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PubMed2006

Delayed satiety-like actions and altered feeding microstructure by a selective type 2 corticotropin-releasing factor agonist in rats: intra-hypothalamic urocortin 3 administration reduces food intake by prolonging the post-meal interval.

Brain corticotropin-releasing factor/urocortin (CRF/Ucn) systems are hypothesized to control feeding, with central administration of 'type 2' urocortins producing delayed anorexia. The present study sought to identify the receptor subtype, brain site, and behavioral mode of action through which Ucn 3 reduces nocturnal food intake in rats. Non-food-deprived male Wistar rats (n=176) were administered Ucn 3 into the lateral (LV) or fourth ventricle, or into the ventromedial or paraventricular nuclei of the hypothalamus (VMN, PVN) or the medial amygdala (MeA), regions in which Ucn 3 is expressed in proximity to CRF(2) receptors. LV Ucn 3 suppressed ingestion during the third-fourth post-injection hours. LV Ucn 3 anorexia was reversed by cotreatment with astressin(2)-B, a selective CRF(2) antagonist and not observed following equimole subcutaneous or fourth ventricle administration. Bilateral intra-VMN and intra-PVN infusion, more potently than LV infusion, reduced the quantity (57-73%) and duration of ingestion (32-68%) during the third-fourth post-infusion hours. LV, intra-PVN and intra-VMN infusion of Ucn 3 slowed the eating rate and reduced intake by prolonging the post-meal interval. Intra-VMN Ucn 3 reduced feeding bout size, and intra-PVN Ucn 3 reduced the regularity of eating from pellet to pellet. Ucn 3 effects were behaviorally specific, because minimal effective anorectic Ucn 3 doses did not alter drinking rate or promote a conditioned taste aversion, and site-specific, because intra-MeA Ucn 3 produced a nibbling pattern of more, but smaller meals without altering total intake. The results implicate the VMN and PVN of the hypothalamus as sites for Ucn 3-CRF(2) control of food intake.

Amygdala↗

PubMed2001

Left ventricular diastolic heart failure with normal left ventricular systolic function in older persons.

Underlying causes and precipitating causes of congestive heart failure (CHF) should be treated when possible. Older persons with CHF and normal left ventricular (LV) ejection fraction should have maintenance of sinus rhythm, treatment of hypertension and myocardial ischemia, slowing of the ventricular rate below 90 beats/minute, and reduction of salt overload. First-line drug treatment in the management of these persons is the use of loop diuretics combined with beta blockers as tolerated. Angiotensin-converting enzyme (ACE) inhibitors should be administered if CHF persists despite diuretics and beta blockers. If persons are unable to tolerate ACE inhibitors because of cough, rash, or altered taste sensation, angiotensin II type 1 receptor antagonists should be given. If CHF persists despite diuretics, beta blockers, and ACE inhibitors or the person is unable to tolerate beta blockers, ACE inhibitors, and angiotensin II type 1 receptor antagonists, isosorbide dinitrate plus hydralazine should be administered. Calcium channel blockers should be used if CHF persists despite administration of diuretics and the person is unable to tolerate beta blockers, ACE inhibitors, angiotensin II type 1 receptor antagonists, and isosorbide dinitrate plus hydralazine. Digoxin, beta blockers, verapamil, and diltiazem may be used to slow a rapid ventricular rate in persons with supraventricular tachyarrhythmias. Digoxin should not be used in persons with CHF in sinus rhythm with normal LV ejection fraction.

Adrenergic beta-Antagonists↗

PubMed1999

Characterization of chloride currents and their noradrenergic modulation in rat taste receptor cells.

Taste receptor cells contain a heterogeneous array of voltage-dependent ion conductances that are essential components for the transduction of gustatory stimuli. Although mechanistic roles have been proposed for several cationic conductances, the understanding of anionic currents is rudimentary. This study characterizes biophysical and pharmacological properties of chloride currents in rat posterior taste cells using whole cell patch-clamp recording technique. Taste cells express a heterogeneous array of chloride currents that displayed strong outward rectification, contained both calcium-dependent and calcium-independent components, and achieved a maximal conductance of almost 1 nS. Reversal potentials altered predictably with changes in chloride concentration. Currents were sensitive to inhibition by the chloride channel pharmacological agents DIDS, SITS, and niflumic acid but were insensitive to 9-AC. Adrenergic enhancement of chloride currents, present in other cell types, was tested on taste cells with the beta-adrenergic agonist isoproterenol (ISP). ISP enhanced the outwardly rectifying portion of the chloride current. This enhancement was calcium dependent and was blocked by the beta-adrenergic antagonist propranolol. Collectively these observations suggest that chloride currents may participate not only in usually ascribed functions such as stabilization of the membrane potential and volume regulation but additionally play active modulatory roles in the transduction of gustatory stimuli.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1990

Membrane currents in taste cells of the rat fungiform papilla. Evidence for two types of Ca currents and inhibition of K currents by saccharin.

Taste buds were isolated from the fungiform papilla of the rat tongue and the receptor cells (TRCs) were patch clamped. Seals were obtained on the basolateral membrane of 281 TRCs, protruding from the intact taste buds or isolated by micro-dissection. In whole-cell configuration 72% of the cells had a TTX blockable transient Na inward current (mean peak amplitude 0.74 nA). All cells had outward K currents. Their activation was slower than for the Na current and a slow inactivation was also noticeable. The K currents were blocked by tetraethylammonium, Ba, and 4-aminopyridine, and were absent when the pipette contained Cs instead of K. With 100 mM Ba or 100 mM Ca in the bath, two types of inward current were observed. An L-type Ca current (ICaL) activated at -20 mV had a mean peak amplitude of 440 pA and inactivated very slowly. At 3 mM Ca the activation threshold of ICaL was near -40 mV. A transient T-type current (ICaT) activated at -50 mV had an average peak amplitude of 53 pA and inactivated with a time constant of 36 ms at -30 mV. ICaL was blocked more efficiently by Cd and D600 than ICaT. ICaT was blocked by 0.2 mM Ni and half blocked by 200 microM amiloride. In whole-cell voltage clamp, Na-saccharin caused (in 34% of 55 cells tested) a decrease in outward K currents by 21%, which may be expected to depolarize the TRCs. Also, Na-saccharin caused some taste cells to fire action potentials (on-cell, 7 out of 24 cells; whole-cell, 2 out of 38 cells responding to saccharin) of amplitudes sufficient to activate ICaL. Thus the action potentials will cause Ca inflow, which may trigger release of transmitter.

Action Potentials↗

PubMed2002

Separate measures of ethanol seeking and drinking in the rat: effects of remoxipride.

Remoxipride, a dopamine D(2) antagonist, decreases responding that results in the presentation of small amounts (approximately 0.1 ml) of ethanol in limited-access paradigms. This type of operant response is a combined appetitive/consummatory response that is differentially affected by changing stimulus properties of consumed ethanol (i.e., taste, pharmacology) over the course of the session. In the present experimental design, ethanol-directed appetitive and consummatory responses were procedurally separated to investigate the specific effects of remoxipride on these distinct behaviors. Male Long-Evans rats were trained to make a series of lever-press responses once each day that resulted in access to a sipper tube spout containing 10% ethanol for 20 min. Three doses of remoxipride were tested: 5.0, 10.0, and 15.0 mg/kg (-30 min, i.p.). In Experiment 1, a response requirement of 20 was used, and both reinforced and nonreinforced sessions were examined. In nonreinforced sessions, subjects were permitted to lever press for 20 min, after which the session ended without sipper tube presentation. These sessions were conducted to remove the possibility that limiting responding might obscure a drug effect on the seeking response. In Experiment 2, a low response requirement (4) was used to investigate the effects of remoxipride on ethanol intake. Average baseline ethanol intake (Experiment 1) was 0.69 g/kg, with blood ethanol concentrations at the end of the session at 64 mg%. At all doses tested, remoxipride had no effect on the measures of ethanol consumption (e.g., total intake, lick latency, lick rate) in either experiment. However, remoxipride dose dependently decreased the number of appetitive responses made, while having no effect on response latency or rate, during both reinforced and nonreinforced sessions in Experiment 1. In these experiments, the systemic antagonism of the dopamine D(2) receptor decreased ethanol seeking without causing a general impairment of motor function. The procedural separation of seeking and intake responses revealed that appetitive responding was more sensitive than consummatory responding to remoxipride treatment.

Alcohol Drinking↗

PubMed2006

Transgenic labeling of taste receptor cells in model fish under the control of the 5'-upstream region of medaka phospholipase C-beta 2 gene.

Vertebrate taste receptor cells express signaling molecules such as taste receptors and effectors to convert taste stimuli to inner cellular signals. Phospholipase C-beta2 (PLC-beta2) is an effector enzyme that is necessary to transduce taste signals in the mouse. It was shown that a subset of the plc-beta2 expressing cells also express taste receptor molecules, T1Rs or T2Rs, in mammals and fish. To label plc-beta2 expressing cells in the model fish species, we constructed a transgene by linking the 5'-upstream region of the medaka plc-beta2 gene to a green fluorescent protein (GFP) gene. The resulting transgenic medaka exhibited GFP signals in taste buds of the lips and the pharyngeal region. Detailed observation revealed that the GFP signals were in a subpopulation of taste bud cells, and co-localized with the transcript of endogenous plc-beta2 gene. Zebrafish introduced with the same transgene showed GFP signals in a subpopulation of taste bud cells of the lips and the pharyngeal region as in the case of medaka. This is the first report of successful labeling of taste receptor cells in two model fish species under the control of the plc-beta2 promoter. This promoter will be a useful genetic tool to study the vertebrate taste system in general.

Animals↗

PubMed2001

Sensory brain areas in mesopelagic fishes.

Four areas of the brain that receive primary projections from chemical senses ([1] olfactory bulb, [2] facial and vagal lobes), the eye ([3] optic tectum), and somato- and mechanosensory systems such as the lateral line, vestibular and auditory systems ([4] trigeminal and octavolateral regions) have been studied and relative size differences used to deduce the sensory specializations of 67 species of mesopelagic fishes. One type of analysis used the average relative volumes of brain areas and identified 'specialists' with only one brain area above-average (36%), species 'dominated' by two sensory brain regions (49%), and generalists (15%), with three areas above-average. In addition, a cluster analysis was performed that separated 49 species which were mostly visually oriented from 18 non-visual species, among which 16 were characterized by an association of above-average trigeminal/octavolateral and gustatory areas, and a single species with a dominant olfactory bulb. The results support the idea that these species occupy a rich sensory environment for which the absence of sunlight is compensated by chemical and mechanosensory stimuli as well as by bioluminescent signals. This has lead to the development of specializations for the perception of single stimulus-modes, most notably for the visual system, as well as for combinations of various receptors and central processing areas, with a preference for associating either the chemical senses, including the olfactory and facial/vagal systems, or the trigeminal/octavolateral systems.

Animals↗

PubMedDate not supplied

[Sugar triggers our reward-system. Sweets release opiates which stimulates the appetite for sucrose--insulin can depress it].

The consumption of sweet food has increased in Sweden, as in other Western countries. The type of food item has changed. The sweet is dominated by soft drinks. Appetite regulation for sucrose has been described in experimental animal models. It has been found that opioids stimulate appetite for sucrose. At the same time sucrose releases endogenous opioids so that a triggering of sucrose consumption occurs. Insulin has been shown to decrease sucrose intake by blocking the opioid response. Sucrose addiction has been described in rat model. With a concentrated sucrose solution to drink an opioid dependence developed with 1) increased consumption of sucrose 2) abstinence symptoms with no sucrose and 3) anxiety with an opiate blocker. Sucrose addiction in man has not been described in the scientific literature. There is an increased liking of sweets with alcoholic persons, which may be significant to support a strongly rewarding effect of sucrose, also in man. We should limit the access to sweet foods, in particular the sweet drinks. Insulin and insulin sensitivity may be an important factor to restrict the intake of sweet food.

Animals↗

PubMed2002

Small molecule insulin mimetics reduce food intake and body weight and prevent development of obesity.

Obesity and insulin resistance are major risk factors for a number of metabolic disorders, such as type 2 diabetes mellitus. Insulin has been suggested to function as one of the adiposity signals to the brain for modulation of energy balance. Administration of insulin into the brain reduces food intake and body weight, and mice with a genetic deletion of neuronal insulin receptors are hyperphagic and obese. However, insulin is also an anabolic factor; when administered systemically, pharmacological levels of insulin are associated with body weight gain in patients. In this study, we investigated the efficacy and feasibility of small molecule insulin mimetic compounds to regulate key parameters of energy homeostasis. Central intracerebroventricular (i.c.v.) administration of an insulin mimetic resulted in a dose-dependent reduction of food intake and body weight in rats, and altered the expression of hypothalamic genes known to regulate food intake and body weight. Oral administration of a mimetic in a mouse model of high-fat diet-induced obesity reduced body weight gain, adiposity and insulin resistance. Thus, insulin mimetics have a unique advantage over insulin in the control of body weight and hold potential as a novel anti-obesity treatment.

Animals↗

PubMed1979

Concept of neuron types in gustation in the rat.

1. In taste neurophysiology, from Pfaffmann's (49, 50) pioneering work until the present, the possibility of types of neurons corresponding in some sense with the "primary" taste qualities of Henning (33) has been entertained: recently types of gustatory neurons in peripheral nerves have been established according to which of the four classical stimuli is the "best stimulus." However, considerable variation occurs in the response profiles within neurons classified as belonging to the same type. The purpose of this research is to determine, using mathematical techniques where appropriate, if the within-type variation is spurious or, instead, indicates the absence of a typology of taste neurons. The data used were counts of the spike discharges of 50 individual taste neurons in the nucleus of the solitary tract of the rat, evoked by 32 diverse chemical stimuli. 2. Using as input the matrix of Pearson r correlation coefficients calculated for the responses of all pairings of neurons to all stimuli, multidimensional scaling analysis revealed a two-dimensional space in which no clear groupings of neurons occurred. 3. In a hierarchical cluster analysis of the neuron response profile similarities, no evidence of grouping was found, suggesting a more-or-less continuous variation among neurons. 4. When the organization of the 32 stimuli utilized was studied by the same techniques, no clear evidence for stimulus types was found, although the possibility of two stimulus types--"sweet" and "nonsweet"--was raised. 5. Construction of a joint neuron-stimulus space supported a spatial model of taste neuron-stimulus interaction, while analysis of the number and pattern of high correlations among neurons--even after allowance for attenuation due to measurement error--failed to support the notion of types of taste neurons with identical response profiles. 6. Aspects of the logical role of types of neurons in gustatory coding were discussed, and the results and methods of the present investigation were related to classification schemes for neurons in general. Suggestions for a formal taxonomy of neurons were given. 7. It should be emphasized that the present study and conclusions are of second-order, CNS neurons, whereas the studies advocating the presence of neurons types were of peripheral neurons. Taken together, the implication to be drawn from these studies is that if neural types do exist in peripheral taste nerves, the typology is lost at the first synapse and is thus unavailable to the CNS for coding purposes, at least in the rat.

Animals↗

PubMed2002

Behavioral processes underlying the intake suppressive effects of melanocortin 3/4 receptor activation in the rat.

RATIONALE: Central application of MTII, a melanocortin 3/4 receptor agonist, reduces food intake. The behavioral mechanisms underlying the anorexia, however, have not been evaluated. OBJECTIVES: We examined the ingestive behavioral effects of MTII at the microstructural level using two complementary approaches. METHODS: Rats were given daily 2-h sessions during which they drank 12.5% glucose solution; the time of occurrence of each lick event was recorded. We compared rats' glucose intake 30 min after the fourth ICV injection of 0.1, 0.33, and 1.0 nmol MTII or vehicle. The licking patterns were examined to discern effects on parameters related to taste processes and others related to post-ingestive inhibitory feedback. A second experiment directly analyzed the effect of MTII on motor performance by examining whether drug treated rats would, like controls, adjust licking output to maintain meal size when lick volume was shifted from 8 to 4 microl. RESULTS: Meal size was reduced by MTII in a dose-dependent manner (20-50%) in both experiments. Rats treated with MTII compensated for decreased lick volume by substantially increasing the number of licks emitted. Licking parameters associated with taste evaluation were not significantly affected by MTII, whereas parameters associated with post-ingestive inhibition varied as a function of treatment. CONCLUSIONS: Results suggest that MTII reduces intake by amplifying post-ingestive feedback inhibition. That MTII-treated rats increase the number of licks emitted in response to the lick volume reduction discounts the suggestion that intake inhibition is secondary to disruption of motor performance.

Animals↗

PubMed1996

Analysis of differential gene regulation in adequate versus inadequate secretory-phase endometrial complementary deoxyribonucleic acid populations from the rhesus monkey.

The ability to create artificial menstrual cycles in the rhesus monkey provides a model for studies on the regulation of genes and gene networks by estradiol or progesterone (P) in the primate endometrium. This model allowed us to create both a normal level of secretory phase P or an inadequate level of secretory phase P, i.e. endometria that cannot support implantation. The objective of our present study focused on PCR analyses of genes for several factors that are believed to be important in the proper maturation of the endometrium. Complementary DNA (cDNA) populations were prepared from endometria harvested on day 13 (peak E level), days 21-23 of an adequate secretory phase (PcDNA) and days 21-23 of an inadequate secretory phase (IcDNA). Although placental protein 14, leukemia inhibitory factor and 17-beta hydroxysteroid dehydrogenase displayed highly upregulated levels in PcDNA (P-activated genes), there was little or no up-regulation in IcDNA. Transforming growth factor-beta 2 and its receptor and insulin growth factor-I and its receptor were up-regulated in PcDNA, whereas little or no expression was observed in IcDNA. Regulators of the cell cycle and transcription, such as retinoblastoma, c-fos, and c-jun genes, were also greatly underexpressed in IcDNA compared with PcDNA. Interestingly, one gene that we studied, keratinocyte growth factor, that was up-regulated by P (peak E levels vs. PcDNA) was more highly expressed in IcDNA. This latter result suggests that low levels of circulating P are sufficient for expression of this gene, whereas high sustained P levels result in an autologous down-regulation. These data show that the regulation of genes that may play pivotal roles in endometrial maturation are differentially expressed in IcDNA vs. PcDNA and may, in part, characterize improper endometrial maturation.

17-Hydroxysteroid Dehydrogenases↗

PubMed2005

Decreased oral self-administration of alcohol in kappa-opioid receptor knock-out mice.

BACKGROUND: Although a large body of evidence suggests a role for the opioid system in alcoholism, the precise role of mu-, delta-, kappa-, and ORL1-opioid receptors and the physiological significance of their natural genetic variation have not been identified. The method of targeted gene disruption by homologous recombination has been used to knock out (KO) genes coding for opioid receptors, and study their effects on alcohol self-administration. Here we examined the effects of targeted disruption of kappa-opioid receptor (KOR) on oral alcohol self-administration and other behaviors. METHODS: Oral alcohol, saccharin and quinine self-administration was assessed in a two-bottle choice paradigm using escalating concentrations of alcohol, or tastant solutions. In preference tests 12% alcohol, 0.033% and 0.066% saccharin, and 0.03 mM and 0.1 mM quinine solutions were used. Open-field activity was determined in an arena equipped with a computer-controlled activity-detection system. Subjects were tested for three consecutive days. Locomotor activity was assessed on days 1 and 2 (after saline injection, i.p.) and on day 3 (after alcohol injection, i.p.). Alcohol-induced locomotor activity was determined as the difference in activity between day 3 and day 2. RESULTS: Male KOR KO mice in preference tests with 12% alcohol consumed about half as much alcohol as wild-type (WT) or heterozygous (HET) mice, showed lower preference for saccharin (0.033% and 0.066%) and higher preference to quinine (0.1 mM) than WT mice. Female KOR KO mice showed similar reduction in alcohol consumption in comparison to WT and HET mice. Partial deletion of KOR in HET mice did not change alcohol consumption in comparison to WT mice. In all genotype-groups females drank significantly more alcohol than males. MANOVA of locomotor activity among KO, WT, and HET mice indicated that strain and sex effects were not significant for alcohol-induced activation (p > 0.05), while strain x sex interaction effects on alcohol-induced activation could be detected (F(1,55) = 6.07, p < 0.05). CONCLUSION: Our results indicating decreased alcohol consumption, lower saccharin preference, and higher quinine preference in KOR KO mice are in line with previous observations of opioid involvement in maintenance of food intake and raise the possibility that the deficient dynorphin/KOR system affects orosensory reward through central mechanisms which reduce alcohol intake and disrupt tastant responses, either as direct effects of absence of kappa-opioid receptors, or as effects of indirect developmental compensatory changes.

Alcohol Drinking↗

PubMed2006

Monoclonal antibody antagonists of hypothalamic FGFR1 cause potent but reversible hypophagia and weight loss in rodents and monkeys.

We generated three fully human monoclonal antibody antagonists against fibroblast growth factor receptor-1 (FGFR1) that potently block FGF signaling. We found that antibodies targeting the c-splice form of the receptor (FGFR1c) were anorexigenic when administered intraperitoneally three times weekly to mice, resulting in rapid, dose-dependent weight loss that plateaued (for doses>4 mg/kg) at 35-40% in 2 wk. Animals appeared healthy during treatment and regained their normal body weights and growth trajectories upon clearance of the antibodies from the bloodstream. Measurements of food consumption and energy expenditure indicated that the rapid weight loss was induced primarily by decreased energy intake and not by increased energy expenditure or cachexia and was accompanied by a greater reduction in fat than lean body mass. Hypophagia was not caused through malaise or illness, as indicated by absence of conditioned taste aversion, pica behavior, and decreased need-induced salt intake in rats. In support of a hypothalamic site of action, we found that, after intraperitoneal injections, anti-FGFR1c (IMC-A1), but not a control antibody, accumulated in the median eminence and adjacent mediobasal hypothalamus and that FGFR1c is enriched in the hypothalamus of mice. Furthermore, a single intracerebroventricular administration of 3 microg of IMC-A1 via the 3rd ventricle to mice caused an approximately 36% reduction in food intake and an approximately 6% weight loss within the ensuing 24 h. Our data suggest that FGF signaling through FGFR1c may play a physiological role in hypothalamic feeding circuit and that blocking it leads to hypophagia and weight loss.

Animals↗

PubMed1993

Ionic basis for endogenous rhythmic patterns induced by activation of N-methyl-D-aspartate receptors in neurons of the rat nucleus tractus solitarii.

1. Activation of N-methyl-D-aspartate (NMDA) receptors in caudal nucleus tractus solitarii (cNTS) neurons elicited endogenous rhythmic activities. We used an in vitro brain stem slice preparation to determine the ionic mechanisms underlying the generation of these activities. 2. Using intracellular recordings, we found several ionic conductances to be responsible for the electrophysiological properties of cNTS neurons. After addition of tetrodotoxin (TTX) to the perfusate, cNTS neurons were still able to generate action potentials (APs). Because these APs were suppressed by the addition of cobalt or by the reduction of calcium, they were likely due to calcium currents (ICa). In addition, the amplitude of the afterhyperpolarization (AHP) that followed a train of TTX-resistant APs was reduced in both low-calcium and cobalt-containing saline. It was therefore suggested that calcium-activated potassium (IKCa) currents were involved in the AHP. Accordingly, application of apamin, a blocker of slow IKCa, also decreased the AHP. cNTS neurons exhibited a delayed excitation phenomenon, characterized by a ramplike depolarization that delayed the onset of neuronal firing, when they were depolarized from hyperpolarizing potential. The underlying current was presumed to be an A-current (IKA), because this phenomenon was suppressed during application of 4-aminopyridine (4-AP). 3. Application of NMDA elicited different types of discharge patterns in cNTS neurons: a repetitive firing at depolarized levels of membrane potential (above -60 mV) and rhythmic patterns characterized by either rhythmic bursting or rhythmic single discharges at hyperpolarized levels (within membrane potential range of -60 to -85 mV). In all neurons, rhythmic patterns were superimposed on oscillations of membrane potential. They were characterized by a sudden shift of membrane potential, followed by a ramp-shaped phase of depolarization that preceded spike elicitation. Addition of TTX to the saline did not suppress NMDA-induced oscillations. Therefore rhythmic patterns were not driven by synaptic mechanisms but resulted from endogenous properties of cNTS neurons. 4. APs superimposed on NMDA-induced depolarizations presented the same characteristics as those elicited by positive current pulses. NMDA-elicited oscillations of membrane potential were eliminated by removing magnesium from the saline. Therefore oscillation generation was based primarily on the NMDA channel properties. 5. Intrinsic conductances of cNTS neurons interacted with NMDA-gated conductances to shape the depolarization waveform. Because removal of calcium from the saline suppressed endogenous oscillations, ICa currents were required for the expression of rhythmic activities. IKCa currents were involved in the repolarization phase of oscillations because apamin increased the duration of the oscillations.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗