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D W Pfaff

Publications and source records attributed to D W Pfaff.

At least 199 records · Page 11Linked to original sources
PubMed1991

Effects of fimbria-fornix and angular bundle transection on expression of the p75NGFR mRNA by cells in the medial septum and diagonal band of Broca: correlations with cell survival, synaptic reorganization and sprouting.

Quantitative in situ hybridization techniques were used to examine the effects of lesions which sever hippocampal cholinergic and cortical afferents on p75NGFR mRNA-expressing cells located in the medial septum (MS) and the vertical (VDB) and horizontal (HDB) limbs of the diagonal band of Broca. Animals received either bilateral transection of the fimbria/fornix, unilateral transection of the angular bundle, or sham surgery. Four days later, animals were sacrificed and sections through the MS, VDB and HDB were processed for detection of the p75NGFR mRNA using in situ hybridization techniques previously described (Mol. Brain Res., 6 (1989) 275-287). Transection of the fimbria/fornix and angular bundle differentially affected p75NGFR-expressing cells in the MS, VDB and HDB within 4 days after injury, in ways which were consistent and correlate with subsequent effects on cell survival, synaptic reorganization and growth. In particular, in the MS and VDB, transection of the fimbria/fornix resulted in a significant decrease in the size of p75NGFR-expressing cells (reductions of 25.9% and 15.1% respectively) which was accompanied by a significant reduction (37.9% and 12.7% fewer grains/cell) in relative levels of p75NGFR mRNA. In contrast, in the HDB, transection of the fimbria/fornix had no significant effect on the average size of p75NGFR-expressing cells; however, a significant increase (49%) in the mean relative level of p75NGFR mRNA was observed which may, in turn, reflect a large increase (as much as 2-3 fold) in the levels of p75NGFR mRNA expressed by a subpopulation of hippocampally projecting cholinergic neurons located in the HDB. Finally, transection of the angular bundle resulted in small, but significant increases (9.4% and 10.9%) in relative levels of p75NGFR mRNA in the MS and VDB, as well as an increase (19.6%) in the number of p75NGFR mRNA-expressing cells in the HDB, on the injured side. No increases in p75NGFR expression in the MS, VDB or HDB contralateral to the lesion were observed; however, a decrease in the size (6.9%) and message content (19.4%) of p75NGFR-expressing cells was detected in the MS contralateral to the lesion. Most importantly, all of these effects are consistent with the subsequent effects of these lesions on the survival of basal forebrain cholinergic cells, and the reorganization and growth of cholinergic afferents to the hippocampal formation.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗
PubMed1991

Estrogenic regulation and sex dimorphism of growth-associated protein 43 kDa (GAP-43) messenger RNA in the rat.

In addition to effects on brain protein synthesis, neurotransmitter release, and electrophysiology, estrogens alter neurite outgrowth and synaptogenesis. This study examined in the adult rat the effects of estrogen and sex on the expression of the GAP-43 gene; encoding a phosphoprotein structurally and physiologically linked to these two processes in the rat CNS. Ovariectomized (OVX) rats were injected with vehicle or estrogen, or male and female rats were either gonadectomized or left intact. Brains were dissected to obtain ventromedial hypothalamus (VMH), posterior hypothalamus (PH), or frontal cortex (CTX). Total RNA from these areas were extracted, and slot-blots of equal masses of total RNA were hybridized to 32P-labeled cDNAs for GAP-43 and beta-actin, and also to synthetic poly-dT. Resultant autoradiograms were scanned by laser densitometry, quantitated, and ratios of the gray scale generated by each probe were compared between experimental groups. GAP-43 mRNA expression, when compared to expression of either beta-actin mRNA or total poly(A)-containing RNA (poly(A) RNA), was higher in VMH and PH as compared to CTX. Estrogen treatment of OVX rats resulted in a 48-74% increase in GAP-43 mRNA levels in the VMH--in one experiment, this increase was noted after 2 h of estradiol treatment, and in another after 3 days of estradiol benzoate treatment; but PH and CTX were unaffected by either estrogen regimen. Conversely, ovariectomy of intact rats decreased GAP-43 mRNA expression by 45% in the VMH, but not in the CTX.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

PLC-alpha: a common mediator of the action of estrogen and other hormones?

The phosphatidyl inositol (PI) second messenger pathway may mediate diverse effects of estrogen, including its potentiation of the effects of other hormones. Both estradiol (E2) and luteinizing hormone-releasing hormone (LHRH) induce a putative isoform of PI-specific phospholipase C-alpha (PLC-alpha). PLC-alpha catalyzes PI hydrolysis, which in turn can increase protein kinase C (PKC) activation, Ca2+ mobilization, and arachidonic acid metabolism. Estrogen activates the PI pathway, and components of the PI pathway can mimic or enhance some effects of estrogen. Furthermore, estrogen potentiates effects of several hormones (e.g., LHRH, prolactin, and insulin) which can also act through the PI system. PLC-alpha may therefore provide a common second messenger pathway mediating the potentiation by E2 of the effects of other hormones; in addition it may also mediate some or all of the many actions of E2, since components of the PI pathway can have secretory, trophic, toxic, and neuromodulatory effects.

Animals↗
PubMed1991

Ultrastructural and morphometric analysis of neurons in the arcuate nucleus of the female rat hypothalamus following estradiol.

Recent evidence suggests that E2 may act in the ventromedial nucleus of the hypothalamus (VMN) and arcuate nucleus (ARC) through mechanisms partly unique to each area. To examine this hypothesis, we investigated early and discontinuous effects of E2 action on neurons within the ARC from an ultrastructural and morphometric perspective. In contrast to our findings of dramatic, rapid effects of E2 on the structure of VMN neurons, no changes in any of the ultrastructural parameters examined, including the nucleolus, nucleus, nucleoplasm, and the nuclear envelope-RER system, were observed in ARC neurons after either 2 hours of E2 or a discontinuous schedule of 2 h on/7 h off/2 h on of E2. No changes were noted in any of the quantitative parameters examined, including nucleolar, nuclear, and somal area, nuclear shape, and nuclear envelope length after either 2 hours of E2 or a discontinuous schedule of 2 h on/7 h off/2 h on of E2. These morphological results support the hypothesis of differential actions of E2 on various E2-concentrating nuclear groups in the brain.

Animals↗
PubMed1991

Gene expression for estrogen and progesterone receptor mRNAs in rat brain and possible relations to sexually dimorphic functions.

A clear neuroendocrine sex difference lies in the ability of the female rat to produce an ovulatory surge of luteinizing hormone. Preoptic neurons, as they respond to estrogen and progesterone, have been proven to be involved in this mechanism, with an emphasis on the possible participation of neurons in the anteroventral periventricular nucleus and the suprachiasmatic portion of the preoptic area (POA). Further, prominent morphological sex differences have been reported in the rat medial POA. To examine expression of the estrogen receptor (ER) and the progesterone receptor (PR) messenger RNAs (mRNAs) in these critical preoptic neurons, we have used in situ hybridization with tritiated single-stranded DNA probes complimentary for ER and PR mRNA. ER mRNA containing cells were found in the periventricular, suprachiasmatic and medical preoptic cell groups, in a manner which agrees with steroid hormone autoradiography. In the female rat, preoptic neurons expressing PR mRNA were distributed very similarly to those for ER mRNA. Moreover, in the male rat brain, all subsets of preoptic neurons which express the PR gene in the female were also detected in the male. Thus, the distribution of PR expressing cells was very similar between females and males. We conclude that the insensitivity to the male to progesterone, as regards the hormonal control of ovulation, cannot be due to a total failure of PR gene expression in a specific subset of POA neurons. Instead, male preoptic neurons must be less sensitive to neural or hormonal inducers in the physiological range or perhaps lack sufficient levels of a transcription factor linking progesterone responsive elements to the start sites of hormone-controlled genes.

Animals↗
PubMed1991

Migration of LHRH-immunoreactive neurons from the olfactory placode rationalizes olfacto-hormonal relationships.

Nerve cells that express luteinizing hormone-releasing hormone (LHRH), essential for reproductive functions, originate in the epithelium of the medial olfactory placode. While the peripheral origin of this physiologically important brain peptide is surprising, associations between olfactory and reproductive systems are well documented in behavioral studies of pheromones and in clinical studies of disorders including hypogonadotropic hypogonadism with anosmia or olfactory-genital dysplasia. Mechanisms underlying this migration include a close association with neural cell adhesion molecules (NCAM), but are likely also to involve other physical and chemical factors.

Animals↗
PubMed1991

Light-dark differences in behavioral sensitivity to oxytocin.

Ovariectomized female rats treated with estradiol benzoate (EB) and progesterone (P) were infused intracerebroventricularly with a low (200 ng) or high (1 microgram) dose of oxytocin (OT). The low dose of OT facilitated lordosis behavior only during the dark phase of the light-dark cycle in females that were pretreated with low doses of EB (2 micrograms) and P (250 micrograms). In contrast, the high dose of OT facilitated lordosis behavior during both the light and the dark phases but only in long-term ovariectomized females that were primed with large amounts of EB (2 x 10 micrograms) and P (500 micrograms). In females that were primed with lower amounts of ovarian steroids, the high dose of OT failed to increase levels of lordosis responding in either the dark or light phase. Thus, when female rats are treated with physiological amounts of ovarian hormones and OT, they are more sensitive to the facilitative effects of the OT on lordosis behavior during the dark phase.

Animals↗
PubMed1991

Sex difference in estradiol regulation of progestin receptor mRNA in rat mediobasal hypothalamus as demonstrated by in situ hybridization.

Previous studies have shown that estrogen increases the level of progestin receptors (PR) to a greater extent in female than in male rat hypothalamus. In order to determine if sex-specific regulation of the PR protein might be attributable to estrogenic effects on the PR message, in situ hybridization was used to assess sex differences in levels of estrogen-inducible PR mRNA in specific brain nuclei. Here, we report a sexually differentiated pattern of estrogen-regulated PR gene expression. In female hypothalamus, estrogen administered to gonadectomized rats induced a 3.6- and a 3.3-fold increase in PR mRNA in the ventrolateral aspect of the ventromedial nucleus and arcuate nucleus, respectively, but failed to alter the level of PR mRNA in the same neuronal groups of the male. Hormone treatment did not affect the levels of PR mRNA in the dorsomedial or medial amygdaloid nuclei of either sex. These results lead towards a molecular explanation of sex differences in female reproductive behavior by revealing an estrogen-dependent up-regulation of the message for PR, a transcription factor, in a region- and sex-specific fashion.

Amygdala↗
PubMed1991

Electrophysiological actions of oxytocin on hypothalamic neurons in vitro: neuropharmacological characterization and effects of ovarian steroids.

Oxytocin (OT) neurotransmission in the brain has a facilitatory effect on sexual receptivity in rats. This effect of OT is dependent on priming by ovarian steroids, estrogen and progesterone. These steroids modulate OT binding in specific brain nuclei, including the ventrolateral portion of the ventromedial hypothalamic nucleus (vlVMN). In the present study, single-unit activity was recorded from the vlVMN in hypothalamic slices to characterize the electrophysiological actions of OT. To examine the effects of ovarian steroids on OT actions, we used brain slices prepared from ovariectomized rats either treated with estrogen or not, and some slices were treated with progesterone in vitro. OT had little modulatory action on neuronal responses to other agents, but affected the activity of large numbers of vlVMN units. Of those neurons affected, 94% responded with excitation. This predominant stimulatory action of OT is consistent with its lordosis-facilitating effect, because increases in the activity of VMN neurons are generally associated with the facilitation of lordosis. Pharmacological analyses with selective OT agonists and antagonists as well as structurally related peptides showed that the excitatory action of OT is mediated by OT receptors. Estradiol modulated several aspects of OT transmission. First, it increased neuronal responsiveness to OT, especially at the lowest concentration used (0.2 nM). In addition, it caused neuronal responses to OT to correlate significantly with responses to acetylcholine and norepinephrine, which also can act on the ventromedial hypothalamus to facilitate lordosis. Finally, estradiol enhanced the excitability of laterally projecting neurons, which have been implicated in lordosis. In estrogen-pretreated slices, addition of progesterone in vitro caused little further effect on responses of individual neurons to exogenous OT. Altogether, the present electrophysiological findings are consistent with the hypothesis that estrogen potentiates OT action by increasing functional OT receptors preferentially in lordosis-relevant neurons, thereby enabling OT to efficiently facilitate female reproductive behavior.

Acetylcholine↗
PubMed1991

Estrogen receptor messenger RNA expression in rat hypothalamus as a function of genetic sex and estrogen dose.

Previously, we showed that estrogen receptor (ER) messenger RNA (mRNA) levels are decreased in cells of the mediobasal hypothalamus of ovariectomized (OVX) female rats following an acute estradiol treatment. Here, we examined whether the level of ER mRNA remains depressed in the continued long-term presence of estradiol, and questioned if there is a systematic relationship between the concentration of estradiol and the decrease in ER mRNA level. OVX female rats were implanted for 2 weeks with silastic capsules containing various concentrations of estradiol. Tissue sections were hybridized with a [3H] single-stranded DNA probe prepared from the region of the rat ER complementary DNA corresponding to the steroid binding domain, and relative mRNA level was assessed by counting grains over cells in specific hypothalamic nuclei. Estradiol induced a dose-dependent decrease in ER mRNA levels. Message levels declined in the ventrolateral aspect of the ventromedial nucleus (VLVM) by 57% and in the arcuate nucleus by 62% at the highest hormone concentrations used. Thus, ER mRNA down-regulation in female rat hypothalamus exhibits orderly dose dependence at a time following hormone treatment which ensures the system is at steady state. A second study determined if there exist differences in basal levels of ER mRNA expression between castrated (CAS) females and males, and if estradiol can down-regulate ER mRNA levels in male hypothalamus. CAS rats of both sexes were exposed acutely to estradiol benzoate (EB) for different periods of time. Again, in females, EB significantly decreased ER mRNA levels in VLVM by 55% (18 h) and in the arcuate nucleus by 74% (18 h). Interestingly, control CAS males had significantly lower basal ER mRNA levels than OVX females (52% lower than female levels in VLVM; 56% in arcuate), suggesting a sex difference in constitutive expression levels. Moreover, EB failed to down-regulate significantly ER message levels in males. There was no significant effect of sex or EB treatment on ER mRNA levels in medial amygdala. Thus, the second study shows sex differences and brain-region specificity in hormonal regulation of ER mRNA. These findings show that differences in basal levels and regulation of ER mRNA could be a substrate for sex differences in ER concentrations in the hypothalamus of the rat, and further raise the possibility of sex differences in concentrations of nuclear proteins related to the control of ER gene expression.

Animals↗
PubMed1991

Thyroidectomy induces Fos-like immunoreactivity within thyrotropin-releasing hormone-expressing neurons located in the paraventricular nucleus of the adult rat hypothalamus.

Effects of thyroidectomy on Fos-like immunoreactivity (IR) in the rat brain were examined using single and double-label immunocytochemical techniques. In particular, the possibility that Fos might be involved in thyroid hormone regulation of thyrotropin releasing hormone (TRH)-containing neurons located in the parvocellular region of the paraventricular nucleus of the hypothalamus (pPVN) was examined. Adult, male, Sprague-Dawley rats were used and all animals received either surgical removal of the thyroid gland or sham surgery. Two experiments were performed. In the first experiment, animals were killed 1, 3, or 6 days after surgery and numbers of Fos-like IR cells in the parvocellular (pPVN) and magnocellular (mPVN) regions of the PVN, the anterior hypothalamic nucleus (AH), the lateral hypothalamic nucleus (LH), and the pyriform cortex were determined. In the second experiment, animals received an intracerebroventricular injection of colchicine 5 days after surgery. The next day, animals were killed and numbers of Fos-like IR cells double-labeled for either TRH, corticotropin releasing factor (CRF), or methionine-enkephalin (met-Enk) were determined. Six days after thyroidectomy there was a significant increase in the number of Fos-like IR cells detected in the pPVN. No induction in the pPVN was observed 1 and 3 days after thyroidectomy, and no effects attributable specifically to thyroidectomy (as opposed to stress) on Fos expression in the mPVN, AH, LH, or pyriform cortex were observed. In addition, a rapid, stress-related, induction of Fos-like IR was detected in the mPVN, AH, and LH and was easily distinguished from Fos expression induced in the pPVN as a function of thyroidectomy. The time course for the effect of thyroidectomy on Fos expression in the pPVN paralleled increased plasma TSH concentration. A significant correlation between numbers of Fos-like IR cells in the pPVN and plasma TSH concentration following thyroidectomy was also observed, suggesting that plasma levels of TSH correlate directly with the number of activated TRH-containing neurons located in the pPVN. Double staining for Fos and TRH, CRF, or met-Enk revealed that thyroidectomy induced Fos-like IR specifically within TRH-, but not within CRF-, or met-Enk, expressing neurons in the pPVN. Taken together, the data suggest that Fos-like IR is induced within TRH-expressing neurons in the pPVN as a consequence of decreasing levels of circulating thyroid hormone (TH). Whether this reflects a direct effect of decreasing TH on Fos expression is not yet known; however, the data are consistent with the hypothesis that Fos is involved in TH-associated regulation of TRH production and release.

Animals↗
PubMed1990

Differential regulation of proenkephalin gene expression by estrogen in the ventromedial hypothalamus of male and female rats: implications for the molecular basis of a sexually differentiated behavior.

The ventrolateral aspect of the ventromedial hypothalamic nucleus (VL-VM) contains many estrogen-concentrating neurons which mediate estrogen facilitation of reproductive behavior. Previous studies have shown that estrogen treatment increases proenkephalin (PE) gene expression in neurons of the VL-VM in ovariectomized female rats, and that enkephalin peptides may stimulate lordosis behavior. To determine whether there is a sex difference in steroid hormone regulation of PE gene expression we have examined the effects of estrogen and testosterone on PE mRNA levels in male rats. Slot blot hybridization analysis of RNA isolated from the ventromedial hypothalamus indicated that estrogen treatment increased PE mRNA levels in the VL-VM of ovariectomized female rats (2.2-fold), but had no measurable effect on PE mRNA levels in gonadectomized males. Testosterone treatment of gonadectomized males also had no effect on PE gene expression. To determine whether the sex difference in estrogen-inducibility of PE gene expression is due to the developmental effects of gonadal steroids, we have investigated the effect of estrogen on PE mRNA levels in the VL-VM of neonatally androgenized female rats. Unlike the genetic male, the androgenized females responded to estrogen treatment with a female-typical increase in PE mRNA levels (1.7-fold). Further, although the androgenized rats clearly exhibited signs of defeminization, they did exhibit estrogen-facilitated lordosis behavior when tested with manual stimulation. The PE mRNA induction in estrogen-treated androgenized rats correlated well with the lordosis scores obtained by manual stimulation testing. These results indicate that estrogen regulation of PE gene expression in the VL-VM is sexually differentiated and support the hypothesis that the enkephalinergic neurons of the VL-VM are involved in the regulation of female reproductive behavior.

Animals↗
PubMed1990

Behavioral effects of progesterone associated with rapid modulation of oxytocin receptors.

The ventromedial nuclei of the hypothalamus (VMN) are important for the control of feminine mating behavior, and hormone action within these nuclei has been causally related to behavior. Estradiol induces receptors for oxytocin in the VMN and in the area lateral to these nuclei over the course of 1 to 2 days, and progesterone causes, within 30 minutes of its application, a further increase in receptor binding and an expansion of the area covered by these receptors lateral to the VMN. The rapid progesterone effect appears to be a direct and specific effect of this steroid on the receptor or membrane, because it was produced in vitro as well as in vivo and was not mimicked by a variety of other steroids. The effect of progesterone occurred in the posterior part of the VMN, where oxytocin infusion facilitated feminine mating behavior; it did not take place in the anterior part of the VMN, where oxytocin infusion had no effect on mating behavior.

Animals↗
PubMed1990

The migration of luteinizing hormone-releasing hormone (LHRH) neurons from the medial olfactory placode into the medial basal forebrain.

Over the years, investigators have noticed, in a wide variety of species of vertebrates, large numbers of cells migrating from the olfactory placode to the forebrain. These cells were considered to be Schwann cells or ganglion cells of the terminalis nerve. Recently, immunocytochemical localization studies have shown that many of these migrating cells contain luteinizing hormone-releasing hormone (LHRH), a brain peptide that regulates reproductive functions by evoking the release of luteinizing hormone and follicle-stimulating hormone from the anterior pituitary gland. The origin of LHRH cells in the epithelium of the medial olfactory placode, their migration across the nasal septum and into the forebrain, with branches of the terminalis nerve, also a derivative of the medial part of the olfactory placode, has led to some interesting speculations, from evolutionary and physiological perspectives, about the origin of these cells and the role of the terminalis nerve in their migration.

Animals↗
PubMed1990

Synaptology of luteinizing hormone-releasing hormone (LHRH)-immunoreactive cells in the nervus terminalis of the gray short-tailed opossum (Monodelphis domestica).

Light and electron microscopic immunocytochemistry were used to examine the structure of LHRH neurons and fibers in the nervus terminalis of the gray short-tailed opossum (Monodelphis domestica). LHRH-immunoreactive neurons and fibers form a loose plexus within the fascicular network of the ganglion terminale on the median surface of the olfactory bulb. There are at least two populations of LHRH-immunoreactive neurons within the network of the ganglion terminale: fusiform and round neurons similar to those described in the forebrain. At the ultrastructural level, axosomatic and axodendritic contacts were seen between LHRH-immunoreactive and nonimmunoreactive elements in the ganglion terminale. These contacts were classified as 1) synaptic input, with asymmetric synapses seen between a nonimmunoreactive axon terminal and a LHRH-immunoreactive cell body or a nonimmunoreactive axon terminal and a LHRH-immunoreactive dendritic process. 2) synaptic output, with symmetric synapses seen between LHRH-immunoreactive and nonimmunoreactive processes. This study is the first systematic examination of the ultrastructure of the LHRH-immunoreactive neurons and their synaptic contacts in the nervus terminalis. The possible integrative roles for this LHRH-immunoreactive system are discussed.

Animals↗
PubMed1990

HIP-70: a protein induced by estrogen in the brain and LH-RH in the pituitary.

Estrogen and luteinizing hormone-releasing hormone (LH-RH) interact to influence both behavior and gonadotropin release. However, little is known about the biochemical mechanisms that mediate the effects of these hormones or their interactions. The most prominent protein induced by estrogen in the ventromedial hypothalamus has the same amino-terminal sequence as the most prominent protein induced by LH-RH in the pituitary in vitro and in vivo; these proteins comigrate on two-dimensional gels. Furthermore, the hormonal induction may be caused by modification of a constitutive protein with the same molecular weight (70,000) but a slightly more acidic isoelectric point, whose level is inversely related to the level of the induced form after estrogen treatment. Thus estrogen and LH-RH may interact by additively or synergistically inducing this protein, which is called HIP-70.

Amino Acid Sequence↗
PubMed1990

Ascending and descending projections to medullary reticular formation sites which activate deep lumbar back muscles in the rat.

The purpose of this study was to determine ascending and descending afferents to a medullary reticular formation (MRF) site that, when electrically stimulated, evoked EMG activity in lumbar deep back muscles. In anesthetized female rats, the MRF was explored with electrical stimulation, using currents less than 50 microA, while EMG activity was recorded from the ipsilateral lateral longissimus (LL) and medial longissimus (ML). MRF sites that evoked muscle activity were located in the gigantocellular nucleus (Gi). At the effective stimulation site, the retrograde fluorescent tracer, Fluoro-Gold (FG), was deposited via a cannula attached to the stimulating electrode. In matched-pair control experiments, FG was deposited at MRF sites that were ineffective in producing EMG activity in LL and ML, for comparison of afferent projections to effective versus ineffective sites. Labeled cells rostral to FG deposition at effective MRF sites were located in the preoptic area, hypothalamus, limbic forebrain and midbrain, with particularly high numbers in the ipsilateral midbrain central gray, tegmentum, paraventricular nucleus and amygdala. At medullary levels, there was a heavy projection from the contralateral Gi. FG labeled cells were also located in the contralateral parvocellular reticular nucleus, and lateral, medial and spinal vestibular nuclei. Labeled cells with ascending projections were observed in greatest number in the rostral cervical spinal cord, with fewer cells at mid cervical levels and even fewer in the lumbar spinal cord. These labeled cells were located primarily in lamina V, VII, VIII and X. Locations of labeled cells following FG deposition at ineffective MRF sites were similar. However, there was a striking difference in the number of cells retrogradely labeled from the effective MRF sites compared to ineffective MRF sites. Significantly greater numbers of labeled cells were observed in the contralateral MRF, the midbrain, and the cervical spinal cord from the FG deposition at effective stimulation sites. These results suggest that one characteristic of MRF sites that activate epaxial muscles is a larger amount of afferent input, from the midbrain central gray and from contralateral Gi, compared to ineffective MRF sites. Ascending and descending inputs converge at the effective MRF sites, and the larger number of descending projections suggests a more powerful contribution of these afferents to deep lumbar back muscle activation.

Animals↗