How societal responses to COVID-19 could contribute to child neglect.

BACKGROUND: The ecosystemic approach to children's needs demands a cohesive response from societies, communities, and families. During the COVID-19 pandemic, the choices societies made to protect their community members from the virus could have created contexts of child neglect. With the closure of services and institutions, societies were no longer available to help meet the needs of children. OBJECTIVE: The purpose of this study is to examine parents' reports on the response their children received to their needs during the COVID-19 crisis. METHODS: During the period of the spring 2020 lockdown, 414 parents in the province of Quebec, Canada, completed an online questionnaire about the impact of the crisis on the response their children received to their needs. RESULTS: Compared to parents of younger children, parents of older children reported less fulfillment of their child's needs in three measured domains, namely cognitive and affective, security, and basic care needs. CONCLUSION: These results are discussed in light of the policies and the resources societies have put in place during the crisis to help families meet the needs of their children. Societies must learn from this crisis to put children at the top of their priorities in the face of a societal crisis. Thoughtful discussions and energy must be given to ensure that, while facing a crisis, the developmental trajectories of children are not sacrificed.

Prevalence and risk factors of child neglect in the general population.

OBJECTIVES: Child neglect is a major public health problem. It is the most frequently reported and substantiated form of maltreatment in youth protective services, and its effects are the most harmful to children. Yet, very few studies have documented its extent and risk factors in the general population. This study aims at documenting the annual prevalence and risk factors of child-neglect behaviours in the general population according to child age and parental gender. STUDY DESIGN: Cross-sectional population survey. METHODS: A sample consisting of 3298 mothers and 1104 fathers of children between six months and 15 years old responded to a telephone survey. The prevalence of neglect was documented using the short version of the Parent-Report Multidimensional Neglectful Behaviour Scale for three child-age categories. RESULTS: Annual prevalence rates vary between 20.6% (95% CI 18.2-23.1) and 29.4% (95% CI 26.6-32.4) depending on the children's age. Although statements do not vary by parent gender, the factors associated with neglect depend on whether they are reported by the mother or the father. Mothers present more mental health problems, while fathers struggle more commonly with difficulties related to their life context. CONCLUSIONS: Measuring neglect in the population presents numerous challenges. Nonetheless, this study made it possible to document the extent of neglectful behaviours in the general population. The results confirm that the risk factors related to neglectful behaviours are similar to those documented in studies concerning situations of neglect reported to the authorities. Other studies are needed to better understand how this phenomenon is manifested in the population.

Endogenous synthesis cannot compensate for absence of dietary oleic acid in rats.

It is important to know whether an organism is able to synthesize all the oleic acid it needs. To determine this, it is sufficient to feed animals a diet containing essential fatty acids but totally lacking oleic acid, and then determine whether tissue concentrations of fatty acids of the (n-9) series are altered due to insufficient endogenous synthesis of oleic acid from stearic acid. In fact, the effects of a total oleic acid deficiency have not previously been studied because all the vegetable oils used in human and animal nutrition contain this fatty acid in variable amounts. Thus, we fed rats semipurified diets whose lipids (triglycerides) were synthesized chemically. Female rats were fed the diets for 3 wk before mating, and their pups (fed the same diets) were killed when 21 and 60 d old. Generally speaking, oleic acid deficiency resulted in a lower level of this acid in the various organs examined (liver, kidney, testes, heart, muscle and sciatic nerve in 21-d-old rats and liver, kidney, heart, muscle and sciatic nerve in 60-d-old rats). Brain, myelin and nerve endings were not affected at either age. This lower level was accompanied by a higher level of 16:1(n-7) and, to a lesser extent, 18:1(n-7). Dietary supplementation with oleic acid (1666 mg/100 g diet) for up to 21 d resulted in normal levels of this fatty acid in some organs (liver, heart, sciatic nerve) but not in others (kidney, muscle, testes) and a decrease in 16:1(n-7), which returned to about the same levels as in the control group in all organs except liver. Adding small or large amounts of stearic acid to the oleic acid-deficient diet had little or no effect on oleic acid levels in the tissues. We conclude that rats (particularly in liver) do not have sufficient synthesizing potential to guarantee the normal fatty acid composition of certain organs if oleic acid is totally absent in the diet.

Rapid and long duration tolerance to the vagal bradycardic effects of 5-HT1A receptor agonists.

Administration of a single dose of the 5-HT1A receptor high intrinsic agonist U-93385E (either 0.3, 1.0 or 3.0 mg/kg, i.v.) results in a 20-30% decrease in heart rate. In contrast, cumulative dosing of U-93385E (0.01-3.0 mg/kg, i.v.) failed to lower heart rate in the spinal cat. Similarly, infusion of 1 mg/kg of U-93385E over a 2 h period failed to lower heart rate and prevented a bradycardic effect of a single bolus dose of U-93385E or flesinoxan. In contrast, the alpha 2-receptor agonist clonidine decreased heart rate in animals receiving the U-93385E infusion. Single bolus doses of flesinoxan or U-93385E failed to decrease heart rate in cats treated for 7 days with U-93385E (3 mg/kg, b.i.d.) and then saline for 3 days. Similarly, U-93385E failed to lower heart rate 12 days following a 14 day infusion of U-93385E (1 mg/kg per day). These data indicate that a rapid and long duration tolerance develops to the vagal bradycardia produced by 5-HT1A receptor agonists.

Role of serotonergic neurons in the maintenance of the 10-Hz rhythm in sympathetic nerve discharge.

We studied the effects of serotonin (5-HT)-receptor agonists and antagonists on the naturally occurring 10-Hz rhythm in sympathetic nerve discharge (SND) of urethan-anesthetized, baroreceptor-denervated cats. Intravenous doses of the 5-HT1A-receptor agonists 8-hydroxy-2(di-n-propylamino)-tetralin (8-OH-DPAT) and U-93385E, which inhibit the firing of serotonergic medullary raphe neurons, decreased the power in the 10-Hz band of SND without affecting the power at frequencies < or = 6 Hz. The inhibitory effects of 8-OH-DPAT and U-93385E were reversed by the 5-HT1A-receptor antagonists spiperone and WAY-100135. Microinjection of 8-OH-DPAT into medullary raphe nuclei also selectively eliminated the 10-Hz rhythm in SND. Intravenous administration of the 5-HT2-receptor antagonist methysergide blocked the 10-Hz rhythm in SND, whereas the 5-HT2-receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane increased peak frequency and power in the 10-Hz band of SND. Microinjection of N-methyl-D-aspartic acid into the medullary raphe also enhanced the 10-Hz rhythm in SND. These data support the view that the naturally occurring discharges of serotonergic medullary raphe neurons preferentially enhance the 10-Hz rhythm in SND.

Effects of inhibitory amino acids on the frequency components in sympathetic nerve discharge.

The effects of the GABA antagonist picrotoxin and the glycine antagonist strychnine on the frequency components in sympathetic inferior cardiac nerve activity were observed. Picrotoxin (0.03-1.0 mg/kg) increased power in the 10-Hz component of sympathetic activity and produced a dramatic shift in the rhythm to higher frequencies. Only small changes were noted in the 2- to 6-Hz component. Strychnine produced a small generalized increase in power in both frequency bands in sympathetic activity. These data suggest that GABA may play an important role in the generation and maintenance of the 10-Hz rhythm in sympathetic activity while glycine likely inhibits activity at a site of convergence of the two rhythms in sympathetic activity.

Tolerance development to the vagal-mediated bradycardia produced by 5-HT1A receptor agonists.

The purpose of this study was to characterize the bradycardic effects of 5-hydroxytryptamine (5-HT)1A receptor agonists in the chloralose-anesthetized spinal cat and to determine if tolerance develops to the bradycardia produced by these drugs. 5-HT1A receptor agonists studied included 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), buspirone, gepirone, flesinoxan and U-93385E (cis-(3aR)-(-)-2,3,3a,4,5,9b-hexahydro-3-propyl-1H-benz[e]indole-9 - carboxamide). These compounds reduced heart rate by 20 to 30% in the spinal cat and lowered arterial blood pressure. The hypotension resulted from a decrease in cardiac output. Atropine reversed and vagotomy prevented the bradycardia produced by a single dose of U-93385E. The decrease in heart rate produced by i.v. bolus doses of flesinoxan or U-93385 was reversed by administration of the 5-HT1A receptor antagonists spiperone or WAY 100135. Administration of a single dose of U-93385E (either 0.3, 1.0 or 3.0 mg/kg i.v.) resulted in a 20 to 30% decrease in heart rate. In contrast, cumulative dosing of U-93385E (0.01-3.0 mg/kg i.v.) failed to lower heart rate in the spinal cat. Similarly, infusion of 1 mg/kg of U-93385E over a 2-hr period failed to lower heart rate and prevented a bradycardic effect of a single bolus dose of U-93385E or flesinoxan. In contrast, the alpha-2 receptor agonist clonidine decreased heart rate in animals receiving the U-93385E infusion. Finally, single bolus doses of flesinoxan or U-93385E failed to decrease heart rate in cats treated for 7 days with U-93385E and then saline for 3 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Impairment of baroreceptor reflexes following kainic acid lesions of the lateral tegmental field.

We examined the effects of kainic acid lesions of the lateral tegmental field on baroreceptor function in the anesthetized cat. Kainic acid lesions prevented the reflex inhibition of inferior cardiac sympathetic nerve activity observed during an increase in blood pressure. The temporal locking of sympathetic slow waves to the cardiac cycle was also abolished following tegmental field lesions. Finally, the periodicity of sympathetic nerve discharge shifted to a higher frequency range following kainic acid lesions. These observations are consistent with the conclusion that lesions of the lateral tegmental field impair baroreceptor reflexes.

Lateral tegmental field involvement in the central sympathoinhibitory action of 8-OH-DPAT.

This study examined the effects of kainic acid and NMDA microinjections into the lateral tegmental field on the sympatholytic effect of the 5-HT1A agonist 8-OH-DPAT. Kainic acid has been reported to destroy cell bodies while leaving fibers of passage intact while NMDA excites the cell bodies but not the axons of neurons. Microinjection of kainic acid was found to block the usual sympatholytic effect of 8-OH-DPAT but not the sympathoinhibition produced by the alpha 2 agonist clonidine. Microinjection of NMDA elicited profound pressor responses related to an increase in sympathetic activity. Sympatholytic effects of 8-OH-DPAT and clonidine were transiently overridden by microinjections of NMDA, but not glutamate. A role for the lateral tegmental field in the generation of sympathetic tone and in the sympatholytic mechanism of 8-OH-DPAT is supported by the chemical lesion and stimulation studies.

8-OH-DPAT-induced inhibition of renal sympathetic nerve activity and serotonin neuronal firing.

The effects of the 5-HT1A receptor 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) administered i.v. on medullary 5-HT neuronal firing and renal sympathetic nerve activity were determined in spontaneously breathing anaesthetized cats. Low doses of 8-OH-DPAT (1-3 micrograms/kg) caused a similar reduction in 5-HT neuronal firing and renal nerve activity while high doses (10-30 micrograms/kg) completely inhibited neuronal firing but caused only 80% inhibition of renal nerve activity. These data are discussed in relationship to the mechanism of sympatholytic action of 8-OH-DPAT and the serotonergic regulation of sympathetic nerve activity.

Evidence that the lateral tegmental field plays an important role in the central sympathoinhibitory action of 8-OH-DPAT.

We examined the effects of 8-OH-DPAT and 5-HT on three types of sympathetic-related neurons identified in the lateral tegmental field of anesthetized cats using spike-triggered averaging techniques. Based on their response to baroreceptor activation, these neurons could be classified as sympathoexcitatory, sympathoinhibitory, or baroreceptor activation unresponsive. 8-OH-DPAT administered intravenously was found to inhibit sympathoexcitatory neurons with a high degree of correlation to inhibition of sympathetic activity, and to excite sympathoinhibitory neurons in a dose-dependent manner. Iontophoretic application of 8-OH-DPAT and 5-HT to the majority of sympathoexcitatory neurons caused inhibition of spontaneous activity while iontophoretic application of 8-OH-DPAT to sympathoinhibitory neurons had variable effects although 5-HT consistently caused excitation. Baroreceptor unresponsive neurons were insensitive to iontophoretic 8-OH-DPAT and showed only limited response to 5-HT. It is concluded that the lateral tegmental field plays an important role in the sympathoinhibitory action of 8-OH-DPAT.

Effects of muscular contraction on discharge patterns of neurons in the medullary raphe nuclei.

Cells of the medullary raphe nuclei were characterized as sympathoinhibitory (SI), sympathoexcitatory (SE) or serotonergic (5-HT). When muscular contraction (MC) was evoked by stimulation of the L7 and S1 ventral roots, putative SI cells were inhibited while putative SE cells were excited. 5-HT cells were unaffected by MC. These data are discussed in relation to integration of somatosensory and cardiovascular reflexes.

Effects of clonidine on sympathoexcitatory neurons in the rostral ventrolateral medulla.

The effects of intravenous and iontophoretic clonidine were determined on the firing rates of sympathoexcitatory neurons in the rostral ventrolateral medulla of the cat. As previously reported in the rat, we found that sympathoexcitatory neurons could be differentiated based on their sensitivity in clonidine. Approximately 50% of the neurons were inhibited by clonidine. There was only a weak correlation between the inhibition of unit activity and whole sympathetic nerve activity. The discharge rates of the remaining neurons were either not altered or were increased by clonidine. Unlike the rat, these two groups of neurons could not be further differentiated on the basis of axonal conduction velocity or discharge frequency. These data are discussed and the effects of clonidine and 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) on sympathoexcitatory neurons are compared.

Pharmacological characterization of medullary serotonin neurons.

In the present study we investigated the characteristics of medullary raphe serotonergic neurons. Specifically, we sought to examine further the similarities between medullospinal 5-HT neurons and the more extensively studied neurons of the dorsal raphe. Intravenous administration of 5-methoxy-dimethyltryptamine (5-MeODMT) produced a dose-related inhibition of the firing of midline medullary 5-HT neurons. Microiontophoretically applied 5-MeODMT also inhibited medullary 5-HT neurons. The inhibitory potency of 5-MeODMT was nearly identical to that observed for dorsal raphe 5-HT neurons. Microiontophoretic or intravenous administration of the 5-HT2 receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) did not alter the firing rate of medullary 5-HT neurons. Intravenous administration of the alpha 1-receptor antagonist prazosin resulted in an inhibition of the medullary 5-HT neuronal firing. The discharge of medullary 5-HT neurons increased during iontophoresis of norepinephrine. These data are discussed in relation to the identification and characterization of medullary 5-HT neurons. In addition, the data suggest that the firing rate of medullary 5-HT neurons is regulated in part by a tonic excitatory noradrenergic input.

Studies on the site and mechanism of the sympatholytic action of 8-OH DPAT.

Studies in our laboratory indicate that the 5-HT1A agonist 8-OH DPAT acts in the central nervous system at postsynaptic receptor sites to inhibit sympathetic nerve activity and lower arterial blood pressure. The present study was designed to investigate possible postsynaptic sites on central sympathetic neurons where 8-OH DPAT might produce its sympatholytic action in anesthetized cats. The sympatholytic effect of 8-OH DPAT was compared in midcollicular transected and sham operated control animals. Administration of 8-OH DPAT (0.01-1.0 mg/kg, i.v.) inhibited sympathetic activity and decreased blood pressure in both the transected and sham animals to a similar degree. The effects of microiontophoretically applied 8-OH DPAT and 5-HT on antidromically identified sympathetic preganglionic neurons were determined. Microiontophoretically applied 5-HT consistently increased the firing rate of sympathetic preganglionic neurons. Iontophoretic 8-OH DPAT failed to affect the firing of sympathetic preganglionic neurons but blocked the excitatory effects of 5-HT. The effects of 8-OH DPAT and 5-HT on the firing of sympathoexcitatory neurons located in the rostral ventrolateral medulla were also determined. Sympathoexcitatory neurons were identified using spike triggered averaging techniques and by their response to baroreceptor activation. Intravenous administration of 8-OH DPAT inhibited the firing of sympathoexcitatory neurons in the rostral ventrolateral medulla. The inhibition of unit firing produced by 8-OH DPAT was exactly paralleled by the shutoff of inferior cardiac nerve activity. Microiontophoretic application of 8-OH DPAT and 5-HT onto sympathoexcitatory neurons in the rostral ventrolateral medulla failed to affect the firing rate of these neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Studies on the site and mechanism of the sympathoexcitatory action of 5-HT2 agonists.

Intravenous administration of the selective 5-HT2 agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), produced an increase in sympathetic activity recorded from the inferior cardiac nerve in chloralose-anesthetized cats. Microiontophoretically applied 5-HT increased the firing rate of antidromically identified sympathetic preganglionic neurons. Microiontophoretic DOI failed to affect the firing of sympathetic preganglionic neurons. The effect of DOI was also studied on medullospinal sympathoexcitatory neurons located in the rostral ventrolateral medulla. Intravenous DOI increased the firing of sympathoexcitatory neurons and sympathetic nerve discharge to a similar extent. Microiontophoretic application of DOI failed to affect the firing of sympathoexcitatory neurons. The data are discussed in relation to the site and mechanism of the sympathoexcitatory action of 5-HT2 agonists.

Studies on the mechanism of the sympatholytic effect of 8-OH DPAT: lack of correlation between inhibition of serotonin neuronal firing and sympathetic activity.

Previous studies indicate that the selective 5-HT1A agonist, 8-OH DPAT, acts in the central nervous system to inhibit sympathetic nerve activity. Based on the observations that: (1) 8-OH DPAT acts at serotonin (5-HT) autoreceptors to inhibit 5-HT neuronal firing; and (2) medullary 5-HT neurons provide a tonic excitatory input to sympathetic preganglionic neurons, we have hypothesized that 8-OH DPAT produces its sympatholytic effects by inhibiting medullary 5-HT neuronal firing and thereby removing an excitatory input to sympathetic preganglionic neurons. The present study was designed to critically test this hypothesis. The sympatholytic effects of 8-OH DPAT were compared in intact animals and in animals which received large electrolytic lesions in the midline area of the lower brainstem. These lesions extended from the obex rostral through the level of the facial motor nucleus and encompassed the brain stem from the dorsal to the ventral surface. The sympatholytic effect of 8-OH DPAT was identical in intact animals and in animals receiving the lesion. The inhibitory effects of 8-OH DPAT on activity recorded simultaneously from the inferior cardiac sympathetic nerve and from medullospinal 5-HT neurons were determined. Medullary 5-HT neurons were identified using criteria modeled after the electrophysiological and pharmacological characteristics previously described for dorsal raphe 5-HT neurons. Medullary 5-HT neuronal activity was more sensitive to the inhibitory effects of 8-OH DPAT than was sympathetic activity. Indeed, low doses of 8-OH DPAT completely suppressed the firing of medullary 5-HT neurons but had little effect on sympathetic nerve activity. These data fail to support the hypothesis that inhibition of 5-HT neuronal firing is responsible for the central sympatholytic effects of 8-OH DPAT. Rather, the data suggest that 8-OH DPAT acts postsynaptically on 5-HT1A receptors located on central sympathetic neurons to inhibit sympathetic nerve activity.

Characterization of midline medulla role in the trigeminal depressor response.

The purpose of the present investigation was to determine the role of the midline medulla in mediating the trigeminal depressor response. Previously we found that lesions of the midline medulla abolished the decrease in blood pressure resulting from electrical stimulation of the spinal trigeminal complex. Electrical stimulation (5 Hz) of the spinal trigeminal tract elicited a decrease in arterial blood pressure that was associated with an inhibition of sympathetic nerve activity recorded from the inferior cardiac nerve of anesthetized cats. The effect of single shocks applied to the trigeminal complex on sympathetic activity was determined using computer-averaging techniques. Single shock stimulation consistently elicited an excitation of sympathetic activity that was followed by an inhibition of sympathetic nerve discharge. The gamma-aminobutyric acid antagonist picrotoxin blocked the depressor response elicited by electrical stimulation of the midline medulla but not by stimulation of the spinal trigeminal complex. Extracellular recordings of the discharges of midline medullary neurons were made to determine the effects of trigeminal stimulation on sympathoinhibitory, sympathoexcitatory, and serotonin neurons. Sympathoinhibitory and sympathoexcitatory neurons were identified by the relationship between unitary discharges and sympathetic nerve activity and by their response to baroreceptor reflex activation. Serotonin (5-HT) neurons were identified using criteria previously developed in our laboratory. These included 1) a slow regular discharge rate, 2) sensitivity to the inhibitory action of the 5-HT1A agonist 8-OH 8-hydroxy-2-(di-n-propylamino)tetralin, 3) failure to respond to baroreceptor reflex activation, and 4) the discharges of the 5-HT neurons were not related to sympathetic activity. Stimulation of the spinal trigeminal complex typically inhibited the discharges of sympathoinhibitory neurons. In contrast, stimulation of the trigeminal complex consistently excited both sympathoexcitatory and 5-HT neurons. These results are discussed in relationship to the role of the midline medulla in mediating the trigeminal depressor response.

Identification of serotonergic and sympathetic neurons in medullary raphe nuclei.

The purpose of the present study was to identify midline medullary serotonin (5-HT) neurons and to determine if these neurons were distinct from previously identified sympathoinhibitory and sympathoexcitatory neurons. Identification of medullary 5-HT neurons was based on electrophysiological and pharmacological similarities to dorsal raphe 5-HT neurons. Sympathoinhibitory and sympathoexcitatory neurons were characterized by an irregular discharge pattern which was temporally related to inferior cardiac sympathetic nerve discharge (SND) and to the cardiac cycle. Sympathoinhibitory neurons increased their discharge rate and the discharge of sympathoexcitatory neurons decreased during baroreceptor reflex activation. A third type of neuron fired in an extremely regular fashion (as judged by interspike interval analysis), fired at a rate of 1.1 spikes/s and had spike durations of approximately 2 ms. The discharges of regularly firing neurons were not temporally related to SND and were not affected during baroreceptor reflex activation. Regularly firing neurons and sympathoinhibitory neurons could be antidromically activated by electrical stimulation of the intermediolateral cell column of the spinal cord. Axonal conduction velocity of sympathoinhibitory neurons (2.4 m/s) was significantly greater than that for regularly firing neurons (1.3 m/s). Regularly firing neurons were completely inhibited by low doses of the 5-HT1A agonist 8-hydroxy-dipropylamino-tetralin (8-OH-DPAT) (i.e. 2 micrograms/kg, i.v.) while much higher doses of the drug failed to affect the discharges of sympathoinhibitory and sympathoexcitatory neurons. Microiontophoretic application of 5-HT and 8-OH-DPAT profoundly depressed the firing of regularly discharging neurons. Based on the striking similarities between regularly firing medullary neurons and dorsal raphe 5-HT neurons it is concluded that the regularly firing neurons were 5-HT-containing neurons. Furthermore, these medullary 5-HT neurons are distinct from sympathoinhibitory and sympathoexcitatory neurons.