Interventions to reduce ambient air pollution and their effects on health: An abridged Cochrane systematic review.

BACKGROUND: A broad range of interventions have been implemented to improve ambient air quality, and many of these have been evaluated. Yet to date no systematic review has been conducted to identify and synthesize these studies. In this systematic review, we assess the effectiveness of interventions in reducing ambient particulate matter air pollution and improving adverse health outcomes. METHODS: We searched a range of electronic databases across multiple disciplines, as well as grey literature databases, trial registries, reference lists of included studies and the contents of relevant journals, through August 2016. Eligible for inclusion were randomized and cluster randomized controlled trials, as well as several non-randomized study designs often used for evaluating air quality interventions. We included studies that evaluated interventions targeting industrial, residential, vehicular and multiple sources, with respect to their effect on mortality, morbidity and the concentrations of particulate matter (PM - including PM10, PM2.5, coarse particulate matter and combustion-related PM), as well as several criteria pollutants, including ozone, carbon monoxide, nitrogen oxides, nitrogen dioxide, nitric oxide and sulphur dioxide. We did not restrict studies based on the population, setting or comparison. Two authors independently assessed studies for inclusion, extracted data and assessed risk of bias. We assessed risk of bias using the Graphic Appraisal Tool for Epidemiological studies (GATE) for correlation studies, as modified and employed by the UK National Institute for Health and Care Excellence. We synthesized evidence narratively, as well as graphically using harvest plots. We assessed the certainty of evidence using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) system. RESULTS: We included 42 studies assessing 38 unique interventions. These comprised a heterogeneous mix of interventions, including those aiming to address industrial sources (n = 5; e.g. the closure of a factory), residential sources (n = 7; e.g. coal ban), vehicular sources (n = 22; e.g. low emission zones), and multiple sources (n = 4; e.g. tailored measures that target both local traffic and industrial polluters). Evidence for effectiveness was mixed. Most included studies observed either no significant association or an association favoring the intervention, with little evidence that the assessed interventions might be harmful. CONCLUSIONS: Given the heterogeneity across interventions, outcomes, and methods, it was difficult to derive overall conclusions regarding the effectiveness of interventions in terms of improved air quality or health. Some evidence suggests that interventions are associated with improvements in air quality and human health, with very little evidence suggesting interventions were harmful. The evidence base highlights the challenges related to establishing the effectiveness of specific air pollution interventions on outcomes. It also points to the need for improved study design and analysis methods, as well as more uniform evaluations. The prospective planning of evaluations and an evaluation component built into the design and implementation of interventions may also be particularly beneficial.

Accumbal dopamine and serotonin in anticipation of the next aggressive episode in rats.

Autonomic and limbic neural activities are linked to aggressive behavior, and it is hypothesized that activities in the cardiovascular and monoaminergic systems play a role in preparing for an aggressive challenge. The objective was to learn about the emergence of monoamine activity in nucleus accumbens before an aggressive confrontation that was omitted at the regular time of occurrence, dissociating the motoric from the aminergic activity. Dopamine, serotonin, heart rate and behavioral activity were monitored before, during and after a single 10-min confrontation in resident male Long-Evans rats fitted with a microdialysis probe in the n. accumbens and with a telemetry sender (experiment 1). DA, but not 5-HT efflux, was confirmed to increase in n. accumbens during and after a single aggressive episode. In aggressive males that confronted an opponent daily for 10 days (experiment 2) heart rate rose 1 h before the regularly scheduled encounter relative to control rats, as measured on day 11 in the absence of any aggression. Concurrently, DA levels increased by 60-70% over baseline levels and 5-HT levels decreased by 30-35% compared to baseline levels. These changes were sustained over 1 h, and contrasted with no significant changes in DA, 5-HT, heart rate or behavioral activity in control rats. The rise in mesolimbic DA appears to be significant in anticipating the physiological and behavioral demands of an aggressive episode, and the fall in 5-HT in its termination, dissociated from the actual execution of the behavior.

Short or continuous social stress: suppression of continuously available ethanol intake in subordinate rats.

We explored the effects of short, intermediate, and continuous social stress on daily ethanol and water intake in rats. The study was designed to: (1) detect increases in intake during hours when animals were not stressed; and (2) detect shifts in preference from solutions with high to low alcohol content. Male Long-Evans rats acquired ethanol self-administration using a sucrose-fading procedure, which was followed by continuous access to 10% and 3% ethanol solutions and water. After intake stabilized, rats were exposed to three periods of five consecutive days of social stress, with 8-10 days without stress in between. Short social stress consisted of being attacked and defeated by an aggressive opponent, followed by 30 min exposure to threats by the aggressive male while in a protective cage. Intermediate and continuous social stress consisted of a 6 h or 24 h 'threat of attack' exposure, respectively. All stress exposures reduced daily intake of 10% ethanol, did not cause changes in intake of 3% ethanol, and caused increases in water intake. No compensatory ethanol consumption was observed on stress days or after stress exposure was discontinued. These results are at variance with the hypothesis for increased alcohol consumption during or following social stress episodes.

Persistent suppression of ethanol self-administration by brief social stress in rats and increased startle response as index of withdrawal.

Excessive alcohol drinking is often linked to the experience of stress, but experimental approaches using animal models of alcohol self-administration have had widely varying outcomes. The objective was to determine how daily exposure to brief, predictable social stress would change alcohol self-administration in rats in a daily limited access protocol. Male Long-Evans rats had either access to a 10% ethanol solution for 15 min in the home cage setting (n=20) or were reinforced with 15% ethanol deliveries for every fifth lever press (n=10). Subsequently, all rats were subjected to brief social stress for five consecutive days. Social stress consisted of attacks by an opponent for 5 min followed by exposure to threats while in a protective cage for 30 min. In both the home cage drinking and operant conditioning groups, social stress exposure significantly decreased alcohol intake or rate of alcohol reinforcements, respectively. When alcohol intake was scheduled immediately before social stress (i.e., 24 h after the previous social stress episode), a decrease was observed with a delay of 1 or 2 days. When alcohol intake was scheduled 4 h after stress, no changes in intake or alcohol reinforcements were observed. Animals that consumed a low dose of ethanol displayed less defensive behavior during social stress compared to water-drinking animals, and showed an increased startle reflex at 8 and 56 h after discontinuation of daily ethanol access. The current experimental protocols of social defeat stress reveal a transient suppression rather than a facilitation of alcohol consumption.

Aggressive behavior, increased accumbal dopamine, and decreased cortical serotonin in rats.

Dopamine (DA) and serotonin have been implicated in the regulation of aggressive behavior, but it has remained challenging to assess the dynamic changes in these neurotransmitters while aggressive behavior is in progress. The objective of this study was to learn about ongoing monoamine activity in corticolimbic areas during aggressive confrontations in rats. Male Long-Evans rats were implanted with a microdialysis probe aimed at the nucleus accumbens (NAC) or medial prefrontal cortex (PFC); next, 10 min samples were collected before, during, and after a 10 min confrontation. Rats continued to display aggressive behavior while being sampled, and they performed two to six attack bites as well as 140 sec of aggressive acts and postures. Dopamine levels in NAC were significantly increased up to 60 min after the confrontation. Peak levels of 140% were achieved approximately 20-30 min after the confrontation. No concurrent changes in accumbal serotonin levels were seen during or after the confrontation. Dopamine and serotonin levels in PFC changed in the opposite direction, with a sustained decrease in serotonin to 80% of baseline levels during and after the confrontation and an increase in dopamine to 120% after the confrontation. The temporal pattern of monoamine changes, which followed rather than preceded the confrontation, points to a significant role of accumbal and cortical DA and 5-hydroxytryptamine in the consequences as opposed to the triggering of aggressive acts. The increase in accumbal DA in aggressive animals supports the hypothesis that this neural system is linked to the execution of biologically salient and demanding behavior.

d-amphetamine "cue" generalizes to social defeat stress: behavioral sensitization and attenuated accumbens dopamine.

RATIONALE: Psychomotor stimulant drugs engender intense euphoria as well as anxiogenic effects, both potentially involving the mesolimbic dopamine system. OBJECTIVES: (1) Do animals that discriminate a psychomotor stimulant drug from saline generalize to a non-pharmacological stressful event such as social defeat? (2) How does the generalization from d-amphetamine to social defeat stress relate to dopamine overflow in the mesocorticolimbic system in response to this stress? METHODS: Adult male Long-Evans rats were trained to discriminate either 1.0 mg/kg d-amphetamine or 10 mg/kg cocaine from saline in a two-lever drug discrimination task; each injection-appropriate tenth lever press was reinforced by milk presentation (fixed ratio, FR10). After confirming systematic cocaine and d-amphetamine dose-effect curves, additional discrimination tests involved exposure to several stress conditions; (1) brief confrontations with an aggressive resident rat that resulted in the intruder's defeat. Rats were administered saline, then exposed to aggressive threats behind a protective screen for 15 min, and subsequently performed the two-lever discrimination task; (2) exposure for 15 min to aggressive threats without prior defeat; (3) exposure to a novel cage for 15 min. A subgroup of rats was prepared for in vivo microdialysis after they generalized the social stress response to the d-amphetamine cue. RESULTS: Nine of 35 d-amphetamine-trained and six of 18 cocaine-trained animals responded at least 80% at the drug-appropriate lever after social defeat stress. Social defeat stress increased dopamine in nucleus accumbens, with a closely similar dopamine response in amphetamine-discriminating rats that were behaviorally sensitized versus those that were not sensitized by amphetamine. CONCLUSIONS: Generalization from social stress to the stimulant "cue" differs among individuals, which may be relevant to the anxiety-like effects of stimulants. By contrast, mesolimbic DA activity and motor activity was increased in response to social defeat stress or a d-amphetamine challenge, regardless of the qualitatively different stimulant-stress generalization. Mesolimbic DA in response to stress or amphetamine appears significant in behavioral activation, but not in the qualitatively divergent internal stimulus properties.

The hypothalamus: cross-roads of endocrine and behavioural regulation in grooming and aggression.

Anatomical and functional studies show that the hypothalamus is at the junction of mechanisms involved in the exploratory appraisal phase of behaviour and mechanisms involved in the execution of specific consummatory acts. However, the hypothalamus is also a crucial link in endocrine regulation. In natural settings it has been shown that behavioural challenges produce large and fast increases in circulating hormones such as testosterone, prolactin, corticotropin and corticosterone. The behavioural function and neural mechanisms of such fast neuroendocrine changes are not well understood. We suggest that behaviourally specific hypothalamic mechanisms, at the cross-roads of behavioural and endocrine regulation, play a role in such neuroendocrine changes. Mild stimulation of the hypothalamic aggressive area, produces stress levels of circulating prolactin, corticotropin, and corticosterone. Surprisingly luteinizing hormone does not change. This increase in stress hormones is due to the stimulation itself, and not caused by the stress of fighting. Similar increases in corticosterone are observed during electrical stimulation of the hypothalamic self-grooming area. The corticosterone response during self-grooming-evoking stimulation is negatively correlated with the amount of self-grooming observed, suggesting that circulating corticosterone exerts a negative feedback control on grooming. Earlier literature, and preliminary data form our laboratory, show that circulating corticosterone exerts a fast positive feedback control over brain mechanisms involved in aggressive behaviour. Such findings suggest that the hormonal responses caused by the activity of behaviourally specific areas of the hypothalamus may be part of a regulation mechanism involved in facilitating or inhibiting the very behavioural responses that can be evoked from those areas. We suggest that studying such mechanisms may provide a new approach to behavioural dysfunctions associated with endocrine disorders and stress.

Increased aggression after ethanol self-administration in male resident rats.

In order to study experimental alcohol intake that leads to heightened aggression, we established ethanol self-administration in aggressive rats. The focus was on low doses of self-administered ethanol and to assess their effects on aggressive behavior in resident rats, using a limited access paradigm followed by a 5-min confrontation with an intruder. In the first phase of the experiment, rats were established as "residents", and their consistent aggressive behavior in confrontations with an intruder was verified. In the second phase, these resident rats were trained to self-administer alcohol, using a sucrose-fading technique. In the third phase, alcohol self-administration was followed by intruder confrontations in order to study the effect of alcohol on aggression. Confrontations after ethanol consumption leading to low (5-20 mg/dl) and moderate (20-50 mg/dl) blood alcohol concentration (BAC) were compared to confrontations without alcohol, each animal serving as its own control. On average, the group showed no change in aggressive behavior after low or moderate ethanol intake. However, six out of 16 individuals significantly increased the number of attack bites and the duration of aggressive behavior by up to 90% after alcohol self-administration. When these rats were assigned post-hoc to an alcohol heightened aggression group, the group was characterized by a 40% increase in number of attack bites and a 90% increase in aggressive posture over control (BAC 0 mg/dl), whereas the alcohol non-heightened aggression group showed no significant changes. These results extend previous observations of increased aggression in a subpopulation of animals after experimenter-administered ethanol in mice, rats and monkeys to self-administered alcohol. Using this animal model, individuals showing enhanced or reduced aggression after oral alcohol self-administration can be characterized behaviorally, physiologically, and neurochemically.

Alcohol, GABAA-benzodiazepine receptor complex, and aggression.

Neurobiological investigations have become productive since experimental protocols were developed that engender large increases in aggressive behavior after acute alcohol challenges in individual experimental animals. Recent developments extended the heightened aggressive behavior to rats that self-administered alcohol shortly before the social confrontation. Quantitative ethological analysis revealed that alcohol prolongs "bursts" of aggressive acts and displays and disrupts communication between the aggressive animal and the opponent who defends, submits, or flees. Pharmacological modulation of the GABAA receptor with benzodiazepine agonists and neuroactive steroids results in dose-dependent biphasic changes in aggressive behavior that mimic the dose-effect function of alcohol; benzodiazepines potentiate the aggression-heightening effects of alcohol as well as the behaviorally suppressive effects; and antagonists at benzodiazepine receptors prevented the aggression-heightening effects of alcohol. The maturational and experiential origins for potentially distinctive GABAA receptor characteristics in individuals who exhibit heightened aggressive behavior await identification.

A time-structured analysis of hypothalamically induced increases in self-grooming and activity in the rat.

Stressors and different manipulations of the paraventricular nucleus of the hypothalamus (PVH) increase self-grooming in the rat. To assess the effect of these PVH manipulations on the timing of grooming in relation to other ongoing behavior, the authors describe these behavioral responses by a time-structured model. The authors show the following: (a) Behavior in each treatment group can be described by a semi-Markov model. Effects of treatments can be described as changes in the parameters of this model, which reflect the tendencies to start and stop grooming and other activities. (b) The PVH manipulations increase self-grooming by increasing the tendencies to start grooming or by extending the period during which grooming occurs. (c) Grooming responses are accompanied by an increase in activity. (d) Different PVH manipulations change the temporal structure of behavior differentially, suggesting that distinct mechanisms within the PVH are involved in the precise timing of grooming in relation to other activities.

Time structure of self-grooming in the rat: self-facilitation and effects of hypothalamic stimulation and neuropeptides.

Specific brain manipulations, such as stimulation of the paraventricular nucleus of the hypothalamus (PVH) or injections of neuropeptides, increase self-grooming in the rat. Such manipulations also affect the different movements that constitute grooming. Using models to assess the time structure of these movements, the authors demonstrate that the rules that control the time structure within grooming are different from the ones that control its initiation. This study also showed that grooming is self-facilitating and that different brain manipulations in the same hypothalamic area induce structurally different kinds of grooming. The authors suggest that this part of the hypothalamus is not only involved in setting priorities to grooming, relative to other behaviors, but is also involved in the timing of different grooming components. These findings suggest that different neural mechanisms may be involved in the initiation and internal time structure of grooming.

Neuronal substrate of electrically induced grooming in the PVH of the rat: involvement of oxytocinergic systems?

Electrical stimulation of the paraventricular (PVH) and adjacent hypothalamic area evokes self-grooming behaviour. Current intensity thresholds for grooming can be obtained depending on the exact localization of the electrode site. Sites localized at greater distance of the center of the grooming area evoke grooming at greater latencies and higher current intensity, or no grooming at all. Results are compared with injections of neuroactive substances into the PVH from previous studies, which showed a similar site specificity for grooming. We found similarity in the distribution of electrode sites in the paraventricular and anterior hypothalamic areas at which grooming is induced, and hypothalamic immunoreactive oxytocinergic neurons and fibres. In addition, we reported earlier that oxytocin infusions into the PVH in resting animals induce grooming, in contrast to other grooming-related peptides, such as alpha-melanocyte-stimulating hormone. We hypothesize that electrical stimulation may induce grooming by activation of oxytocinergic systems originating from the PVH.

PVH lesions do not inhibit stressor-induced grooming in the rat.

Electrical and chemical stimulation of specific parts of the paraventricular hypothalamus (PVH) and the adjacent hypothalamus induce self-grooming responses in the rat. The function of this hypothalamic grooming area (HGA) is not understood. The localization of the HGA in the hypothalamus suggests that grooming, a behavioural response to stressors, is somehow linked to the neuroendocrine response to stressors. In this study it is shown that grooming induced by the stressors, mild restraint and moistening of the fur of the rat, is not inhibited by complete, bilateral radiofrequency lesions of the HGA. The changes in grooming patterns observed following lesions suggest that the HGA may have a function in the timing of different grooming elements.

Effect of environmental stressors on time course, variability and form of self-grooming in the rat: handling, social contact, defeat, novelty, restraint and fur moistening.

Grooming is often related to dearousal following stressors. Interestingly, electrical and chemical stimulation of the paraventricular nucleus of the hypothalamus (PVH), at levels that are known to activate the hypothalamus-pituitary adrenal axis (HPA), also elicits grooming. At the level of the PVH, the neuroendocrine stress response is apparently still linked to the behavioural response to stressors. However the precise nature of this relation is not fully understood. Here we report on grooming in rats following exposure to different stressors which are known to activate the HPA axis. Stressors such as handling, restraint, novelty, encounters with aggressive or non-aggressive conspecifics, or moistening the fur, change the amount and time course of grooming upon return in the home cage, as compared with controls that are just handled. However, the amount of grooming is not directly related to the strength of the stressor. Defeated intruders groom less upon return in their home cage. Novelty and non-aggressive encounters with conspecifics reduce the variation in the amount of grooming between rats. The time course of grooming over the 20-min observation period also differs between treatments. Following restraint, or exposure to non-aggressive conspecifics, grooming first increases and then decreases. Moistened rats immediately start grooming which subsequently decreases. Rats used as intruders in the territory of another rat maintain a constant low level of grooming. Rats placed in a novel cage steadily increase grooming during the 20-min observation period. These results suggest that grooming cannot be simply understood as an immediate response necessary to reduce arousal following stressors. Following exposure to a stressor, grooming rather seems temporary suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Neuropharmacological characteristics of individual differences in alcohol effects on aggression in rodents and primates.

Many violent crimes have been associated with alcohol intoxication, but experimental research in laboratory animals has been largely inconclusive on alcohol effects on aggression. A focus on individual differences rather than group statistics has revealed that low doses of ethanol cause large and repeatable increases in aggressive behavior in subgroups of rodents and primates. The recent progress using in vivo neuropharmacological techniques makes it feasible to explore differences in brain mechanisms in animals that show enhanced aggression after ethanol vs those that do not. Effects of ethanol on three major neurotransmitter systems (i.e. GABA, serotonin, dopamine) are examined. Since these neurotransmitter substances are critically important in the neurobiology of various kinds of aggressive behavior in rodent and primate species, they are potential mechanisms by which ethanol alters aggressive behavior. Direct research on the relevance of the physiological interaction between ethanol and the GABA receptor suggests that at least some of the effects of alcohol on aggression involve the GABA(A)-benzodiazepine receptor complex. The role of serotonin (5-HT) will have to be newly defined in light of the findings that ethanol increases 5-HT release in several forebrain areas, in a dose range that can stimulate aggressive behavior in a subgroup of individuals. Recent in vivo studies show that acute exposure to ethanol increases dopamine release in discrete dopamine terminal areas, and that the initiation and execution of aggressive and defensive behavior are also synchronized with increased dopamine activity in these brain regions.

Periaqueductal gray lesions do not affect grooming, induced electrically in the hypothalamic paraventricular area in the rat.

Electrical stimulation inducing behavioral responses from the hypothalamus seems to activate systems involved in the execution phase of the behaviour rather than in the introductory or decision-making phase. However, the pathways involved are not fully understood. Projections originating from hypothalamic areas involved in specific behavioral responses are rather complex. The periaqueductal gray (PAG) has been proposed to be an essential output station of hypothalamic behavioral mechanisms. Here we report that lesions of the periaqueductal gray area have no effect on grooming responses evoked by electrical stimulation of the hypothalamic paraventricular area. Neither threshold current intensities needed to evoke grooming, nor latencies were affected 7 or 14 days after lesioning. The lesions caused severe behavioural deficits. Animals did not drink or eat spontaneously, had problems with motor coordination and sometimes showed strong defensive reactions upon touch. However, their grooming responses induced by hypothalamic stimulation were not changed. The PAG may have a modulatory role on grooming behaviour; however, this modulatory effect apparently is overruled during electrical stimulation of the hypothalamus.

Initiation of self-grooming in resting rats by local PVH infusion of oxytocin but not alpha-MSH.

The present study was designed to discriminate between factors that initiate and/or prolong self-grooming. The study of factors initiating the grooming response is complicated by the fact that rats may groom already as a consequence of the injection procedure, due to release of endogenous substances after needle insertion or just handling of the animal. Therefore we used an infusion technique that allowed the rats to settle down quietly after they had been connected to an infusion pump, before the actual infusion of the peptide took place. In a previous report, we showed that direct injections of ACTH1-24 and alpha-melanocyte-stimulating hormone (alpha-MSH) into the paraventricular nucleus of the hypothalamus (PVH) prolong self-grooming caused by the injection procedure. Whether these peptides can also initiate grooming, however, is not yet clear. In this report, we compare the effects of alpha-MSH and oxytocin after infusion into the PVH in resting animals. Oxytocin is abundantly present in the PVH and is known to be involved in the regulation of grooming behavior. Slow infusions of oxytocin (0.1 microgram) do initiate grooming, but alpha-MSH (0.1 microgram) is without any behavioral effect. This suggests that oxytocin in the PVH is involved in the initiation of self-grooming, whereas alpha-MSH and probably ACTH do maintain grooming initiated otherwise, either by mechanical activation of the PVH and/or by the handling procedures. Infusion of substances in resting animals apparently is a way to avoid interactions between ongoing overt behavior and peptide-induced effects.

Induction of grooming in resting rats by intracerebroventricular oxytocin but not by adrenocorticotropic hormone-(1-24) and alpha-melanocyte-stimulating hormone.

Adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) injected i.c.v. induce so called 'excessive grooming'. Whether these peptides play a role in the initiation of grooming is not clear, since rats will groom even as a consequence of a particular environmental stimulation, such as handling and/or a novel environment. In most studies, therefore, the first 15 min after i.c.v. injection are not examined. Here we report on the effects of slow i.c.v. infusions of ACTH-(1-24), alpha-MSH and oxytocin in resting rats in their home cages. Interestingly, i.c.v. infusions of oxytocin did initiate grooming in a dose-related way. In contrast, i.c.v. infusions of both ACTH-(1-24) and alpha-MSH in resting rats were without effect on grooming. Oxytocin is apparently involved in the initiation of self-grooming in rats, whereas ACTH and alpha-MSH prolonged grooming initiated by other means, e.g. handling procedures and/or a novel environment. We conclude that the effects of alpha-MSH and ACTH on grooming are conditional, depending on the behavioural state (active or resting) of the animal.

Differential effect of ACTH1-24 and alpha-MSH induced grooming in the paraventricular nucleus of the hypothalamus.

Injection of ACTH1-24 as well as alpha-MSH in the paraventricular nucleus of the hypothalamus (PVH) induces intense grooming in the rat. While comparing the details of MSH, ACTH and control grooming, we found that the induction of grooming was highly site specific. Even injection of saline in that specific area produced some grooming, possibly due to the release of endogenous substances. To distinguish between effects caused by the peptides and the effects caused by the injection procedure, we compared the behavioural effects of saline and peptide injections in sites with exactly the same location in the PVH, in a post-hoc matched pairs design. Using this design we found that the grooming response induced by saline is of a limited duration. ACTH1-24 and alpha-MSH prolong grooming beyond that period. Interestingly, rats receiving alpha-MSH continued to groom, while rats receiving ACTH1-24 changed to scratching. This confirms earlier findings suggesting that grooming and scratching have a differential organization at the level of the PVH. Whether the peptides also have a role in the initiation of the grooming response, or just prolong a response caused by other local factors requires another experimental approach.

Behavioural effects of NMDA injected into the hypothalamic paraventricular nucleus of the rat.

Electrical stimulation of the hypothalamic paraventricular nucleus (PVH) and of the adjacent dorsal hypothalamic area (DHA) evokes grooming behaviour. Microinjections of low doses of kainic acid, an agonist of the kainate type of glutamate receptors, into the same area evokes the same behaviour. To test whether other glutamate receptors are involved, microinjections with N-methyl-D-aspartic acid (NMDA) were made into the PVH/DHA area and the behaviour was observed. From the total observation time (30 min) up to 73% was spent on grooming, accompanied by yawning. Pronounced feeding behaviour was also noticed at 3 injection sites but not until 23 min after injection. Conclusions are that neurones within the PVH/DHA area are involved in grooming behaviour, possibly via glutamatergic innervation. The interaction between grooming and feeding behaviour at the level of the PVH is discussed.