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PubMed2000

Regulation of rat cortex function by D1 dopamine receptors in the striatum.

Interactions between the basal ganglia and the cerebral cortex are critical for normal goal-directed behavior. In the present study, we used immediate-early genes (c-fos, zif 268) as functional markers to investigated how basal ganglia output altered by stimulation/blockade of D1 dopamine receptors in the striatum affects cortical function. Systemic administration of the mixed D1/D2 receptor agonist apomorphine (3 mg/kg) increased immediate-early gene expression in the striatum and throughout most of the cortex. Unilateral intrastriatal infusion of the selective D1 receptor antagonist SCH-23390 (0.5-10 microg) blocked this response bilaterally in striatum and cortex in a dose-dependent manner. Even apparently regionally restricted blockade of striatal D1 receptors attenuated gene expression throughout striatum and cortex in both hemispheres. Intrastriatal administration of the D1 antagonist inhibited apomorphine-induced sniffing/whisking, whereas other motor behaviors were unaffected. To determine whether such changes in cortical gene expression could reflect altered cortical function, we examined the effects of blocking striatal D1 receptors on whisker stimulation-evoked immediate-early gene expression in the sensorimotor cortex. Apomorphine increased sensory stimulation-evoked gene expression in the barrel cortex, and intrastriatal infusion of SCH-23390 attenuated this effect. These results suggest that stimulation of D1 dopamine receptors in the striatum exerts a widespread facilitatory effect on cortical function.

Animals↗
PubMed2006

Nicotinamide treatment reduces behavioral impairments and provides cortical protection after fluid percussion injury in the rat.

This study examined the ability of nicotinamide (vitamin B3) to improve functional outcome in a dose-dependent manner following fluid percussion injury (FPI). Injured (duration of unconsciousness mean = 85.8 sec; apnea = 9.9 sec), rats were administered nicotinamide (500 or 50 mg/kg; ip) or saline at 15 min and 24 h. Serum analysis of nicotinamide concentrations were conducted 1 h following the last injection. Sensorimotor and cognitive tests were conducted for 35 days following FPI. Both the 500 and 50 mg/kg doses of nicotinamide significantly facilitated recovery on the vibrissae-forelimb placing test compared to saline treatment, which showed chronic impairments. Both treatments also significantly improved performance on the bilateral tactile adhesive removal test. On the cognitive tests, the 500 mg/kg dose, but not the 50 mg/kg dose, improved performance on a working memory task in the Morris water maze (MWM). However, acquisition of a reference memory task in the MWM was not improved. Serum analysis showed that the 500 mg/kg dose significantly raised nicotinamide concentrations by 30-fold and the 50 mg/kg dose by 3-fold compared to the saline administration. This study demonstrated that raising nicotinamide concentrations resulted in the reduction of the behavioral impairments following FPI. In fact, the 500 mg/kg dose prevented the occurrence of the behavioral deficits on the bilateral tactile removal and working memory tests. Both doses significantly reduced tissue loss and glial fibrillary acid protein (GFAP) expression in the cortex. The 500 mg/kg dose reduced GFAP expression in the hippocampus. This data suggests that nicotinamide has substantial preclinical efficacy for TBI, and there appears to be some differences in the ability of the doses to improve performance in the MWM.

Animals↗
PubMed1987

Somatosensorimotor function of the superior colliculus, somatosensory cortex, and lateral hypothalamus in the rat.

The role of the superior colliculus in multimodal sensory function is unsettled, in large part because a clear distinction between the somatosensory effects and the postural/motor effects of damage to the deep layers of the superior colliculus has not been obtained. Unilateral lesions of the entire superior colliculus impair orienting of the head and eyes to tactile, visual, and auditory stimuli presented on the side of the body contralateral to the lesion; however, even in the absence of sensory stimulation animals with such a lesion tend to circle ipsiversively and fail to make contralateral head movements. To determine whether or not unilateral damage to the superior colliculus produces a somatosensory asymmetry independently of head movement/circling biases, a neurological test was used in which lateral head or trunk movements were not required. Small pieces of adhesive-backed paper were attached to each forelimb and the latencies to contact and remove the stimuli were recorded. A battery of standard neurological tests was administered as well. The entire superior colliculus was removed unilaterally, and for comparison, the sensorimotor cortex or lateral hypothalamus were damaged in additional groups. Lesions of the superior colliculus produced the expected deficit in contralateral orienting and ipsilateral circling/postural biases, but failed to produce a somatosensory asymmetry in the head movement-independent sensorimotor test. In contrast, both sensorimotor cortex and lateral hypothalamus lesions produced a severe asymmetry in the head-movement-independent sensorimotor test. We conclude that the superior colliculus is involved in the control of lateral head movements and that its role in somatosensory function is fundamentally different from that of the sensorimotor cortex or lateral hypothalamus regions.

Animals↗
PubMed2004

Acute effect of an extract of Ambrosia paniculata (Willd.) O. E. Schultz (mugwort) in several models of experimental epilepsy.

The acute effect of Ambrosia paniculata was studied in several animal models of epilepsy. Intraperitoneal injections (0.01 mL/g body wt) of a decoction of the dry leaves significantly enhanced the latency to the first convulsion and survival time in mice injected with picrotoxin (7 mg/kg) or isoniazid (210 mg/kg). Epileptic spikes were induced by topical application of penicillin through a glass electrode filled with a penicillin-agar-saline mixture and recorded in sensorimotor and occipital cortices, in rats immobilized with d-tubocurarine. The plant decoction reduced significantly the spike amplitude in both sites. The mentioned effects were elicited at doses that also reduced general motor activity (Irwin test) and exploratory behavior. The decoctions were not effective against electroshock-induced convulsions in mice. The convulsions induced by isoniazid, picrotoxin, and penicillin differed from those induced by electroshock implicating selective disruption of GABAergic neurotransmission. The results suggest that A. paniculata, like several conventional antiepileptic drugs, might act by enhancing GABAergic neurotransmission, a hypothesis that requires further demonstration. These results explain and justify the traditional use of the plant in epilepsy.

Ambrosia↗
PubMed2003

Prepulse inhibition deficits of the startle reflex in neonatal ventral hippocampal-lesioned rats: reversal by glycine and a glycine transporter inhibitor.

BACKGROUND: Neonatal ventral hippocampal (NVH) lesions in rats induce behavioral abnormalities at adulthood thought to simulate some aspects of the positive, negative, and cognitive deficits classically observed in schizophrenic patients. Such lesions induce a postpubertal emergence of prepulse inhibition (PPI) deficits of the startle reflex reminiscent of the sensorimotor gating deficits observed in a majority of schizophrenic patients. To study the potential involvement of the glycinergic neurotransmission in such deficits, we investigated the capacity of glycine (an obligatory N-methyl-D-aspartate [NMDA] receptor co-agonist) and ORG 24598 (a selective glycine transporter 1 inhibitor) to reverse NVH lesion-induced PPI deficits in rats. METHODS: Ibotenic acid was injected bilaterally into the ventral hippocampus of 7-day-old pups. Prepulse inhibition of the startle reflex was measured at adulthood. RESULTS: Glycine (.8 and 1.6 g/kg IP) and ORG 24598 (10 mg/kg IP) fully and partially reversed lesion-induced PPI deficits, respectively. CONCLUSIONS: These findings confirm that an impaired glutamatergic neurotransmission may be responsible for PPI deficits exhibited by NVH-lesioned rats and support the hypoglutamatergic hypothesis of schizophrenia. They also suggest that drugs acting either directly at the NMDA receptor glycine site or indirectly on the glycine transporter 1 could offer promising targets for the development of novel therapies for schizophrenia.

Amino Acid Transport Systems, Neutral↗
PubMed1997

Testing hypotheses of spatial learning: the role of NMDA receptors and NMDA-mediated long-term potentiation.

The role of NMDA receptors and NMDA-mediated hippocampal long-term potentiation (LTP) in spatial learning was studied in rats using the competitive, systemically administered NMDA receptor antagonists CGS19755 ((+/-)-cis-4-phosphonomethyl-2-piperidine carboxylic acid) and NPC17742 (2R,4R,5S-2-amino-4,5-(1,2-cyclohexyl)-7-phosphonoheptanoic acid). CGS19755 caused sensorimotor disturbances and disrupted acquisition of the water maze in naive rats. The sensorimotor disturbances were greatly reduced and maze learning was normal in spite of the blockade of dentate gyrus LTP by CGS19755 in rats that had first been familiarized with the general task requirements by non-spatial pretraining. In a second experiment, antagonism of NMDA receptors caused small, but reliable, impairments in Y-maze and visible platform visual discrimination tasks. The results indicate that NMDA receptors are not crucial for water maze acquisition using a spatial learning strategy, and that NMDA antagonists cause visual and other sensorimotor disturbances in naive rats that could help account for their poor performance in this task.

Amino Acids↗
PubMed1990

Motivational-sensorimotor interaction controls aphagia and exaggerated treading after striatopallidal lesions.

This study examined the relationship between sensorimotor and motivational functions of the corpus striatum. In rats, excitotoxic lesions of the corpus striatum (neostriatum and globus pallidus) caused by kainic or quisqualic acid can produce both aversive aphagia and a "choreic" sensorimotor syndrome: an exaggerated treading of the forepaws that is triggered by oral sensory stimulation. Experiment 1 used a recovery-of-function approach to show that (a) aphagia induced by ventroposterior striatopallidal lesions was accompanied by an enhancement of aversion (a specific motivational process) to sweet stimuli, which was expressed in taste reactivity measures of affective evaluation; (b) aphagia and enhanced aversion recovered together; and (c) exaggerated treading did not disappear with aphagia-aversion but narrowed the range of its eliciting trigger to sour and bitter stimuli. Experiment 2 used a partial lesion approach to show that this dissociation of enhanced aversion and exaggerated treading could be reproduced by smaller lesions immediately after striatopallidal damage. Experiment 3 used a conditioned aversion procedure to show that the stimulus for exaggerated treading was aversion (natural or conditioned) and not a simple sensory feature of oral stimulation. Three conclusions were made: (a) Exaggerated treading after a small lesion or after partial recovery from a larger one results from a restructuring of a sensorimotor relations that is nested within a system of aversive reaction, (b) exaggerated treading is elicited only by tastes that elicit natural or conditioned aversion, and (c) more extensive lesions potentiate aversion to tastes that are normally palatable and expand the range of treading elicitors to include those tastes. In other words, affective and sensorimotor systems interact in a hierarchial manner in the production of choreic treading. These results demonstrate a specific hierarchical link between motivational and sensorimotor functions mediated by striatopallidal circuits.

Affect↗
PubMedDate not supplied

[The dopaminergic system and addictions].

AIM: All psychoactive substances with a high abuse potential are characterized by altering the mesocorticolimbic dopaminergic neurotransmission system. In this article it is proposed to review the neurobiological mechanisms that comprise the foundation of the development of addiction. DEVELOPMENT: The acute drug intake provokes an increase in extracellular dopamine which, in vulnerable individuals, could be the start of the addictive process. Chronic drug use is accompanied by a reduction in the dopaminergic function with the development of neuroadaptive changes in the mesolimbic and mesocortical pathways. In the prefrontal cortex, the changes in dopaminergic function produce an inbalance between receptors D1 and D2, which leads to a predominance of inhibitatory function. Dopaminergic innervation in the amygdala and its interaction with the nucleus accumbens plays an essential role in the conditioning of environmental stimuli, and can trigger the craving and relapse. In drug dependent patients, dopaminergic changes extend from the limbic regions to the associative and sensorimotor striatum, and affect the cortico-striatico-cortical circuits. CONCLUSION: The involvement of the dopaminergic systems is crucial in the development of addiction, from the early phases in which drug use begins as an object-directed instrumental behavior, to the consolidation of the addiction as a compulsive habit, controlled by stimulus-response mechanisms, which progressively invade all aspects of the life of an individual.

Dopamine↗
PubMedDate not supplied

[Effect of damage to the parietal associative cortex on the function of acquired motor coordination in dogs].

The effect of ablation of the parietal associative cortex on the performance of a complex food instrumental reaction was studied in dogs. The reaction consisted in two movements of the forelimb which were of similar pattern, but differed by their coordination. The first one was the lifting and holding of the paw at a required level for a required time, with the head in natural position (lifted), and the second one was the same movement of the paw with the head bent down for feeding, i.e. a new coordination, for the natural coordination consists in lowering of the forelimb associated with lowering of the head. During two sessions after the lesion, both reactions became irregular (so that the dogs performed only one of two movements or none). In the course of four months, the precision of the first movement was reduced, the amplitude of lifting the paw and duration of holding it were diminished. The new coordination persisted after ablation of the parietal associative cortex, though the holding (fixation) of the paw was less perfect. As was shown before by one of the present authors (M. E. Ioffe), lesion of the sensorimotor cortex resulted in profound disturbance of acquired coordination.

Animals↗
PubMed2005

The effect of low estrogen state on serotonin transporter function in mouse hippocampus: a behavioral and electrochemical study.

Defects in serotonergic transmission, including serotonin transporter (SERT) function, have been implicated in depression, anxiety disorders and some aspects of schizophrenia. The sex steroid hormone estrogen is known to modulate functional SERT activity, but whether it is up- or down-regulated is unclear. The aim of the present study was to examine the effect of a low estrogen state in mice on the behavioral effect of drugs acting through the SERT, serotonin uptake kinetics and SERT density in the hippocampus. We compared control mice, ovariectomized (OVX) C57BL/6J mice and aromatase knockout (ArKO) mice that are unable to produce estrogen. Fluoxetine treatment, but not fenfluramine treatment, significantly increased prepulse inhibition (PPI), a measure of sensorimotor gating, in C57BL/6J mice. The effect of fluoxetine was greater in OVX compared to sham-operated mice. In ArKO and J129 wild-type mice, fluoxetine increased PPI to the same extent while fenfluramine increased PPI more in ArKO mice compared to controls. Measurement of the time-course for diffusion and reuptake of exogenous serotonin in the CA3 region of the hippocampus showed that, in OVX mice, the fluoxetine-induced slowing of signal decay after application of serotonin was enhanced when compared to sham-operated controls. Similarly, in ArKO mice, the effect of fluoxetine was enhanced, suggesting that SERT function was greater than in J129 wild-type controls. Measurement of SERT density by [3H]-citalopram autoradiography, revealed an 18% decrease in hippocampus of OVX mice compared to intact controls. SERT density was also significantly reduced in nucleus accumbens (26%) but not in other regions, such as the raphe nuclei. Together, these results suggest that a low estrogen state increases SERT activity in the hippocampus despite an apparent reduction in SERT density. The behavioral consequences of these changes depend on the model of estrogen state used.

Analysis of Variance↗
PubMed1997

Characterization of the disruptions of prepulse inhibition and habituation of startle induced by alpha-ethyltryptamine.

Alpha-ethyltryptamine (AET), a monoamine oxidase inhibitor and potent monoamine releasing agent, has been sold illicitly as a substitute for the entactogen 3,4-methylenedioxy-N-methylamphetamine (MDMA), and is the first example of an indolealkylamine analog demonstrated to substitute in MDMA-trained animals. Previous studies have demonstrated that MDMA and AET have similar effects on unconditioned motor behavior in rats. Furthermore, the locomotor-activating effects of both MDMA and AET are blocked by pretreatment with fluoxetine, a selective serotonin (5-HT) uptake inhibitor, suggesting that the two compounds may share a presynaptic mechanism of action. This study examined the effects of AET using measures of startle plasticity, specifically prepulse inhibition (PPI), and habituation. PPI, a measure of sensorimotor gating, is reduced in rats treated with hallucinogens, 5-HT releasers, and dopamine agonists. In contrast, startle habituation is reduced in rats treated with hallucinogens and 5-HT releasers. AET (1.25, 2.5, 5, and 10 mg/kg) decreased PPI of acoustic startle and reduced the habituation of tactile startle. To determine whether AET produces these effects via pre- or postsynaptic actions, fluoxetine (10 mg/kg) was used as a pretreatment. By itself, fluoxetine did not disrupt PPI, but did reduce startle habituation. Fluoxetine pretreatment prevented the AET-induced disruption of PPI and reduced the AET-induced disruption of startle habituation. Combined with previous findings, these results confirm that AET produces behavioral effects that mimic those of other indirect 5-HT agonists and that the effects of AET on startle plasticity are due to the release of presynaptic 5-HT.

Animals↗
PubMed2002

Intra- and intertask relationships in a behavioral test battery given to Tg2576 transgenic mice and controls.

Several transgenic mouse models for Alzheimer's disease (AD) that develop -amyloid deposition have recently been advanced, including the Tg2576 mouse. Thorough behavioral phenotyping of this, or any mouse line/population, requires not only analysis of multiple behavioral measures through a comprehensive battery of tasks, but also a clear understanding of the interrelationships between behavioral measures in such a battery. In our accompanying study (King et al., this volume), Tg2576 transgenic (Tg+) and nontransgenic (Tg-) mice aged 3-19 months were administered an extensive behavioral test battery. The present study involved correlation analysis between those behavioral measures. Numerous correlations were evident for all 169 mice (Tg+ and Tg-) combined, with additional correlations being dependent on genotype or age. For all mice combined, intratask measures in water maze and circular platform were highly correlated; in addition, several measures of activity correlated with each other, as did various measures of balance/agility. A number of correlations between the six cognitive-based tasks of the test battery (e.g. Y-maze, Morris water maze, circular platform, visible platform, passive avoidance, and active avoidance) were also evident, as were correlations between cognitive and sensorimotor measures. In as much as some correlations were found to be exclusive to either Tg+ or Tg- animals alone, separate analysis by genotype is clearly warranted whenever two or more genotypes are involved. Likewise, some correlations were age-dependent, being present either in young adulthood (3 months) or in old age (19 months). These correlation analysis results in mice indicate that: (1) performance in one or several behavioral measures can be predictive of performance in others and (2) both genetic background and age influence the degree and profile of intra-/intertask relationships in an extensive behavioral test battery.

Aging↗
PubMed1994

IGF-I and IGF-I24-41 but not IGF-I57-70 affect somatic and neurobehavioral development of newborn male mice.

Insulin-like growth factor (IGF-I) is a trophic factor for both neurons and glial cells. Its presence in developing and adult nervous system suggests an important role for this peptide in the development of neural circuitries. Neonatal male mice of the CD-1 outbred strain were injected intracerebroventricularly with either recombinant IGF-I, synthetic IGF-I fragment 24-41 or IGF-I fragment 57-70 on postnatal days (PND) 2, 4, and 7. Physical traits such as body weight gain, body length, and tail length were recorded daily from PND2 to PND13. Sensorimotor development was scored according to a modified Fox's scale. The ultrasonic vocalization pattern on PND8 and homing performance on PND10 were also recorded. Measures for body weight gain and tail length of the pups were significantly increased following treatment with the whole IGF-I peptide. However, neither IGF-I nor the smaller fragments affected mice sensorimotor development. IGF-I and IGF-I24-41 but not IGF-I57-70 increased the rate of ultrasonic calls of the pups measured on PND8. These data provide evidence that IGF-I regulates somatic growth and behavioral development when administered in newborn mice and that different portions of the peptide can exert different effects.

Animals↗
PubMed2000

Forward modeling allows feedback control for fast reaching movements.

Delays in sensorimotor loops have led to the proposal that reaching movements are primarily under pre-programmed control and that sensory feedback loops exert an influence only at the very end of a trajectory. The present review challenges this view. Although behavioral data suggest that a motor plan is assembled prior to the onset of movement, more recent studies have indicated that this initial plan does not unfold unaltered, but is updated continuously by internal feedback loops. These loops rely on a forward model that integrates the sensory inflow and motor outflow to evaluate the consequence of the motor commands sent to a limb, such as the arm. In such a model, the probable position and velocity of an effector can be estimated with negligible delays and even predicted in advance, thus making feedback strategies possible for fast reaching movements. The parietal lobe and cerebellum appear to play a crucial role in this process. The ability of the motor system to estimate the future state of the limb might be an evolutionary substrate for mental operations that require an estimate of sequelae in the immediate future.

Journal Article↗
PubMed2002

Development of the EEG from 5 months to 4 years of age.

OBJECTIVES: This report provides a systematic longitudinal analysis of the EEG from infancy into early childhood. Particular emphasis is placed on the empirical confirmation of a 6-9 Hz alpha-range frequency band that has previously been used in the infant EEG literature. METHODS: EEG data in 1-Hz bins from 3 to 12 Hz were analyzed from a longitudinal sample of 29 participants at 5, 10, 14, 24, and 51 months of age. RESULTS: Inspection of power spectra averaged across the whole sample indicated the emergence of a peak in the 6-9 Hz range across multiple scalp regions. Coding of peaks in the power spectra of individual infants showed a clear developmental increase in the frequency of this peak. A rhythm in the 6-9 Hz emerged at central sites that was independent of the classical alpha rhythm at posterior sites. The relative amplitude of this central rhythm peaked in the second year of life, when major changes are occurring in locomotor behavior. CONCLUSIONS: The 6-9 Hz band is a useful alpha-range band from the end of the first year of life into early childhood. The findings also complement other research relating the infant central rhythm with the adult sensorimotor mu rhythm.

Aging↗
PubMed1992

Stooling problems in patients with myelomeningocele.

In children with myelomeningocele fecal and urinary incontinence lowers self-esteem and decreases social interaction. The defects in the lumbosacral spine disturb the sensory and motor nerves supplying the skin and muscles of the perianal region, including the puborectalis muscle, and the external anal sphincter. The sensations in the region, as well as the motor functions of the striated muscles suffer, compromising the dynamics of continence and the normal process of stooling and leading to incontinence and constipation. Constipation has been treated by disimpaction of stools from the colon and rectum, administration of stool softeners, and a healthy diet containing adequate bulk-forming items. Incontinence has usually been managed by behavior modification of self-initiating stooling after meals and positive reinforcement of this process. This method has helped up to 75% of patients to become socially continent. Biofeedback training has been helpful in patients who have preservation of some sensorimotor functions in the perianal region and who understand and cooperate in the process of biofeedback training. The enema continence catheter has been used to empty the rectosigmoid every 48 hours; most children treated in this manner have achieved social continence. Electric stimulation of the pudendal nerves using a neuroprosthetic device has been used in some patients. The pudendal nerve is stimulated continuously to achieve continence; stimulation is discontinued only for stooling and/or urination.

Biofeedback, Psychology↗
PubMed2005

Enhanced prepulse inhibition following adolescent ethanol exposure in Sprague-Dawley rats.

OBJECTIVES: Recent studies have demonstrated that ethanol exposure differentially affects adolescents and adults. The current studies were designed to compare the effects of 2-week exposure to ethanol during adolescence or adulthood on the acoustic startle response (ASR) and prepulse inhibition (PPI) METHODS: Male Sprague-Dawley rats were exposed to ethanol vapor 12 hr/d (on from 6 pm to 6 am) for 14 days during adolescence or adulthood. Six days after the cessation of ethanol vapor exposure, the ASR and PPI were assessed. RESULTS: During ethanol treatment, overall blood alcohol levels averaged 230 to 250 mg/dl in the adolescent and adult treatment groups. Assessment of the ASR revealed that latency to startle was more rapid in adolescents than in adults, but ASR latency was not altered by ethanol exposure. In addition, ASR magnitude was lower in adolescents and was decreased in ethanol-exposed rats on startle trials. Ethanol exposure significantly enhanced PPI, but only after adolescent exposure CONCLUSIONS: These data further demonstrate a differential sensitivity of adolescents and adults to the effects of ethanol exposure. Specifically, a 2-week period of ethanol exposure during adolescence selectively enhanced PPI, a neurobehavioral index of sensorimotor gating. However, ASR magnitude was decreased by ethanol exposure regardless of age. On the basis of previous studies, the effects of ethanol exposure on PPI data could indicate that adolescent rats exposed to ethanol are more likely to exhibit behavioral inflexibility and that ethanol exposure acts as a more potent physical stressor in adolescent rats.

Acoustic Stimulation↗
PubMedDate not supplied

Quantitation of contacts among sensory, motor, and serotonergic neurons in the pedal ganglion of aplysia.

Present models of long-term sensitization in Aplysia californica indicate that the enhanced behavioral response is due, at least in part, to outgrowth of sensory neurons mediating defensive withdrawal reflexes. Presumably, this outgrowth strengthens pre-existing connections by formation of new synapses with follower neurons. However, the relationship between the number of sensorimotor contacts and the physiological strength of the connection has never been examined in intact ganglia. As a first step in addressing this issue, we used confocal microscopy to examine sites of contact between sensory and motor neurons in naive animals. Our results revealed relatively few contacts between physiologically connected cells. In addition, the number of contact sites was proportional to the amplitude of the EPSP elicited in the follower motor neuron by direct stimulation of the sensory neuron. This is the first time such a correlation has been observed in the central nervous system. Serotonin is the neurotransmitter most closely examined for its role in modulating synaptic strength at the sensorimotor synapse. However, the structural relationship of serotonergic processes and sensorimotor synapses has never been examined. Surprisingly, serotonergic processes usually made contact with sensory and motor neurons at sites located relatively distant from the sensorimotor synapse. This result implies that heterosynaptic regulation is due to nondirected release of serotonin into the neuropil.

Animals↗