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PubMed2000

Neuronal and behavioral correlations in the medial prefrontal cortex and nucleus accumbens during cocaine self-administration by rats.

Up to 31 neurons per animal were simultaneously recorded from the medial prefrontal cortex and nucleus accumbens in 15 rats during i.v. cocaine self-administration sessions, using a multi-channel, single-unit recording technique. Alterations of neuronal activity (both excitatory and inhibitory) were found a few seconds before each lever press for cocaine infusion; we have called these pre-lever press neuronal activations "anticipatory responses". A detailed video analysis revealed that these neuronal firing alterations were associated with specific portions of the behavioral sequence performed before each lever press in both recording areas. Some of the simultaneously recorded neurons displayed similar firing patterns in relation to a given behavioral episode within the behavioral sequence (turning, raising head, etc.), while others fired at different times relative to each behavioral event. Cross-correlational analyses revealed inter-regional and intra-regional correlated firing patterns between pairs of simultaneously recorded medial prefrontal cortex and nucleus accumbens neurons. This correlated firing occurred in the neurons with and without anticipatory responses, although the incidence of correlations between anticipatory neuron pairs was much higher than that between non-anticipatory neuron pairs (18.4% vs 3.6%). Many correlated neuron pairs displayed a time lag in the peak of correlational activity that indicated a temporal sequence in correlated activity. In contradiction to our hypothesis, the temporal pattern of correlation reveals that there are more cases in which nucleus accumbens neurons fired ahead of medial prefrontal cortex neurons. The results suggest that multiple mesocorticolimbic neuronal circuits may code sequential steps during the behavioral sequence performed to obtain an infusion of cocaine. The observed correlated firing between the medial prefrontal cortex and the nucleus accumbens indicates that dynamic, coherent activity occurs within the mesocorticolimbic circuit. Because this circuit is hypothesized to drive drug-seeking behavior, we suggest that this correlated firing between the nucleus accumbens and the medial prefrontal cortex may participate in the control of cocaine self-administration. In addition, the finding that correlated activity within the nucleus accumbens more often precedes that of the medial prefrontal cortex suggests that the nucleus accumbens may play a prime role in the initiation of cocaine self-administration.

Animals↗
PubMed1995

In vivo assessment of dopamine uptake in rat medial prefrontal cortex: comparison with dorsal striatum and nucleus accumbens.

In vivo electrochemistry was used to characterize dopamine clearance in the medial prefrontal cortex and to compare it with clearance in the dorsal striatum and nucleus accumbens. When calibrated amounts of dopamine were pressure-ejected into the cortex from micropipettes adjacent to the recording electrodes, transient and reproducible dopamine signals were detected. The local application of the selective uptake inhibitors GBR-12909, desipramine, and fluoxetine before the application of dopamine indicated that at the lower recording depths examined (2.5-5.0 mm below the brain surface), locally applied dopamine was cleared from the extracellular space primarily by the dopamine transporter. The norepinephrine transporter played a greater role at the more superficial recording sites (0.5-2.25 mm below the brain surface). To compare clearance of dopamine in the medial prefrontal cortex (deeper sites only), striatum, and nucleus accumbens, varying amounts of dopamine were locally applied in all three regions of individual animals. The signals recorded from the cortex were of greater amplitude and longer time course than those recorded from the striatum or accumbens (per picomole of dopamine applied), indicating less efficient dopamine uptake in the medial prefrontal cortex. The fewer number of transporters in the medial prefrontal cortex may be responsible, in part, for this difference, although other factors may also be involved. These results are consistent with the hypothesis that regulation of dopaminergic function is unique in the medial prefrontal cortex.

Animals↗
PubMed1975

Afferents to prefrontal cortex from the thalamic mediodorsal nucleus in the rhesus monkey.

Thalamic afferents to Macaque prefrontal cortex from the mediodorsal nucleus were examined by techniques specific for anterograde degeneration and axoplasmic transport. The sampling procedure employed permits establishing the extent of topographic projections to cortex from subcortical foci for the same brain which was surveyed subsequently in tracing specific neuronal connections by electron microscopy. Topographic and general laminar distribution of thalamic terminals are presented in terms of 3 subareas of prefrontal cortex. The dorsolateral and ventral (orbital) surfaces of prefrontal cortex receive respectively projections from the lateral and medial subdivision of the mediodorsal nucleus. In addition, the medial wall of the frontal lobe, including the dorsomedial part of the lateral convexity, heretofore regarded as athalamic, receives input from the caudal-dorsomedial aspect of the mediodorsal nucleus. Preliminary evidence suggests that axons from the mediodorsal nucleus terminate in the head of caudate nucleus, as Sachs-81 described 65 years ago in the first orthograde study of thalamo-prefrontal cortex connections.

Animals↗
PubMed1997

Effects of imipramine on raphe nuclei and prefrontal cortex extracellular serotonin levels in the rat.

The effect of acute administrations of three doses of imipramine (1, 5 and 10 mg/kg s.c.), a widely used tricyclic antidepressant, on extracellular levels of serotonin (5-HT) has been studied by intracerebral microdialysis in raphe nuclei and prefrontal cortex of conscious rats. Imipramine 1 mg/kg s.c. did not change extracellular 5-HT in either raphe nuclei and prefrontal cortex. However, with the dose of 5 mg/kg s.c. imipramine induced in raphe nuclei, a brief increase of extracellular 5-HT followed by a lowering (55-65% basal release) of the neurotransmitter. The same dose of imipramine decreased (60-70% of basal value) extracellular 5-HT in prefrontal cortex. Imipramine 10 mg/kg s.c. significantly increased 5-HT levels in both raphe nuclei (190 +/- 20% above basal value) and prefrontal cortex (280 +/- 15% above basal value). Pretreatment with (-)pindolol (5 mg/kg s.c.), a non-selective 5-HT1A subtype receptor antagonist, 30 min before imipramine 5 mg/kg, modified the effect of the antidepressant: an increase, instead of a decrease, on prefrontal cortex dialysate 5-HT was observed. (-)Pindolol (10 mg/kg s.c.) increased extracellular 5-HT in both raphe nuclei (155 +/- 20% above basal value) and prefrontal cortex (160 +/- 8% above basal value). These data show that acute administration of imipramine modifies extracellular 5-HT at the level of the raphe nuclei and prefrontal cortex. 5-HT1A autoreceptors in the raphe nuclei, which this study suggests to be tonically active, may be stimulated after systemic administration of high doses of imipramine.

Adrenergic beta-Antagonists↗
PubMed2002

The mid-ventrolateral prefrontal cortex and active mnemonic retrieval.

The role of the mid-ventrolateral prefrontal cortex in memory retrieval is examined and compared with the role of the mid-dorsolateral prefrontal cortex in the monitoring of information in memory. It has been argued that the mid-ventrolateral prefrontal cortex (areas 47/12 and 45) is involved in the active retrieval of information from posterior cortical association areas. Active retrieval is required when stimuli in memory do not bear stable relations to each other and therefore retrieval cannot be automatically driven by strong, stable, and unambiguous stimulus or context relations. Data from functional activation studies with normal human subjects are presented that have demonstrated specific changes in activity within the mid-ventrolateral region of the frontal cortex in relation to the active retrieval of information from memory. By contrast, increases in activity in the mid-dorsolateral region of the frontal cortex occur when the performance of the tasks requires monitoring of information in memory.

Humans↗
PubMed1981

Subcortical connections of the prefrontal cortex in dogs: afferents to the medial cortex.

Afferent subcortical connections to the medial prefrontal cortex (PFC) in the dog were investigated using the horseradish peroxidase retrograde transport method. The dorsal and ventral regions of the medial PFC receive different projections both from the mediodorsal and the ventral thalamic nuclei. The dorsomedial PFC receives projection from a dorsolateral region of the "parvocellular" MD subdivision, while the ventromedial PFC - from the medial, "magnocellular" MD subdivision. The area precruciata medialis (XM) is involved in significant MD projection and should be included in the "prefrontal" not the "premotor" cortex. The ventral thalamic nuclei project mainly to the dorsomedial but not the ventromedial cortex. The distribution of this projection was correlated with antero-posterior cortical localization of injections. The main criterion for distinguishing "prefrontal" and "motor" cortex remains its projections either from MD or from VL nuclei. Only the ventromedial prefrontal cortex receives projection from anterior thalamic nuclei. The caudal region of the ventromedial prefrontal cortex seems to receive richer projection from "non-specific" thalamic nuclei as well as from the amygdaloid complex.

Afferent Pathways↗
PubMed1992

The anatomy of dopamine in monkey and human prefrontal cortex.

This chapter reviews recent evidence establishing the comparable organization of dopamine afferents and dopaminergic receptors in the human and monkey prefrontal cortex. Light microscopy using a dopamine-specific antibody reveals that the dopamine innervation in the human prefrontal cortex exhibits a distinct bilaminar distribution with dense bands of fibers in the upper and deeper strata of the cortex, closely resembling the patterning of dopamine fibers in the monkey prefrontal cortex. Also, EM-immunohistochemistry has now revealed identical synaptic complexes both in human and monkey. In both species, dopamine axons from symmetric synapses predominantly on the spines of pyramidal cells. In many cases, the same spine is apposed by an asymmetric, putatively excitatory synapse. Finally, both in human and monkey prefrontal cortex, the dopamine D1-specific ligand, 3H-SCH23390, and the D2-specific ligand, H3-raclopride, label binding sites in laminar positions which match the location of the densest dopamine innervation. These results indicate that the organization of the cortical dopamine system is essentially the same in macaque monkey and human and that the nonhuman primate is a suitable animal model for analysis of dopamine function in prefrontal cortex.

Afferent Pathways↗
PubMed2000

Collateral projection from the amygdalo--hippocampal transition area and CA1 to the hypothalamus and medial prefrontal cortex in the rat.

Amygdaloid and hippocampal neurons projecting to both the medial prefrontal cortex and hypothalamus by way of axon collaterals were examined in the rat by double labeling method using fluorescence retrograde tracers. Fluoro-gold was injected in the medial prefrontal cortex, while Fluoro-red was injected into the ventromedial and ventral premammillary nuclei of the hypothalamus. The results indicated that neurons which sent axon collaterals to both the medial prefrontal cortex and hypothalamus constituted 50 or 30% of populations of medial prefrontal cortex-projecting neurons in the amygdalo-hippocampal transition area or in CA1, respectively. Possible roles of the neurons with axon collaterals in sexually related aggressive and/or defensive behavior were discussed.

Amygdala↗
PubMed2001

The role of the dorsolateral prefrontal cortex during sequence learning is specific for spatial information.

Many studies have implicated the dorsolateral prefrontal cortex in the acquisition of skill, including procedural sequence learning. However, the specific role it performs in sequence learning has remained uncertain. This type of skill has been intensively studied using the serial reaction time task. We used three versions of this task: a standard task where the position of the stimulus cued the response; a non-standard task where the color of the stimulus was related to the correct response; and a combined task where both the color and position simultaneously cued the response. We refer to each of these tasks based upon the cues available for guiding learning as position, color and combined tasks. The combined task usually shows an enhancement of skill acquisition, a result of being driven by two simultaneous and congruent cues. Prior to the performance of each of these tasks the function of the dorsolateral prefrontal cortex was disrupted using repetitive transcranial magnetic stimulation. This completely prevented learning within the position task, while sequence learning occurred to a similar extent in both the color and combined tasks. So, following prefrontal stimulation the expected learning enhancement in the combined task was lost, consistent with only a color cue being available to guide sequence learning in the combined task. Neither of these effects was observed following stimulation at the parietal cortex. Hence the critical role played by the dorsolateral prefrontal cortex in sequence learning is related exclusively to spatial cues. We suggest that the dorsolateral prefrontal cortex operates over the short term to retain and manipulate spatial information to allow cortical and subcortical structures to learn a predictable sequence of actions. Such functions may emerge from the broader role the dorsolateral prefrontal cortex has in spatial working memory. These results argue against the dorsolateral prefrontal cortex constituting part of the neuronal substrate responsible for general aspects of implicit or explicit sequence learning.

Adult↗
PubMed2002

NMDA and AMPA/kainate glutamatergic agonists increase the extracellular concentrations of GABA in the prefrontal cortex of the freely moving rat: modulation by endogenous dopamine.

Using microdialysis in the prefrontal cortex, this study investigated first the effects of the ionotropic glutamatergic agonists NMDA and AMPA on extracellular concentrations of GABA, and second, the modulation of these effects by increasing endogenous dopamine. NMDA (20, 100, and 500 microM) and AMPA (1, 20, and 100 microM), perfused through the microdialysis probe for 60 min, produced a dose-related increase of extracellular concentrations of GABA in the prefrontal cortex of the awake rat. NMDA 100 and 500 microM produced a maximal increase of extracellular GABA of 150 +/- 38% and 245 +/- 75% of baseline, respectively. AMPA 20 and 100 microM produced a maximal increase of extracellular GABA of 140 +/- 17% and 195 +/- 41% of baseline, respectively. NMDA and AMPA also increased extracellular concentrations of glutamate. Increases of extracellular GABA, and also of glutamate, produced by NMDA (500 microM) and AMPA (100 microM) were significantly blocked by the NMDA antagonist CPP (100 microM) and the AMPA/kainate antagonist DNQX (100 microM), respectively. To investigate whether dopamine modulates the increases of GABA produced by NMDA and AMPA, endogenous dopamine was increased with the dopamine uptake inhibitor nomifensine. Nomifensine (1, 100, and 1000 microM) produced a dose-related increase of dialysate dopamine (from 0.1 to 1.0 nM) but did not modify basal extracellular concentrations of GABA in the prefrontal cortex. However, increases of endogenous dopamine at 0.5-0.7 nM did potentiate the increases of extracellular GABA produced by AMPA (20 microM) (from 140% to 240% of baseline), but not by NMDA (100 microM), in this area of the brain. These effects were attenuated by the perfusion of (-)sulpiride (D2 antagonist), but not by the perfusion of SCH-23390 (D1 antagonist). These results suggest that glutamate, through the activation of both NMDA and AMPA/kainate ionotropic receptors, facilitates GABAergic transmission in the prefrontal cortex, and that dopamine can modulate the effects of glutamate through AMPA/kainate receptors on GABA transmission in this area of the brain.

Animals↗
PubMed2004

Prefrontal cortex serotonin, stress, and morphine-induced nucleus accumbens dopamine.

Uncontrollable, but not controllable, stress produces a persistent potentiation of morphine-induced nucleus accumbens dopamine (DA) efflux and morphine-induced medial prefrontal cortex serotonin (5-HT) efflux. Here we investigate medial prefrontal cortex 5-HT mediation of this potentiation. Male Sprague-Dawley rats received bilateral medial prefrontal cortex microinjections of the neurotoxin 5,7-dihydroxytriptamine (5,7-DHT, 8 microg/microl/side), which selectively depleted medial prefrontal cortex 5-HT, or vehicle (Sham), and cannula implantation in the nucleus accumbens shell. After 2 weeks, rats received either uncontrollable stress or no stress. Microdialysis and morphine (3 mg/kg) treatment were performed the following day. Morphine produced an enhanced increase in DA in the Stress-Sham group that was completely blocked by 5,7-DHT lesions, suggesting that 5-HT in the medial prefrontal cortex mediates this potentiation.

5,7-Dihydroxytryptamine↗
PubMed2004

Aripiprazole, a novel antipsychotic drug, preferentially increases dopamine release in the prefrontal cortex and hippocampus in rat brain.

Aripiprazole,7-(4-[4-(2,3-dichlorophenyl)-1-piperazinyl]butyloxy)-3,4-dihydro-carbostycil (OPC-14597), a novel atypical antipsychotic drug, is a dopamine D2 receptor partial agonist with functional 5-HT2A receptor antagonist, and 5-HT1A receptor partial agonist properties as well. Other atypical antipsychotic drugs, e.g. clozapine, but not typical antipsychotic drugs, e.g. haloperidol, produce significant increases in dopamine and acetylcholine release in the medial prefrontal cortex in rats, effects believed to be related to the ability to improve cognitive function. The increase in the medial prefrontal cortex dopamine release by the atypical antipsychotic drugs has been shown to be partially inhibited by N-[2[4-)2-methoxyl)-1-piperazinyl]ethyl]-N-(2-pyridinyl)cyclohexanecarboxamide trihydrochloride (WAY100635), a selective 5-HT1A receptor antagonist. Aripiprazole, 0.1 and 0.3 mg/kg, significantly increased dopamine release in the hippocampus. Moreover, aripiprazole, 0.3 mg/kg, slightly but significantly increased dopamine release in the medial prefrontal cortex but not in the nucleus accumbens. These increases were significantly inhibited by WAY100635. By contrast, aripiprazole, 3.0 mg/kg and 10 mg/kg, significantly decreased dopamine release in the nucleus accumbens but not the medical prefrontal cortex. However, aripiprazole 10 mg/kg significantly decreased dopamine release in the both regions. Aripiprazole had no effect on acetylcholine release in the medial prefrontal cortex, hippocampus, or nucleus accumbens at any dose, except for 3.0 mg/kg, which decreased acetylcholine release in the nucleus accumbens only. Aripiprazole, 0.3 mg/kg, transiently potentiated haloperidol (0.1 mg/kg)-induced dopamine release in the medial prefrontal cortex but inhibited that in the nucleus accumbens. The present study demonstrated that aripiprazole, at low doses of 0.1 and 0.3 mg/kg, increases dopamine release in the medial prefrontal cortex and hippocampus. It also suggests that the function of both the medial prefrontal cortex and hippocampus may contribute to the ability of aripiprazole to improve negative symptom and cognition.

Acetylcholine↗
PubMed1999

Prefrontal cortex regulates inhibition and excitation in distributed neural networks.

Prefrontal cortex provides both inhibitory and excitatory input to distributed neural circuits required to support performance in diverse tasks. Neurological patients with prefrontal damage are impaired in their ability to inhibit task-irrelevant information during behavioral tasks requiring performance over a delay. The observed enhancements of primary auditory and somatosensory cortical responses to task-irrelevant distractors suggest that prefrontal damage disrupts inhibitory modulation of inputs to primary sensory cortex, perhaps through abnormalities in a prefrontal-thalamic sensory gating system. Failure to suppress irrelevant sensory information results in increased neural noise, contributing to the deficits in decision making routinely observed in these patients. In addition to a critical role in inhibitory control of sensory flow to primary cortical regions, and tertiary prefrontal cortex also exerts excitatory input to activity in multiple sub-regions of secondary association cortex. Unilateral prefrontal damage results in multi-modal decreases in neural activity in posterior association cortex in the hemisphere ipsilateral to damage. This excitatory modulation is necessary to sustain neural activity during working memory. Thus, prefrontal cortex is able to sculpt behavior through parallel inhibitory and excitatory regulation of neural activity in distributed neural networks.

Animals↗
PubMed1985

Cytoarchitectonic development of the prefrontal cortex in the rat.

This paper gives an account of the cytoarchitectonic characteristics that make it possible to delineate, from as early as day 6, different subareas of the prefrontal cortex of the rat. Three phases can be distinguished during postnatal development. The first phase (from day 1 until day 18) is dominated by differentiation of the neurons within the cortical plate and by the formation of the cortical layers. At day 1, regional differences are observed in the cytoarchitecture of the cortical plate which correspond to the future subareas of the prefrontal cortex. The formation of layer IV occurs in the dorsolateral cortex around day 6, and from this age the agranular prefrontal cortex is well demarcated from the other parts of the frontal cortex. Between day 6 and day 10, the cortical plate has disappeared and all cortical layers can be recognized in the prefrontal cortex. Differentiation of the cells within the cortical layers changes the cytoarchitectonic character of the layers through day 18. During the second phase (from day 18 until day 30) little change occurs in the cytoarchitectonic characteristics of the prefrontal subareas. During the third phase (from day 30 until day 90) the delineation of the cortical layers becomes less clear in Nissl-stained sections, and the individual cytoarchitectonic variance increases. On the basis of cytoarchitectonic criteria it can be concluded that the orbital prefrontal cortex develops earlier than does the medial prefrontal cortex.

Aging↗
PubMed1993

Maturation of the dopamine innervation during postnatal development of the prefrontal cortex in gerbils (Meriones unguiculatus). A quantitative immunocytochemical study.

Dopamine (DA)-immunoreactivity was investigated in the prefrontal cortex of gerbils (Meriones unguiculatus). For that purpose, a sensitive and selective antibody against glutaraldehyde-conjugated dopamine was applied. All detectable fragments of dopamine-immunoreactive nerve fibres were identified in selected consecutive frontal sections and their total length was determined in both the medial and orbital prefrontal cortex on postnatal days 7, 14, 23, 30, 60, and 90. Dopamine immunoreactivity revealed exponential growth until postnatal day 30, and further increased until postnatal day 90 with reduced increments. Due to higher initial percentage growth rates the dopamine innervation in the orbital prefrontal cortex achieved maturity earlier than in the medial prefrontal areas. Quantitative maturation of the prefrontal DA innervation is discussed with current data on functional and structural development of the prefrontal cortex.

Aging↗
PubMed1998

An ultrastructural study of the neural circuit between the prefrontal cortex and the mediodorsal nucleus of the thalamus.

Synaptic connectivity between the prefrontal cortex (PFC) and the mediodorsal thalamic nucleus (MD) of the rat has been investigated with the electron microscope after labeling both the pre- and postsynaptic elements. Prefrontal corticothalamic fibers end exclusively as small axon terminals with round synaptic vesicles (SR boutons), which make asymmetrical synaptic contacts with distal dendritic segments of MD neurons. Thalamocortical terminals from MD in PFC are also of the SR type and form asymmetrical synaptic contacts predominantly with dendritic spines arising from the apical or basal dendrites of pyramidal cells whose somata reside in layers III, V and VI. At least some pyramidal cells in layer III that receive MD afferents are callosal cells, whereas deep layer pyramidal cells projecting to MD receive directly some of the thalamocortical terminations from MD, suggesting that the recurrent loop to MD is monosynaptically mediated. Thus, taken together with recent evidence that both the PFC-MD and MD-PFC pathways are glutamatergic and excitatory, the cortical excitation exerted by afferent fibers from MD is transferred, not only back to MD itself through deep pyramidal cells, but also the contralateral prefrontal cortex via pyramidal cells in layer III of the ipsilateral prefrontal cortex. Concerning modulatory and inhibitory inputs, fibers to MD from the ventral pallidum and substantia nigra pars reticulata have been shown to be inhibitory and GABAergic. In addition, fibers from the ventral tegmental area preferentially make symmetrical membrane thickenings (i.e. inhibitory synapses) on deep pyramidal cells in PFC that receive synaptic endings from MD. From these morphological grounds, therefore, cells in the ventral pallidum, the substantia nigra pars reticulata and the ventral tegmental area may mediate, to some extent, an inhibitory effect on the reverberatory excitation between PFC and MD.

Animals↗
PubMed2001

Place and response learning of rats in a Morris water maze: differential effects of fimbria fornix and medial prefrontal cortex lesions.

The question examined in this study is concerned with a possible functional dissociation between the hippocampal formation and the prefrontal cortex in spatial navigation. Wistar rats with hippocampal damage (inflicted by a bilateral lesion of the fimbria fornix), rats with damage to the medial prefrontal cortex, and control-operated rats were examined for their performance in either one of two different spatial tasks in a Morris water maze, a place learning task (requiring a locale system), or a response learning task (requiring a taxon system). Performance of the classical place learning (allocentric) task was found to be impaired in rats with lesions of the fimbria fornix, but not in rats with damage of the medial prefrontal cortex, while the opposite effect was found in the response learning (egocentric) task. These findings are indicative of a double functional dissociation of these two brain regions with respect to the two different forms of spatial navigation. When the place learning task was modified by relocating the platform, the impairment in animals with fimbria fornix lesions was even more pronounced than before, while the performance of animals with medial prefrontal cortex lesions was similar to that of their controls. When the task was again modified by changing the hidden platform for a clearly visible one (visual cue task), the animals with fimbria fornix lesions had, at least initially, shorter latencies than their controls. By contrast, in the animals with medial prefrontal cortex damage this change led to a slight increase in escape latency.

Animals↗
PubMed1998

Convergent prefrontal cortex and mamillary body projections to the medial pontine nuclei: a light and electron microscopic study in the rat.

To study the convergence of medial prefrontal cortex and mamillary body projections to the medial pontine nuclei, light and electron microscopic, neuroanatomical, tract-tracing experiments were performed. Injections of horseradish peroxidase conjugated to wheat germ agglutinin (WGA-HRP), biotin conjugated to dextran (BD), or rhodamine conjugated to dextran (RD) were made individually or in combinations into the cerebral cortex, hypothalamus, or pons. In addition, injections of WGA-HRP into the medial prefrontal cortex and electrolytic lesions of the mamillary body were made to study the synaptology of afferent projections to the pontine nuclei. In the light microscopic studies, injections of WGA-HRP into the rostromedial pontine nuclei produced dense, retrograde labeling both in the dorsal peduncular area of the medial prefrontal cortex and in the medial mamillary nucleus, pars medialis. Injections of the anterograde tracers BD and RD into the medial prefrontal cortex and the medial mamillary nuclei, respectively, resulted in partially overlapping terminal fields in the rostromedial pontine nuclei. In the electron microscopic studies, injections of WGA-HRP into the dorsal peduncular area and electrolytic lesions of the mamillary body produced anterogradely labeled axon terminals and degenerating axon terminals that synapsed on the same dendrites or neuronal somata in the rostromedial pontine nuclei. The results demonstrate that the medial prefrontal cortex and the medial mamillary nuclei have partially overlapping projections to the rostromedial pontine nuclei and implicate precerebellar relay nuclei in the integration of limbic and/or autonomic functions mediated by convergent projections from the cerebral cortex and the hypothalamus.

Animals↗