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PubMed1988

Organization of cortical and subcortical projections to medial prefrontal cortex in the cat.

We have analyzed the cortical and subcortical afferent connections of the medial prefrontal cortex (MPF) in the cat with the specific aim of characterizing subregional variations of afferent connectivity. Thirteen tracer deposits were placed at restricted loci within a cortical district extending from the proreal to the subgenual gyrus. The distribution throughout the forebrain of retrogradely labeled neurons was then analyzed. Within the thalamus, retrogradely labeled neurons were most numerous in the mediodorsal nucleus and in the ventral complex. The projection from each region exhibited continuous topography such that more medial thalamic neurons were labeled by tracer from more ventral and posterior cortical deposits. Marked retrograde labeling without any sign of topographic order occurred in a narrow medioventral sector of the lateroposterior nucleus. Several additional thalamic nuclei contained small numbers of labeled neurons. In a subset of nuclei closely affiliated with the limbic system (the parataenial, paraventricular, reuniens, and basal ventromedial nuclei), retrograde labeling occurred exclusively after deposits at extremely ventral and posterior cortical sites. Within the amygdala, retrogradely labeled neurons occupied the anterior basomedial nucleus, the posterior basolateral nucleus, and a narrow strip of the lateral nucleus immediately adjoining the basolateral nucleus. The number of labeled neurons was greater after more ventral deposits. Very ventral deposits resulted in extensive labeling of the cortical amygdala. Within the cerebral cortex, the distribution of labeled neurons depended on the location of the tracer deposit. Comparatively dorsal deposits produced prominent retrograde transport to the anterior and posterior cingulate areas, to the agranular insula, and to lateral prefrontal cortex. Comparatively ventral deposits gave rise to prominent labeling of the hippocampal subiculum, various parahippocampal areas, and prepiriform cortex. On the basis of afferent connections, it is possible to divide the cat's medial prefrontal cortex into an infralimbic component, MPFil, marked by strong afferents from prepiriform cortex and the cortical amygdala, and a dorsal component, MPFd, without afferents from these structures. Further, within MPFd, it is possible to define an axis, running from ventral and posterior to dorsal and anterior levels, along which limbic afferents gradually become weaker and projections from cortical association areas gradually become stronger.

Acetylcholinesterase↗

PubMed1990

Differential effects of forced locomotion, tail-pinch, immobilization, and methyl-beta-carboline carboxylate on extracellular 3,4-dihydroxyphenylacetic acid levels in the rat striatum, nucleus accumbens, and prefrontal cortex: an in vivo voltammetric study.

In vivo voltammetry with carbon fiber electrodes was used to assess extracellular 3,4-dihydroxyphenylacetic acid (DOPAC) levels in striatum, nucleus accumbens, and anteromedial prefrontal cortex of freely moving rats subjected to altered motor activity or anxiogenic stimuli. Forced locomotion on a rotarod for 40 min caused an increase in extracellular DOPAC levels in the striatum and to a lesser extent in the nucleus accumbens but not in the prefrontal cortex. Subcutaneous injection of the anxiogenic agent methyl-beta-carboline carboxylate (10 mg/kg) increased extracellular DOPAC levels to a similar extent in prefrontal cortex and nucleus accumbens. Immobilization for 4 min augmented dopamine (DA) metabolism preferentially in the nucleus accumbens and to a lesser extent in the prefrontal cortex. Tail-pinch caused a selective activation of DA metabolism in the nucleus accumbens. None of these stimuli altered extracellular striatal DOPAC levels. These results confirm the involvement of dopaminergic systems projecting to the striatum and nucleus accumbens in motor function and suggest that mesolimbic and mesocortical dopaminergic systems can be specifically activated by certain kinds of anxiogenic stimuli; the relative activation of either of these latter systems could depend primarily on the nature (sensory modality, intensity) of the acute stressor.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1991

Prefrontal cortex alpha 2 adrenoceptors and energy balance.

The sulcal prefrontal cortex (SPC) influences thermogenesis, energy substrate utilization and feeding behaviour. The present study examined the role of SPC alpha noradrenergic receptors in these effects. Fifty nmol norepinephrine (NE) injected into the SPC produced a large and long-lasting increase in respiratory quotient (RQ), indicating enhanced carbohydrate utilization and fat synthesis. This dose also reduced energy expenditure without corresponding decreases in locomotor activity, suggesting an inhibition of thermogenesis. Neither a lower dose of NE (25 nmol) injected into the SPC, nor injections of NE (50 nmol) into a variety of sites adjacent to the SPC affected energy balance. The alpha 2 agonist clonidine (20 nmol) injected into the SPC produced similar effects to 50 nmol NE, with a large increase in RQ and a decrease in thermogenesis. Forty nmol clonidine, however, decreased RQ and reduced both energy expenditure and activity. The alpha 1 agonist L-phenylephrine (20 and 40 nmol) injected into the SPC had no clear effect on energy balance. Finally, it was shown that clonidine or NE injected into the SPC promotes food intake. These results implicate alpha 2 adrenoceptors in the sulcal prefrontal cortex in the control of food intake, thermogenesis and metabolic substrate utilization.

Animals↗

PubMed1978

Subcortical afferents to the prefrontal cortex in rabbits.

The origins of cells projecting to the prefrontal cortex of the rabbit were studied, using horseradish peroxidase (HRP) technique. HRP injected into the prefrontal cortex labeled cells in the basal forebrain, lateral hypothalamus, raphe nuclei and locus coeruleus area on both sides. Labeled cells appeared also in the nucleus medialis dorsalis of the thalamus and other thalamic nuclei on the injection side.

Afferent Pathways↗

PubMed1989

Stimulation in prefrontal cortex area inhibits cardiovascular and motor components of the defence reaction in rats.

In the present investigation it was shown that electrical or chemical (D,L-homocysteic acid, DLH) stimulation in a defined area of the medial prefrontal cortex inhibits cardiovascular components of the defence reaction elicited by stimulation in the basal nucleus of the amygdala or in the hypothalamus in rats anaesthetized by Saffan. Electrical stimulation in the dorsal part of the nucleus accumbens or ventral part of the nucleus caudate had the same effect, while chemical stimulation (DLH) in these areas was not effective. In unanaesthetized rats stimulation in the prefrontal cortex or the nucleus accumbens inhibited cardiovascular and motor components of the defence reaction induced from the amygdala or hypothalamus. Stimulation in the described areas of the medial prefrontal cortex or nucleus accumbens does not induce general inhibition of motor activity since it did not affect operant, appetitive bar pressing. It is therefore concluded that the inhibition is selectively addressed to the motor activities associated with the defence reaction. It is suggested that inhibition of the cardiovascular components of the defence reaction must occur below hypothalamic level. The inhibition is most likely presynaptic since stimulation in the prefrontal cortex or nucleus accumbens alone did not produce any cardiovascular changes. It is unlikely that the efferent pathway originating in the prefrontal inhibitory area relays in the nucleus accumbens since microinjection of DLH into this nucleus was ineffective. Stimulation in "sympatho-inhibitory' areas (anterior hypothalamus, anterior cingulum) or in the nucleus raphe obscurus had no inhibitory effect on the cardiovascular components of the defence reaction.

Animals↗

PubMed1991

Neuronal activity related to saccadic eye movements in the monkey's dorsolateral prefrontal cortex.

1. Single-neuron activity was recorded from the prefrontal cortex of monkeys performing saccadic eye movements in oculomotor delayed-response (ODR) and visually guided saccade (VGS) tasks. In the ODR task the monkey was required to maintain fixation of a central spot throughout the 0.5-s cue and 3.0-s delay before making a saccadic eye movement in the dark to one of four or eight locations where the visual cue had been presented. The same locations were used for targets in the VGS tasks; however, unlike the ODR task, saccades in the VGS tasks were visually guided. 2. Among 434 neurons recorded from prefrontal cortex within and surrounding the principal sulcus (PS), 147 changed their discharge rates in relation to saccadic eye movements in the ODR task. Their response latencies relative to saccade initiation were distributed between -192 and 460-ms, with 22% exhibiting presaccadic activity and 78% exhibiting only postsaccadic activity. Among PS neurons with presaccadic activity, 53% also had postsaccadic activity when the monkey made saccadic eye movements opposite to the directions for which the presaccadic activity was observed. 3. Almost all (97%) PS neurons with presaccadic activity were directionally selective. The best direction and tuning specificity of each neuron were estimated from parameters used to fit a Gaussian tuning curve function. The best direction for 62% of the neurons with presaccadic activity was toward the contralateral visual field, with the remaining neurons having best directions toward the ipsilateral field (23%) or along the vertical meridian (15%). 4. Most postsaccadic activity of PS neurons (92%) was also directionally selective. The best direction for 48% of these neurons was toward the contralateral visual field, with the remaining neurons having best directions toward the ipsilateral field (36%) or along the vertical meridian (16%). Eighteen percent of the neurons with postsaccadic activity showed a reciprocal response pattern: excitatory responses occurred for one set of saccade directions, whereas inhibitory responses occurred for roughly the opposite set of directions. 5. Sixty PS neurons with saccade-related activity in the ODR task were also examined in a VGS task. Forty of these neurons showed highly similar profiles of directional specificity and response magnitude in both tasks, 13 showed saccade-related activity only in the ODR task, and 7 changed their response characteristics between the ODR and VGS tasks.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1992

Electrophysiological influences of the parietal cortex and dorso-medial thalamic nucleus on the prefrontal cortex of the cat.

Lesion studies have shown that the functional integrity of prefrontal and posterior parietal cortex is necessary for complex behavioural performance. Recordings were made from 137 prefrontal cells in awake cats. Parietal cortex stimulation affected fifty-four cells (39.5%); thirty-four (63%) increased and twenty (37%) decreased their discharge frequency. Thalamic stimulation affected forty-seven cells; twenty-eight increased their discharge and nineteen decreased it. These responses suggest firstly that the organization between parietal and prefrontal cortex is similar to that in monkeys, and secondly that prefrontal cortex has an integrative role.

Animals↗

PubMed1991

Dopamine D1 autoreceptor function: possible expression in developing rat prefrontal cortex and striatum.

Synthesis-modulating dopamine (DA) autoreceptor function was studied in vivo using gamma-butyrolactone (GBL) to block propagation along DA axons. DA synthesis was measured by the accumulation of L-3,4-dihydroxyphenylalanine (L-DOPA) after inhibition of aromatic L-amino acid decarboxylase. GBL treatment markedly increased DOPA accumulation in both the striatum and prefrontal cortex of developing rats. The selective DA partial D1 agonist SKF-38393 inhibited this GBL-induced rise in DA synthesis in both the striatum and prefrontal cortex of 15- and 22-day-old rats, but not in adults. The effects of SKF-38393 in developing rats were mimicked by the non-catechol D1 partial agonist CY-208-243, and were blocked by the D1 antagonist SCH-23390, suggesting receptor mediation. The mixed D2/D3 agonist quinpirole attenuated DA synthesis in striatum of both two-week-old and adult rats, but failed to inhibit the GBL-induced increase in DA synthesis in the developing prefrontal cortex. These findings suggest that synthesis-modulating D1-like receptor function may emerge transiently in the developing mammalian forebrain. In the adult striatum these functions appear to be subsumed by D2-like receptors, whereas all synthesis-modulating DA receptor function in prefrontal cortex appears to be essentially lost with maturation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1990

Metabolic effects obtained from excitatory amino acid stimulation of the sulcal prefrontal cortex.

Indirect calorimetry was used to assess metabolic changes in rats following injections of the excitatory amino acid D,L-homocysteic acid (DLH) into the sulcal or medial prefrontal cortex. Injection of 7 nmol of DLH into the sulcal prefrontal cortex (SPC) increased respiratory quotient (RQ), indicating increased utilization of carbohydrate as an energy substrate. This treatment also decreased energy expenditure in the absence of related changes in motor activity, suggesting an inhibition of thermogenesis. A larger dose of DLH (50 nmol) injected into the SPC caused opposite effects, with a significant decrease in RQ and increased energy expenditure and motor activity. Rectal temperature was also increased by 20 or 50 nmol DLH but decreased with 7 nmol DLH. The anatomical specificity of these effects was indicated in that equivalent injections DLH into the medial prefrontal cortex did not affect energy balance. From this and related evidence it is concluded that SPC neurons exert a potent influence upon thermogenesis and metabolic substrate utilization that is bidirectional according to the magnitude of the excitatory stimulation that is applied.

Analysis of Variance↗

PubMed1992

Cocaine facilitation of prefrontal cortex self-stimulation: a microstructural and pharmacological analysis.

A novel self-stimulation methodology involving a fixed-interval (FI-5 s) schedule of reinforcement, microanalysis and threshold evaluation was used to investigate the effects of cocaine on rats lever pressing for electrical stimulation of the prefrontal cortex. Cocaine (15 mg/kg) increased medial prefrontal cortex (MPC) self-stimulation rates under FI-5 by a mean of 269% and reduced current thresholds for self-stimulation. A similar facilitation was evident with self-stimulation of the sulcal prefrontal cortex. Microanalysis showed that cocaine decreased inter-response times and post-reinforcement pauses, increased responding in the second and third quartiles of the inter-reinforcement interval (IRI) and decreased responding in the fourth IRI quartile. Schedule control of responding was still evident following cocaine despite the profound facilitation of response rates. Increased response rates were seen up to 48 h following a single dose of cocaine, suggesting sensitization of the PFC reinforcement substrate. The acute effects of cocaine on MPC self-stimulation were completely reversed by the dopamine (DA) D1 antagonist SCH 23390 0.02 mg/kg) and the D2 antagonist raclopride (0.3 mg/kg) but not by naloxone (0.5 mg/kg). These results are consistent with previous studies demonstrating the PFC as part of the neural substrate mediating cocaine reward. Further, these results implicate DA receptors in the reinforcing properties of both cocaine and MPC self-stimulation.

Animals↗

PubMed1992

Effects of acute and chronic clozapine on dopaminergic function in medial prefrontal cortex of awake, freely moving rats.

We previously showed that chronic administration of the clinically atypical and clinically superior antipsychotic drug clozapine selectively reduces dopamine (DA) release in the nucleus accumbens but not neostriatum, and that this effect appears mediated by anatomically selective mesolimbic DA depolarization blockade. The present study extends that research to another mesocorticolimbic DA locus, the medial prefrontal cortex. Acute clozapine challenge (5-40 mg/kg i.p.) produced dose-dependent increased extracellular levels of DA and its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in the medial prefrontal cortex of awake, free-moving rats as measured by in vivo brain microdialysis. Chronic clozapine treatment (20 mg/kg/day for 21 days) did not significantly change basal extracellular levels of DA, DOPAC or HVA. Acute clozapine challenge on day 22 in the chronic clozapine-treated animals produced no significant differences in medial prefrontal cortex DA, DOPAC or HVA as compared to chronic vehicle-treated animals, indicating that tolerance to clozapine does not develop in the mesocortical DA system, in contrast to the mesolimbic system. The DA agonist apomorphine (100 micrograms/kg) produced decreased basal extracellular levels of DA, DOPAC and HVA in medial prefrontal cortex of both chronic clozapine-treated and chronic vehicle-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗

PubMedDate not supplied

Adrenergic receptors in aging and Alzheimer's disease: decreased alpha 2-receptors demonstrated by [3H]p-aminoclonidine binding in prefrontal cortex.

Biochemical and pathological studies have described abnormalities in the brainstem locus coeruleus noradrenergic neurones in Alzheimer's disease (AD) and in aging. Loss of cortical noradrenergic fibers originating from the locus coeruleus may cause a decrease in presynaptic receptors or induce an increase in postsynaptic receptors, similar to "denervation supersensitivity" in animal models. Thus far it is unclear whether alpha 2-adrenergic receptors are affected in AD. In this study, we assessed the specific binding of [3H]p-aminoclonidine, an agonist at alpha 2-receptors and at imidazoline-preferring binding sites, to prefrontal cortex and other regions including hippocampus, temporal cortex, putamen and cerebellum from subjects with AD and aging controls. We particularly focused on the prefrontal cortex because of its relatively rich monoaminergic innervation and recent evidence suggesting involvement of noradrenergic mechanisms in cognition in aging nonhuman primates. The other regions, which are also innervated by noradrenergic fibers, were examined for comparison. Ligand binding to prefrontal cortex decreased with age of controls and was also significantly reduced by approximately 50% in AD subjects compared to age-matched controls. This change in AD was related to the maximum binding capacity (Bmax) rather than to an altered affinity of the ligand for the receptor. There were no significant changes in any of the other regions studied. Binding did not change with postmortem delay or with duration of tissue storage. We suggest that presynaptic alpha 2-receptors presumably labeled by [3H]p-aminoclonidine on noradrenergic synapses are those that are selectively decreased in the prefrontal cortex in AD and in aging.

Adult↗

PubMed1989

Adrenergic receptors in aging and Alzheimer's disease: increased beta 2-receptors in prefrontal cortex and hippocampus.

Loss of pigmented noradrenergic locus ceruleus neurons occurs in Alzheimer's disease (AD) and, to a lesser extent, in aging. We studied beta-adrenergic receptors and their subtypes, beta 1 and beta 2, by the specific binding of 125I-pindolol to particulate membrane preparations from prefrontal cortex, hippocampus, putamen, and cerebellum and to sections from frontal cortex by in vitro autoradiography. In prefrontal cortex from controls, numbers of total beta- and beta 2-adrenoceptors did not significantly correlate with age, but number of beta 1-adrenoceptors showed a weak but significant negative correlation. Binding in tissue particulate preparations to total beta-receptors did not reveal significant differences in samples from prefrontal cortex between AD subjects and age-matched controls. However, beta 1-adrenoceptors were decreased and beta 2-adrenoceptors were increased in number by approximately 30-50% in AD subjects. Thus, the relative ratio of beta 1-/beta 2-receptors was decreased in AD. Binding by in vitro receptor autoradiography performed in a subset of samples of frontal cortex also showed beta 2-adrenoceptors, and less consistently total beta- and beta 1-receptors, to be increased significantly in number in cortical laminae II, III, IV, and V of tissue sections from AD subjects. In these subjects, number of locus ceruleus cells and norepinephrine concentrations in putamen and frontal cortex were markedly reduced compared with values in controls. In the hippocampus, total beta- and both beta 2- and beta 1-adrenoceptors were increased in number in AD. In contrast, in the putamen, where beta 1-receptors predominate, total beta- and beta 1-receptors were significantly decreased in number with no consistent change in content of beta 2-receptors in AD. There were no significant changes in the cerebellum. Specific pindolol binding was not affected by interval between death and sampling of tissue at autopsy. Our results indicate selective changes in number of beta-receptors in AD. These changes in the cortex and hippocampus suggest receptor upregulation in response to noradrenergic deafferentation from the locus ceruleus or may simply reflect glial proliferation in AD.

Aged↗

PubMed1989

Selectivity of the hippocampal projection to the prelimbic area of the prefrontal cortex in the rat.

Afferent connections of the medial and lateral prefrontal cortex of the rat arising from the hippocampal formation were investigated using iontophoretic application of the fluorescent tracer, Fluoro-gold. Our results demonstrate that the projection which originates in the temporal part of the CA1 hippocampal field and in the prosubiculum is restricted to the prelimbic area of the prefrontal cortex.

Animals↗

PubMed1992

Neuromedin N decreases self-stimulation of the medial prefrontal cortex.

Intracerebral microinjections of neurotensin (NT) decrease intracranial self-stimulation (ICSS) of the medial prefrontal cortex (MPC) in the rat. This effect could be due to the ability of NT to bind dopamine. To test this hypothesis we studied the effects of intracerebral microinjections of neuromedin N, a natural NT analogue that does not bind dopamine, on ICSS of the rat MPC. Unilateral microinjections of neuromedin N into the MPC at doses of 2.5, 5, 10, 20 and 40 nmol produced a dose-related decrease in ICSS of the ipsilateral MPC. ICSS of the contralateral MPC, used as a control, was not affected by the microinjections. These results suggest that the inhibitory effect of NT on ICSS is independent of NT-dopamine binding. Because neuromedin N is also present in the MPC, these results also suggest a possible neuromodulatory role of this neuropeptide on ICSS of the prefrontal cortex.

Animals↗

PubMed1991

Effects of haloperidol administration on in vivo extracellular dopamine in striatum and prefrontal cortex after partial dopamine lesions.

The effects of haloperidol on striatal and prefrontal cortical extracellular fluid dopamine (DA) concentrations were examined in sham-operated control rats and in rats which had received partial lesions of their dopamine systems. In control rats haloperidol administration produced increases in extracellular fluid DA concentrations in both the striatum and prefrontal cortex. However, in rats which had been partially lesioned with intracerebroventricular 6-hydroxydopamine, haloperidol produced an increase in extracellular fluid DA concentration in the prefrontal cortex but failed to alter striatal DA release. These data suggest that nigrostriatal and mesocortical DA neurons have different response capabilities following partial DA lesions.

Animals↗

PubMed1991

Contrasting effects of stress on medial and sulcal prefrontal cortex self-stimulation.

Male Wistar rats were subjected to either 25 controllable or uncontrollable footshocks and then tested for changes in fixed-interval 5-second (FI-5) self-stimulation of the medial prefrontal cortex (MPC), sulcal prefrontal cortex (SPC) or nucleus accumbens (NAS). Controllable footshock caused a moderate facilitation of MPC self-stimulation (30% above baseline rates) but inhibited SPC self-stimulation (32% below baseline rates). Uncontrollable footshock had no effect on MPC self-stimulation but inhibited SPC self-stimulation (52% below baseline rates). An inhibition of SPC self-stimulation was also evident 24 hours following controllable or uncontrollable footshock. NAS self-stimulation was unaffected by footshock. Changes in locomotor activity were not consistently related to changes in self-stimulation following footshock. These results are discussed in terms of the different effects of mild stress on the release of reward-relevant neurotransmitters in the MPC, SPC and NAS. The possible role of stress-induced hypoalgesia in determining the stress-induced facilitation of MPC self-stimulation is also discussed.

Animals↗

PubMed1992

Determinants of the slow acquisition of medical and sulcal prefrontal cortex self-stimulation: an individual differences approach.

Stimulation-naive rats were tested for motor activity during noncontingent electrical stimulation of the medial prefrontal cortex (MPC) or sulcal prefrontal cortex (SPC). Defecation during stimulation was also measured. The rats were then tested using a conditioned taste aversion paradigm for aversion to a novel flavor (0.1% saccharin) paired with stimulation. Finally, the rats were trained to acquire self-stimulation over 26 days of training. Large individual differences were seen in motor activity, defecation, and conditioned taste aversion to initial stimulation and in the subsequent speed of self-stimulation acquisition. In the MPC-stimulated group, acquisition speed was positively correlated with motor activity to initial stimulation and negatively correlated with defecation to this stimulation. In the SPC-stimulated group, the same correlations were evident, but only when rats suffering seizures prior to self-stimulation acquisition were excluded from the analysis. Such preacquisition seizures, which were only found in the SPC-stimulated group, retarded self-stimulation acquisition. In most rats, MPC or SPC stimulation failed to condition a taste aversion to saccharin. These results suggest that the slow acquisition of MPC and SPC self-stimulation may be partly related to the motor suppressive, aversive, and convulsive properties of initial stimulation.

Animals↗