperidol into the contralateral nucleus accumbens had no effect. The spontaneous discharge rates of neurons of the ventral tegmental area, identified by their electrophysiological characteristics as dopaminergic, were both increased and decreased in response to single pulse stimulation of sites in the medial forebrain bundle from which feeding responses had been elicited. These observations suggest that mesolimbic dopaminergic neurons may have a role in feeding behavior and indicate the need for chronic electrophysiological recording experiments to see whether or not the activity of these neurons is correlated with the initiation of elicited and spontaneous feeding responses.

Animals↗
PubMedDate not supplied

Prolonged medial forebrain bundle unit responses to rewarding and aversive intracranial stimuli.

In unanesthetized cerveau isolé rats, brief medial forebrain bundle (MFB) and dorsal midbrain reticular (RET) stimulus trains elicited prolonged MFB unit responses lasting up to ten or more seconds. On the MFB unit responses studied, the effects of MFB and RET stimuli were basically similar, although the stimulations were probably rewarding and aversive respectively. These data agree with the previously reported anatomical localization, in medial regions of thalamus and pallidum, of opposite single cell responses to the behaviorally opposite inputs, and suggest that unit responses to rewarding stimuli should not be characterized as reward-related when aversive stimuli elicit similar responses in the same unit.

Animals↗
PubMed1983

Role of medial forebrain bundle catecholaminergic fibers in the modulation of glucocorticoid negative feedback effects.

The possible role of medial forebrain bundle (MFB) catecholaminergic fibers in the previously observed MFB-mediated modulation of hypothalamic sensitivity to glucocorticoid negative feedback effects has been investigated. MFB catecholaminergic fibers were destroyed by bilateral MFB injections of 6-hydroxydopamine (6-OHDA) to adult male rats. The inhibitory effect of dexamethasone (10 micrograms, i.p., 4 h) upon the adrenocortical secretory response to ether stress, as estimated by serum corticosterone levels, was enhanced in the 6-OHDA-treated animals, as compared to vehicle-injected controls. This study suggests that MFB noradrenergic neurons are at least partially responsible for the MFB-mediated modulation of hypothalamic sensitivity to glucocorticoid hormones.

Animals↗
PubMed1973

Directionality of rewarding impulses within the medial forebrain bundle self-stimulation system of the rat.

Self-stimulation performance of rats was tested with conditioning pulses to the anterior preoptic area of the medial forebrain bundle followed at various intervals by test pulses to the contralateral posterior hypothalamic area of this bundle. Alternatively, conditioning pulses were delivered through the posterior electrode and test pulses were sent through the anterior electrode. The animals' performance in these two test sequences was indicative of (i) synaptic facilitation and (ii) a posterior convergence site of "self-stimulation impulses" in the medial forebrain bundle.

Animals↗
PubMed1987

Anatomical dissociation of the substrates of medial forebrain bundle self-stimulation and exploration.

The purpose of this research was to determine whether brain stimulation reward and exploration are induced by activation of the same set of neurons along the medial forebrain bundle. The behavioral version of the collision test was utilized with electrodes in the lateral hypothalamus (LH) and the ventral tegmental area (VTA). A collision effect obtained between LH and VTA in one behavior at the exclusion of the other was treated as evidence of the involvement of two different sets of fibers. In 4 rats, a collision effect was observed only in self-stimulation, whereas in 1 rat, a collision was obtained in exploration at the exclusion of self-stimulation. Three animals showed no collision in either behavior. These data suggest that coexistence of self-stimulation and exploration following medial forebrain bundle stimulation can be explained by current spread on two different sets of fibers.

Animals↗
PubMed1993

Bilaterally recorded multiple-unit activity of the cingulate cortex during head turning conditioning with unilateral medial forebrain bundle stimulation.

Cats were conditioned to turn their heads using a tone conditioned stimulus (CS) and medial forebrain bundle stimulation (MFB) unconditioned stimulus (US). The CS+ was delivered to one ear at a time, in random order, followed by the US. A tone of a different frequency was used as a CS-. The cats learned to respond differentially to the CSs showing head movements of greater acceleration to the CS+ than CS- over sessions. Bilateral recordings of cingulate cortex multiple-unit activity showed increased response amplitudes over sessions and larger responses in the hemisphere ipsilateral to the US. Since ipsilateral multiple-unit responses did not differ for the CSs, the asymmetry was probably due to the sensitizing effect of the unilateral US. Although increases in cingulate cortex neural activity coincided with increases in conditioned head movements, larger activation of the cingulate cortex ipsilateral to the US suggests that the neural changes were independent of these movements.

Animals↗
PubMed1988

The region of medial forebrain bundle is involved in tonic maintenance of arterial pressure and heart rate.

The role of the medial forebrain bundle (MFB) in central regulation of cardiovascular system was studied in freely moving rats. Injection of lidocaine into the ventral, but not other portions of the MFB, produced transient (approximately ten minutes) pressor and tachycardic responses. These responses resulted from an increase in sympathetic tone, since they were abolished by ganglionic blockade. The pressure response was attenuated by alpha-adrenoceptor blockade and both pressor and tachycardic responses were diminished by beta-adrenoceptor blockade. Electrolytic lesion of the same site caused long lasting pressor and tachycardic responses. Injection into the MFB of the excitatory amino acids, kainate (KA) and N-methyl-D,L-aspartate (NMDA) produced pressor and tachycardic responses accompanied by behavioral excitation, whereas no effects were produced by L-glutamate. The cardiovascular responses induced by KA and NMDA were abolished by ganglionic blockade. These results suggest that a selective region of MFB contains fibers of passage and/or cell bodies, with receptor specificity for excitatory amino acids, that are capable of influencing sympathetic sympathetic control of arterial pressure.

Amino Acids↗
PubMed2000

Temporary inactivation of the retrorubral fields decreases the rewarding effect of medial forebrain bundle stimulation.

Prior studies indicate that lesioning the retrorubral fields (RRF) decreases the rewarding effect of medial forebrain bundle (MFB) stimulation, although these studies did not make the RRF their primary target. This study directly investigates the role of the RRF in MFB self-stimulation using transient lidocaine-induced inactivation of target tissue rather than permanent lesioning. In 18 rats with MFB stimulation electrodes, inactivation of the RRF via 0. 5 and 1.0 microl of 4% lidocaine produced immediate, substantial upward shifts in the frequency required to maintain half-maximal self-stimulation response rates whereas injecting comparable volumes of saline did not. Bilateral inactivation was particularly effective, especially at medium and high stimulation currents, although unilateral inactivation ipsilateral to the stimulation site was also effective. Contralateral inactivation alone did not substantially change the stimulation's reward value, although contralateral inactivation appeared to contribute to the effectiveness of bilateral inactivation. The frequency required to maintain half-maximal responding returned to baseline levels by 15-20 min after lidocaine infusion. In seven rats whose infusion sites were not in the RRF, lidocaine inactivation did not consistently degrade the stimulation's reward value. These results indicate that some neural elements located in the RRF contribute to the rewarding effect of MFB stimulation. Possible roles for these elements in the anatomical substrate for MFB self-stimulation are discussed.

Anesthetics, Local↗
PubMed1985

Unilateral lesion of the intrinsic cells in the medial forebrain bundle depresses self-stimulation but not stimulus-bound locomotor activity.

The intrinsic neurons of the medial forebrain bundle were unilaterally destroyed, in rats, through local injection of ibotenic acid (4 micrograms in 0.5 microliter). Ten days later, electrodes were bilaterally implanted, one in the lesioned lateral hypothalamus, the other into the contralateral hypothalamus. Firstly, self-stimulation was studied with stimulation of each electrode separately. Later on, the effect of non-contingent electrical stimulation on evoked locomotor activity in the open-field was analysed for each electrode. While self-stimulation of the lesion area was greatly depressed in comparison with the unlesioned lateral hypothalamus, the increase in locomotor activity produced by stimulation, at the intensity applied, was the same whether the stimulated hypothalamus was lesioned or not.

Animals↗
PubMed1998

Midbrain periaqueductal lesions do not degrade medial forebrain bundle stimulation reward.

To investigate the possible role of the midbrain central grey and dorsal raphe in medial forebrain bundle (MFB) self-stimulation, 12 rats received monopolar stimulation electrodes in both the lateral hypothalamic and ventral tegmental MFB and an ipsilateral lesioning electrode in either the central grey or dorsal raphe. Baseline rate-frequency data were collected at several currents at each stimulation site until the frequency required to maintain half-maximal responding stabilized and then an electrolytic lesion was made by passing either 20 or 60 s of anodal constant current through the lesioning electrode. Post-lesion rate-frequency data indicated that lesions of the central grey and dorsal raphe had little appreciable effect on the rewarding nature of MFB stimulation. One rat's lesion damaged the median raphe and produced sustained downward shifts in required frequency, suggesting post-lesion enhancement of the stimulation's rewarding effect.

Animals↗
PubMed1989

Medial forebrain bundle stimulation or D-2 dopamine receptor activation increases preproenkephalin mRNA in rat striatum.

Electrical stimulation of the medial forebrain bundle, in a manner that augmented the release of dopamine in the forebrain, rapidly increased the striatal content of preproenkephalin (but not preprotachykinin) mRNA. This effect was mimicked by administration of either the indirect (dopamine-releasing) agonist methamphetamine or by the D-2 dopamine receptor agonist quinpirole, but not by the D-1 agonist SKF 38393. These data suggest that D-2 receptors, which mediate a stimulatory effect on enkephalin gene expression, may be subsaturated under basal conditions and, therefore, responsive to increases in synaptic dopamine.

Animals↗
PubMed1985

Forebrain origins and terminations of the medial forebrain bundle metabolically activated by rewarding stimulation or by reward-blocking doses of pimozide.

Using [14C]-2-deoxyglucose autoradiography, we determined which forebrain and diencephalic areas showed metabolic alterations in response to unilateral electrical stimulation of the posterior medial forebrain bundle at parameters chosen to produce a just-submaximal rewarding effect. At these parameters, only a few areas were activated. There was no detectable activation anterior or dorsal to the genu of the corpus callosum. Just anterior to the anterior commissure, there was strong activation of the vertical limb of the diagonal band of Broca, with a focus in the nucleus of the diagonal band. Just posterior to the anterior commissure, there was strong activation of compartment "c" of the medial forebrain bundle (MFB), with weaker activation of the bed nucleus of the stria terminalis and the medial preoptic area. At midhypothalamic levels, the dorsolateral, dorsomedial, and ventral MFB all showed activation. There was bilateral suppression of activity in the lateral habenula. Activation appeared to end in the anterior ventral tegmental area of Tsai. Reward-blocking doses of the neuroleptic pimozide activated the caudate and the lateral habenula but did not alter any of the unilateral effects of stimulation. Using longer pulse durations and/or shifting the site of stimulation to the substantia nigra activated many of the systems not activated in the first experiment, including all of the major dopaminergic projection systems, proving the capacity of the technique to reveal activation of these systems. The results permit one to define a discrete projection system that merits electrophysiological investigation as a likely substrate for the rewarding effect of MFB stimulation. They also suggest that dopaminergic projection systems may not form part of the reward pathway itself.

Animals↗
PubMed2001

Crossed unilateral lesions of medial forebrain bundle and either inferior temporal or frontal cortex impair object recognition memory in Rhesus monkeys.

In monkeys, section of the fornix, amygdala and anterior temporal stem results in a severe anterograde amnesia. Immunolesions of the cholinergic cells of the basal forebrain suggest that this amnesia is a result of isolating the inferior temporal cortex and medial temporal lobe from their cholinergic basal forebrain afferents. In this experiment, six monkeys were trained in a delayed match-to-sample task and then received a section of the medial forebrain bundle in one hemisphere and an ablation of either the frontal or inferior temporal cortex in the opposite hemisphere. All the animals were severely impaired in the performance of this task following this surgery, and the severity of the impairment was independent of the cortical area from which the medial forebrain bundle was disconnected. These results support a model of fronto-temporal interaction via the basal forebrain in new learning, in which midbrain sites related to reward modulate the cholinergic basal forebrain activity.

Animals↗
PubMed1983

Some dorsal raphe axons of the cat bifurcate to project into bilateral medial forebrain bundles.

Seventy-one dorsal raphe (DR) neurons of the cat were antidromically activated by electrical stimulation of the medial forebrain bundle (MFB). It was found that not a small number of DR neurons send their axons contralaterally. Seven out of 67 DR neurons (10.4%) responded to stimulation of both sides of MFB. Positive collision test for the bilaterally evoked responses indicates that single axons of these DR neurons bifurcate to innervate bilateral forebrain structures.

Animals↗
PubMed2003

Temporal and sequential analysis of microglia in the substantia nigra following medial forebrain bundle axotomy in rat.

Dopaminergic neurons in the substantia nigra pars compacta undergo apoptosis after transection of the medial forebrain bundle. We have assessed the temporal and sequential activities of microglia in these events by examining the complement-3 (OX-42), major histocompatibility complex class II antigen presentation (OX-6) and phagocytic activity (ED1), and correlating these indicators with dopaminergic neuronal loss. Microglia in the ipsilateral substantia nigra pars reticulata evinced activation morphology at 12 h postaxotomy. Phagocytic microglia apposed dying dopaminergic neurons in the pars compacta starting at 3 days postlesion; their number increased through 14 days and slowly decreased. Nuclear chromatin condensation and significant loss of tyrosine hydroxylase-positive dopaminergic neurons occurred around 7 days postlesion. In contrast to microglial expression of interleukin-1beta and inducible nitric oxide synthase at the axotomy site, nigral microglia were interleukin-1beta and inducible nitric oxide synthase-negative. Consistently, RNase protection assays showed that interleukin-1beta and inducible nitric oxide synthase transcripts in nigra were equivocal. The present data support the idea that phagocytosis of axotomized neurons by activated microglia is not limited to dead neurons but includes dying neurons probably without cytotoxic effects of inflammatory substances, such as interleukin-1beta or nitric oxide.

Animals↗