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PubMed2000

Sensory innervation of the sacroiliac joint in rats.

STUDY DESIGN: The segmental levels of dorsal root ganglions innervating the sacroiliac joint in rats were investigated using the retrograde transport method. The pathways and functions of the nerve fibers supplying the sacroiliac joint were determined by immunohistochemical detection of transported tracer. OBJECTIVES: To study the sensory innervation of the sacroiliac joint and to elucidate the neural pathways of low back pain originating from the sacroiliac joint. SUMMARY OF BACKGROUND DATA: The sacroiliac joint is a possible source of low back pain. The L4-S4 spinal nerves have been regarded as the nerves innervating the sacroiliac joint in humans. However, the origins of nerve fibers have not been analyzed experimentally with tracer methods. METHODS: Cholera toxin B subunit, a neural tracer, was injected into the left sacroiliac joint of adult rats, and the bilateral dorsal root ganglions were immunohistochemically examined 4 days after injection. In another rat group, the dorsal root ganglions were examined using the same methods after resection of the left sympathetic trunk from L2 to the most caudal level. Thus, the pathways of the nerve fibers supplying the sacroiliac joint were investigated. RESULTS: Labeled neurons were mainly located in the ipsilateral dorsal root ganglions from L1 to S2 of the unsympathectomized rats and in the ipsilateral dorsal root ganglions from L4 to S2 of the sympathectomized rats. CONCLUSIONS: The sacroiliac joint was innervated by sensory neurons in dorsal root ganglions ipsilateral to the joint from L1 to S2. Sensory fibers from the L1 and L2 dorsal root ganglions passed through the paravertebral sympathetic trunk.

Adrenergic Fibers↗

PubMed1984

Morphology and behavior of quail neural crest cells in artificial three-dimensional extracellular matrices.

Neural crest cells migrate extensively through a complex extracellular matrix (ECM) to sites of terminal differentiation. To determine what role the various components of the ECM may play in crest morphogenesis, quail (Coturnix coturnix japonica) neural crest cells have been cultured in three-dimensional hydrated collagen lattices containing various combinations of macromolecules known to be present in the crest migratory pathways. Neural crest cells migrate readily in native collagen gels whereas the cells are unable to use denatured collagen as a migratory substratum. The speed of movement decreases linearly as the concentration of collagen in the gel increases. Speed of movement of crest cells is stimulated in gels containing 10% fetal calf serum and chick embryo extract, 33 micrograms/ml fibronectin cell-binding fragments, 3 mg/ml chondroitin sulfate, or 3 mg/ml chondroitin sulfate proteoglycan when compared to rates of movement through collagen lattices alone. Low concentrations of hyaluronate (250-500 micrograms/ml) in a 750 micrograms/ml collagen gel do not alter rates of movement over collagen alone, but higher concentrations (4 mg/ml) greatly inhibit migration. Conversely, hyaluronate (250 micrograms/ml) significantly increases speed of movement if the crest cells are cultured in high concentration collagen gels (2.5 mg/ml), suggesting that hyaluronate is expanding spaces and consequently enhancing migration. The morphology and mode of movement of neural crest cells vary with the matrix in which they are grown and can be correlated with their speed of movement. Light and scanning electron microscopy reveal rounded, blebbing cells in matrices associated with slower translocation, whereas rounded cells with branching filopodia or lamellipodia are associated with rapid translocation. Bipolar cells with long processes are observed in cultures of rapidly moving cells that appear to be adhering strongly, as well as in cultures of cells that are stationary for long periods. These data, considered with the known distribution of macromolecules in the early embryo, suggest the following: (1) Both collagen and fibronectin can act as preferred substrata for migration. (2) Chondroitin sulfate and chondroitin sulfate proteoglycan increase speed of movement, but probably do so by decreasing adhesiveness and thereby producing more frequent detachment. In the embryo, crest cells would most likely avoid regions containing high concentrations of chondroitin sulfate. (3) Hyaluronate cannot act as a substratum for migration, but in low concentrations it can open spaces in the matrix and consequently may stimulate movement. The complex interactions of combined matr

Animals↗

PubMed2003

Pregnancy-induced hyperphagia is associated with increased gene expression of hypothalamic agouti-related peptide in rats.

Pregnancy is characterized by an increase in food intake that, in turn, produce a positive energy balance in order to face the considerable metabolic demands associated with the challenge of reproduction. Since hypothalamus is a key brain region involved in many peripheral signals and neuronal pathways that control energy homeostasis and food intake, we investigated if during pregnancy the increase in food intake is mediated by stimulating orexigenic and/or inhibiting anorexigenic neural pathways. We examined hypothalamic gene expressions of Ob-Rb, NPY, AgRP, POMC, MC4-R, and preproorexins in pregnant Wistar rats at day 19 of gestation. Food intake and body weight were increased progressively during the pregnancy. Visceral fat mass depots and serum leptin levels were also increased when compared with virgin animals. No differences were found in mRNA expression of Ob-Rb, POMC, MC4-R, NPY or preproorexin between virgin and pregnant animals. However, pregnancy produced a selective increase in AgRP mRNA levels. These results indicate that the positive energy balance that occurred during pregnancy can hardly be explained by changes in Ob-Rb despite hyperleptinemia associated with pregnancy. The enhanced expression of AgRP suggests the involvement of this neuropeptide in mediating pregnancy-associated hyperphagia.

Agouti-Related Protein↗

PubMed2000

Abnormal cerebral processing of oesophageal stimuli in patients with noncardiac chest pain (NCCP).

In noncardiac chest pain (NCCP), altered visceral perception may result from abnormal cerebral processing of sensory input rather than abnormalities of afferent pathways. However, the interactions between symptoms, autonomic function and oesophageal stimuli are poorly studied. Oesophageal stimulation elicits reproducible cortical evoked potentials [CEP] and modulates heart rate variability via vagal pathways, as visible on power spectrum analysis of heart rate variability [PS-HRV]. These methods are increasingly used to study the function of visceral afferent neural pathways in human. The aim of this study was to compare EP and PS-HRV during oesophageal stimuli in NCCP and controls. Twelve healthy volunteers (one female, 11 male; aged 24-51 years; mean 32 +/- 8 years), and eight NCCP patients (three female, five male; age range 26-58, mean 40.5 +/- 10 years) were studied. Electrical oesophageal stimulation (EOS; 200 microseconds, 0.2 Hz, 25 stimuli) was applied to the oesophageal wall 5 cm above the lower oesophageal sphincter (LOS), and perception thresholds (measured in mA) determined. EP responses were recorded using 22 standard electroencephalogram scalp electrodes. Autonomic activity was assessed using PS-HRV, before, during, and after oesophageal stimulation. Measured PS-HRV indices included high frequency (HF; 0. 15-0.5 Hz) and low frequency (LF; 0.06-0.15 Hz) power, respectively, assessing vagal and sympathetic activity, and the LF/HF ratio. EOS perception occurred at lower thresholds in NCCP than in controls (3. 6 +/- 1 vs. 7.8 +/- 2 mA, P < 0.05). EP amplitude was greater (13 +/- 2 vs. 6 +/- 1 microV, P < 0.0001), and latency longer in controls vs. NCCP (191 +/- 7 ms vs. 219 +/- 6 ms, P < 0.001). In NCCP, EOS decreased sympathetic outflow (low frequency peak on PS-HRV) and increased cardiovagal activity (high frequency peak, P < 0.02) to a significantly higher degree in comparison with controls. During EOS, heart rate decreased in NCCP from 68 vs. 62 beats min-1 (P < 0.003) but not in controls. In NCCP patients, EOS was perceived at lower intensities and was associated with a greater cardiovagal reflex response. EP responses associated with EOS were smaller in NCCP than in controls, suggesting that an increased perception of oesophageal stimuli results from an enhanced cerebral processing of visceral sensory input in NCCP, rather than from hyperalgesic responses in visceral afferent pathways.

Adult↗

PubMed2006

Transformation of vestibular signals into motor commands in the vestibuloocular reflex pathways of monkeys.

Parallel pathways mediate the rotatory vestibuloocular reflex (VOR). If the VOR undergoes adaptive modification with spectacles that change the magnification of the visual scene, signals in one neural pathway are modified, whereas those in another are not. By recording the responses of vestibular afferents and abducens neurons for vestibular oscillations at frequencies from 0.5 to 50 Hz, we have elucidated how vestibular signals are processed in the modified versus unmodified VOR pathways. For the small stimuli we used (+/- 15 degrees/s), the afferents with the most regular spontaneous discharge fired throughout the cycle of oscillation even at 50 Hz, whereas afferents with more irregular discharge showed phase locking. For all afferents, the firing rate was in phase with stimulus head velocity at low frequencies and showed progressive phase lead as frequency increased. Sensitivity to head velocity increased steadily as a function of frequency. Abducens neurons showed highly regular spontaneous discharge and very little evidence of phase locking. Their sensitivity to head velocity during the VOR was relatively flat across frequencies; firing rate lagged head velocity at low frequencies and shifted to large phase leads as stimulus frequency increased. When afferent responses were provided as inputs to a two-pathway model of the VOR, the output of the model reproduced the responses of abducens neurons if the unmodified and modified VOR pathways had frequency-dependent internal gains and included fixed time delays of 1.5 and 9 ms. The phase shifts predicted by the model provide fingerprints for identifying brain stem neurons that participate in the modified versus unmodified VOR pathways.

Acoustic Stimulation↗

PubMed1977

The caudal luminous organs of lanternfishes: general innervation and ultrastructure.

Neuroanatomical, light and electron microscopic investigations of the caudal luminous organs of two lanternfish species, Stenobrachius leucopsarus and Parvilux ingens, were conducted in a search for morphological correlates underlying their luminescent behavior and control mechanisms. Complex neural pathways involving the spinal nerves and the sympathetic nerve chain of the caudal peduncle are associated with profuse segmental innervation to both the supracaudal and infracaudal organs. Neural composition of these segmental subunits indicates that pre-ganglionic (spinal) as well as post-ganglionic (sympathetic) fibers are involved in the neural control of luminescence of these organs. Neuro-photocyte units, in which multiple nerve branches are sandwiched between two lamellar photocytes and establish large surface areas of close appposition, as well as gap junctions apparently interconnecting all photocytes throughout the luminous organs, may account for the very rapid and simultaneous displays of spontaneous or electrically driven luminescence. The organization of the caudal luminous organs is compared with that of lanternfish photophores. Relatively few granular and agranular synaptic vesicles are present in some nerve processes of the photocyte units, suggesting that adrenergic neurotransmission as well as electrotonic spread of excitation may be involved at the neuro-photocyte junctions.

Animals↗

PubMed1975

Temporal frequency characteristics of spatial interaction in human vision.

In psychophyscial experiments the bright-dark contrast effects observed in a steady test-field were measured as a function of the temporal frequency of an inducing-field modulated symmetrically about the test-field luminance. The frequency-contrast functions obtained from these measurements were interpreted as reflecting the temporal frequency characteristics of the lateral pathways within the B and D systems (the on-center and off-center neurons) in human vision. Psychophysical evidence is further presented that the lateral neural pathways have lower temporal cut-off frequencies than the "straight-through" pathways. The results are discussed in terms of the frequency characteristics of the center and surround of the receptive fields of on-center and off-center neurons. It is doubtful, however, whether the psychophysical results can be fully explained by the properties of the single-unit receptive field mechanisms.

Humans↗

PubMed1989

Amyloidosis mimics achalasia's effect on lower esophageal sphincter.

Esophageal involvement in systemic amyloidosis is common. Manometric studies have been few in number and have revealed a variety of findings compatible with deposition of amyloid in myopathic as well as neuropathic patterns. This report describes a patient with primary amyloid whose esophageal dysfunction was limited to the lower esophageal sphincter, with both a hypertensive sphincter and impaired relaxation after swallows. Pharmacologic testing confirmed a mild abnormality of the inhibitory pathway to the LES with an intact excitatory pathway and sphincter muscle. This case suggests that amyloidosis, like idiopathic achalasia and carcinoma of the lower esophagus, can produce dysphagia by selective impairment of the inhibitory neural pathway to the lower esophageal sphincter.

Amyloidosis↗

PubMed2005

Reduced sensorimotor inhibition in the ipsilesional motor cortex in a patient with chronic stroke of the paramedian thalamus.

OBJECTIVE: Unilateral or bilateral paramedian infarction in the region of the thalamus and upper midbrain may lead to hypersomnia. To determine whether unilateral infarction of the paramedian thalamus leads to changes in excitability of ipsilesional primary motor hand area (M1). METHODS: We describe a patient with chronic stroke of the right dorsomedian and intralaminar thalamic nuclei, who suffered from mild persistent hypersomnia. We studied the excitability of the right and left M1 with transcranial magnetic stimulation (TMS) in the patient, and in 10 healthy controls. RESULTS: In contrast to healthy controls, contralateral electrical stimulation of the median nerve failed to induce short-latency afferent inhibition (SAI) in the ipsilesional M1. Other measures of corticomotor excitability and somatosensory evoked potentials were normal. CONCLUSIONS: The selective loss of ipsilateral SAI in a patient with paramedian thalamic stroke suggests that during wakefulness, the intact paramedian thalamus facilitates the excitability of intracortical inhibitory circuits, which process thalamocortical sensory inputs in the ipsilateral M1. This preliminary finding suggests that measurements of SAI may provide a means of probing the integrity of some neural pathways, which are involved in the control of wakefulness and arousal. SIGNIFICANCE: In addition to the established role of the paramedian thalamus in arousal and memory, our observation suggests that thalamocortical projections from the paramedian thalamus contribute to the integration of sensory input at the cortical level during wakefulness.

Adult↗

PubMed2001

Role of central melanocortin signaling in eating disorders.

Melanocortins are derived from posttranslational processing of the precursor protein pro-opiomelanocortin (POMC). The central melanocortinergic system consists of endogenous agonist alpha-melanocyte-stimulating hormone, the naturally occurring antagonist Agouti-related protein (AGRP), and two melanocortin receptors (MC3R, MC4R). Activation of central melanocortin receptors inhibits feeding and leads to weight loss, whereas blockade of the central melanocortin signaling pathway increases food consumption and promotes weight gain. This review will focus on the role of central melanocortin signaling in eating behavior and will evaluate studies of the neural pathways of POMC and AGRP systems, the effects of the central melanocortinergic system on food intake and body weight, and the regulation of hypothalamic POMC and AGRP neurons in response to altered feeding state and energy balance. In addition, this review will explore what is known about the interplay between the central melanocortinergic system and peripheral signals of energy homeostasis, i.e., leptin and glucocorticoids. Furthermore, evidence will be presented that genetic defects within the melanocortin signaling system are involved in determining susceptibility to obesity and anorexia in humans, and the therapeutic potential of melanocortin agonists and antagonists in the treatment of these disorders will be discussed.

Animals↗

PubMed1980

Segmental reflex sympathetic dystrophy syndrome.

The classical findings of Reflex Sympathetic Dystrophy Syndrome (RSDS), OR Sudeck's atrophy, include pain, swelling, limitation of motion, and patchy demineralization, all of which usually affect an entire extremity. This report presents two cases of RSDS which involve only a portion of an extremity--the fourth and fifth fingers. It is concluded that this segmental distribution is best explained by neural pathway transmission.

Female↗

PubMed1993

Synaptic inputs of neuropeptide Y-immunoreactive noradrenergic nerve terminals to neurons in the nucleus preopticus medianus which project to the paraventricular nucleus of the hypothalamus of the rat: a combined immunohistochemical and retrograde tracing method.

The nucleus preopticus medianus (POMe) is known to serve as a relay site in the neural pathway, from the subfornical organ to the paraventricular nucleus of the hypothalamus (PVN), and to play an important role in the regulation of fluid balance and cardiovascular control. A neural connection of noradrenergic nerve terminals in the POMe was examined using electron microscopic immunohistochemistry with the retrograde tract tracing method. Double immunofluorescent labeling revealed nerve terminals immunoreactive to both tyrosine hydroxylase (TH) and neuropeptide Y (NPY) and those immunoreactive to both TH and noradrenaline in the POMe. This indicates that there is an NPY-immunoreactive noradrenergic innervation in the POMe. At the electron microscopic level, nerve terminals immunoreactive to TH or NPY in the POMe formed synapses with dendrites or cell bodies of neurons which were retrogradely labeled after injection of the retrograde tracer, WGA-HRP-colloidal gold, in the PVN. These observations suggest that neurons in the POMe with projections to the PVN may be directly affected by NPY-immunoreactive noradrenergic afferent fibers which presumably originate in the brainstem.

Animals↗

PubMed2003

On reversible deafness, generalized anxiety disorder, and the motoric brain: a psychophysiological perspective.

Electromyographic (EMG) recording during presentation of loud sounds revealed central motor inhibition in a rare case of conversion disorder with deafness. Two subjects in whom hypnotic deafness was induced resembled the patient. In contrast, patients with generalized anxiety disorder (GAD) showed a significantly delayed return of EMG to baseline, compared with normals and schizophrenics following administration of auditory startle stimuli. Blood pressure (BP) of GAD patients was also slower to return to baseline than that of normals and schizophrenics. BP recorded continuously during seven consecutive tests revealed a striking difference between GAD patients and controls. While the controls' BP generally decreased during the session, pressure of the GAD patients remained at their initial levels. These data are interpreted in relation to allodynamic autonomic regulation as affected by vagal blockade, which appeared to decrease in controls while remaining undiminished in GAD patients. It is suggested that intrusions of uncontrollable worry in GAD patients, and their consequent overuse of certain rostral neural pathways involved in preparation for action prolonged their vagal blockade. A GAD case with typically high frontalis EMG is presented. Frontalis EMGs may provide an exceptionally sensitive indication of neural activity of relevance to GAD. EMG gradients in normal subjects draw attention to Sperry's motoric brain concept, whose influence is strong throughout the paper. Sperry's principle states that the main function of the brain is that of moving the animal in ways that are advantageous for satisfying basic needs and avoiding dangers. Also, with a focus on the motoric brain, some discoveries resulting from brain-recording experiments in freely moving rats are described.

Acoustic Stimulation↗

PubMed1985

Vasopressin secretion in progressive autonomic failure: evidence for defective afferent cardiovascular pathways.

Patients with progressive autonomic failure with multiple system atrophy show a severely blunted response of plasma arginine vasopressin to the stimulus of head-up tilt. Whether this could be due to lesions either at one or more sites within ascending neural pathways from cardiovascular stretch receptors in the thorax or, alternatively, to lesions affecting vasopressin secreting cells within the hypothalamus was investigated. The arginine vasopressin response to an intravenous infusion of hypertonic saline was determined in six patients with progressive autonomic failure. The mean plasma concentration of arginine vasopressin rose from 1.0 to 3.7 pmol/l, a change comparable to that observed in normal controls. This demonstrates normal functioning of the efferent connections from the osmoreceptors within the hypothalamus and suggests that the loss of vasopressin response to head-up tilt is due to lesions in ascending pathways from cardiovascular receptors. There was a significant rise in mean blood pressure during the infusions on patients with progressive autonomic failure, a change which was not observed with the controls. This may have been at least partly caused by the rise in circulating arginine vasopressin concentrations, since these patients have been reported to be extremely sensitive to the pressor effects of arginine vasopressin.

Afferent Pathways↗

PubMed2003

Mechanisms involved in the loss of excitatory post-stimulus responses by inflammation.

AIM: Electrical stimulation of colonic muscles elicits a response during the stimulation period, and a transient excitation after the stimulus. Post-stimulus or "rebound" excitation has been linked to pathways involving inhibitory neurotransmitters, prostaglandins and substance P but the mechanism is incompletely understood. Because rabbit colitis is characterized by a loss of inhibitory neurotransmission we hypothesized it might affect the rebound response. Therefore we characterized rebound responses in non-inflamed and inflamed tissue by comparing the effect of antagonists/blockers of putative (nitric oxide [NO], ATP, substance P, prostaglandins) and new (serotonin) neurotransmitters. METHODS: Strips from rabbits with colitis induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS) were subjected to electrical field stimulation. Because rebound responses are more prominent under nonadrenergic noncholinergic (NANC) conditions, the effect of specific antagonists (N(omega)-nitro-L-arginine methyl ester (L-NAME), indomethacin, SR140333, methiothepin) on the rebound response was compared under normal and NANC conditions. RESULTS: NANC-conditions increased rebound responses in non-inflamed strips, but this effect was reduced or abolished in inflamed strips. Rebound responses were reduced by pretreatment with the NO-synthase inhibitor, L-NAME, under NANC conditions in non-inflamed strips but not affected in inflamed tissue. In contrast, the P(2) purine receptor antagonist, suramin, did not affect rebound responses in inflamed and non-inflamed strips. The effect of the cyclo-oxygenase inhibitor (COX), indomethacin, on rebound responses was reversed from excitatory to inhibitory by inflammation. Under NANC conditions rebound contractions were also reduced by the neurokinin-1 (NK(1)) antagonist, SR140333, both in normal and inflamed strips. The most pronounced reduction in rebound responses in inflamed and non-inflamed strips under normal conditions was observed with the 5-hydroxytryptamin (1,2) (5-HT(1,2)) antagonist, methiothepin. CONCLUSION: Rebound responses are mainly non-cholinergic and involve NO, substance P, serotonin and inhibitory prostaglandins. In inflamed tissue the nitrergic pathway is absent, excitatory prostaglandins prevail and the cholinergic and tachykinergic components are relatively more important. However there remains an important serotonergic contribution. Our data suggest that inflammation damages different neural pathways to a different extent and is most selective for nitrergic pathways.

Adenosine Triphosphate↗

PubMed2001

Correspondence between short-latency somatosensory evoked brain potentials and cortical magnetic fields following median nerve stimulation.

We investigated the somatosensory evoked cortical magnetic field (SEF) components corresponding to the somatosensory evoked potential (SEP) components between 20 and 30 ms after median nerve stimulation. SEP and SEF were simultaneously recorded after right median nerve stimulation in seven healthy subjects. Twenty single-sweep epochs of SEF and SEP were selected, in which the first SEF component at 20 ms, 1M, and the second component at 30 ms, 2M, were identifiable. The selected epochs were re-averaged at the peaks of 1M and 2M as the triggering periods (zero ms). The width of the deflection, the temporal dispersion (TD), of SEP components, P20 and N30 (Fz-A2), N20, cP25 and cN30 (C3-Fz), N20 and pP30 (P3-A2), and N20 and P30 (P3-Fz), were compared between three averaging conditions. The N20/P20 components showed significantly smaller TDs when the epochs were averaged at the 1M peak (one-way factorial ANOVA, P<0.02) than those of the control, but averaging at the 1M peak did not decrease the TD of N30/P30. On averaging at the 2M peak, the TDs of N30/P30 components recorded from Fz-A2 and P3-Fz were smaller than those of the control. Neither the averaging at the 1M peak nor that at the 2M peak decreased the TD of the cP25 and cN30 components. Source analysis showed that the equivalent current dipoles (ECDs) for both 1M and 2M were located around the central sulcus, possibly in the primary somatosensory cortex (SI). We confirmed that the 1M and 2M temporally linked with N20/P20 and N30/P30, respectively. The difference of TD of N20/P20 and N30/P30 indicated that the neural pathways to the responses to N20/P20 and N30/P30 might be independent.

Adult↗

PubMed1981

Acoustic augmentation and inhibition of the human eyeblink.

The human eyeblink elicited by a mechanically produced tap to the glabella was inhibited by a mild acoustic stimulus presented 200 msec prior to the tap and was augmented when the same acoustic stimulus was presented simultaneously with the tap. Monaural presentation of the acoustic stimulus prior to the tap yielded more reflex inhibition than when that same stimulus was presented binaurally. Binaural presentation of the acoustic stimulus simultaneously with the tap yielded more reflex augmentation than when that same stimulus was presented monaurally. These findings lend credence to the proposition that reflex inhibition and reflex augmentation are mediated by separate neural pathways.

Acoustic Stimulation↗

PubMed1980

Amygdala neurones: converging synaptic inputs produced by median eminence and medial preoptic area stimulations in rats.

1. Amygdaloid afferent inputs from the median eminence and the medial preoptic area were studied electrophysiologically in urethane-anaesthetized female rats.2. Stimulation of the surface of the median eminence produced orthodromic responses in about 80% of the forty-seven amygdala units tested and about 65% of the responsive cells showed an excitation.3. Stimulation of the ipsilateral medial preoptic area orthodromically excited seventeen and inhibited twenty of the forty-nine units tested.4. Stimulation of the contralateral medial preoptic area evoked orthodromic excitation in nine and inhibition in three of the twenty-two units tested. These stimuli were ineffective for producing antidromically conducted impulses in the tested units.5. Sixteen of the thirty amygdala units tested for responses to both median eminence and ipsilateral medial preoptic area stimulation responded orthodromically with either excitation or inhibition. The latency of the response to median eminence stimulation was approximately equal to that of the response to ipsilateral preoptic area stimulation in four of these sixteen units.6. A characteristic bursting discharge was observed in eleven amygdala units during and after ipsilateral preoptic area stimulation. A transitory inhibition was evoked simultaneously with the bursting discharge in some units. Seven of the eleven units were also tested for median eminence stimulation, and a transitory excitation was observed in each of these units.7. These results suggest the existence of converging synaptic inputs both from tuberoinfundibular neurones and the ipsilateral medial preoptic area to certain amygdala neurones. They also demonstrate the existence of a specific neural pathway mediating a characteristic self-sustained bursting discharge in some amygdala neurones after such stimulation.

Afferent Pathways↗