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PubMed2000

Proximal and distal segments of the possum sphincter of Oddi respond differently to neural and cholecystokinin octapeptide stimulation in vitro.

BACKGROUND/AIMS: Previous studies have demonstrated separate pancreatic duct (PD) and bile duct (BD) components of the sphincter of Oddi (SO) and suggested distinct proximal and distal functional segments. This study was designed to determine if proximal and distal segments of the BD component of the SO (BD-SO) and PD component of the SO (PD-SO) responded equally to (1) activation of SO-duodenal neural pathways, and (2) exogenous cholecystokinin octapeptide (CCK-8). METHODS: Intact SO-duodenum preparations from Australian brush-tailed possums (n = 6) were mounted in organ baths. SO activity was recorded from the proximal and distal segments of BD-SO and PD-SO +/- electrical activation of duodenal nerves at two separate sites. Full thickness muscle strips from the proximal and distal segments of the BD-SO and PD-SO were prepared (n = 8), mounted in organ baths, and exposed to CCK-8 (10(-9)- 10(-6) M), +/- tetrodotoxin. RESULTS: Activation of duodenal nerves evoked different responses in some segments of the BD-SO and PD-SO, depending on the site of duodenal electrical stimulation. CCK-8 induced a concentration-dependent, tetrodotoxin-insensitive decrease in the contraction amplitude of SO muscle strips from the proximal but not the distal SO. BD-SO and PD-SO strips were not different. CONCLUSIONS: The SO is composed of BD and PD components each of which contains proximal and distal segments that can respond independently to appropriate stimuli.

Animals↗

PubMed2003

Reduced dipsogenic response induced by angiotensin II activation of subfornical organ projections to the median preoptic nucleus in estrogen-treated rats.

The present study was carried out to investigate whether estrogen modulates the drinking response induced by activation of angiotensinergic neural pathways from the subfornical organ (SFO) to the median preoptic nucleus (MnPO). Microinjection of angiotensin II (ANG II, 10(-10) M, 0.2 microl) into the SFO elicited drinking in ovariectomized (OVX) female rats that were treated with either propylene glycol (PG) vehicle or estrogen benzoate (EB). The amount of water intake induced by the ANG II injection was significantly greater in the PG-treated than in the EB-treated animals. In both groups of female rats, previous injections of saralasin (Sar, 10(-10) M, 0.2 microl), a specific ANG II antagonist, into the MnPO resulted in the significant attenuation of the drinking response to ANG II, showing that the ANG II-induced drinking response may be mediated in part by the angiotensinergic SFO projections to the MnPO. Injections of ANG II (10(-10) M, 0.2 microl) into the MnPO caused drinking in both groups, while no significant difference was found between the groups in the amount of water intake. These results suggest that increases in the circulating level of estrogen may attenuate the drinking response induced by ANG II activation of the SFO projections to the MnPO.

Angiotensin II↗

PubMed2003

Capsaicin-sensitive extrinsic afferents are involved in acid-induced activation of distinct myenteric neurons in the rat stomach.

Challenge of the rat gastric mucosa with 0.5 mol L(-1) HCl activates nitrergic neurons in the myenteric plexus as visualized by c-Fos immunohistochemistry. In the present study, we characterized the activated neurons more extensively by their chemical coding and investigated whether a neural pathway that involves capsaicin-sensitive extrinsic afferents and/or cholinergic neurons transmitting via nicotinic receptors contributes to the activation of myenteric neurons. In multiple labelling experiments, c-Fos was examined for co-localization with nitric oxide synthase (NOS), vasoactive intestinal peptide (VIP), neuropeptide Y (NPY), enkephalin (ENK), gastrin-releasing peptide (GRP), substance P (SP), calbindin D-28k (CALB) and neurofilament 145 (NF 145). All c-Fos-positive neurons were immunoreactive for NOS, VIP, NPY and NF 145, but not for SP, ENK, GRP and CALB. Nerve fibres co-expressing NOS, VIP and NPY were predominantly found in the external muscle layer and in the muscularis mucosae but rarely in the mucosa. Pre-treatment with capsaicin or hexamethonium or a combination of both pre-treatments reduced HCl-induced c-Fos expression by 54, 66 and 63%, respectively. Acid challenge of the stomach, therefore, leads to activation of presumably inhibitory motor neurons responsible for muscle relaxation. Activation of these neurons is partly mediated by capsaicin-sensitive afferents and involves ganglionic transmission via nicotinic receptors.

Animals↗

PubMed1986

Acute hypercalcemia and cardiac autotransplantation in dogs: long-term hemodynamic adaptability.

Cardiac autotransplantation (excision and reimplantation) is a unique model that isolates totally the cardiac afferent and efferent neural pathways and results in hemodynamic misadaptability to many provocative tests. Since the cardiovascular response to acute hypercalcemia is modulated by numerous factors among which the autonomic innervation plays a major role, the hemodynamic response to bolus administration of calcium gluconate was compared in normal and cardiac autotransplanted dogs. Twenty-two animals underwent an autotransplantation while a sham procedure was performed in 18 animals. Each dog was equipped with an electromagnetic flow probe positioned around the ascending aorta and with central venous and aortic catheters. Hemodynamic data were collected daily during 1 month, before and during rapid intravenous administration of calcium gluconate (0.90 mEq). Baseline hemodynamic studies indicate that for both groups myocardial failure is evident in the immediate postoperative period; despite progressive recovery, the autotransplants always show lower cardiovascular performance. Calcium administration elicits transient positive inotropism, which is more important in presence of myocardial failure; this is true for both control and autotransplanted dogs. In the early postoperative period, hemodynamic adaptability to this stress is impaired in the autotransplants. However, long-term results indicate that minimal differences subsist over time in response to calcium administration, and when they are observed, they result from interferences in baroreceptor regulation and reflexes.

Animals↗

PubMedDate not supplied

[Musical perception and cognitive functions. Is there such a thing as the Mozart effect?].

INTRODUCTION: Throughout the second half of the 20th century important advances were made in the study of neurobiology related to the processing of music, the differences and similarities between the neural pathways involved in language and in music, the role played by each hemisphere in recognising these stimuli, and the effects that exposure to certain specific pieces of music could have on the cognitive functions. DEVELOPMENT: The objective of this study is to review the literature concerning music and the central nervous system, bearing in mind the above-mentioned aspects. Likewise, we also wanted to analyse the reports referring to the Mozart effect and Tomatis, in addition to those dealing with formal musical education and its effects. The increased capacity to respond in visuospatial-type tasks after exposure to music by Mozart has triggered a commercial boom which makes use of isolated data, while the real extent of the effect remains unknown. CONCLUSIONS: After reviewing the scientific literature on this subject, it was found that the effects of exposure to music by Mozart (the 'Mozart effect') when they actually occurred, were limited to a specific skill that did not last for more than a few minutes. Formal musical education, on the other hand, shows more permanent positive effects but which can be attributed to the individual attention the pupil receives and to the stimulation in basic skills for general learning.

Auditory Perception↗

PubMed1990

Substantia nigra-mediated anticonvulsant action: a possible role of a dopaminergic component.

A number of neural pathways may mediate nigral control of epilepsy. According to the literature, a GABAergic nigrotectal pathway may be responsible for the control exerted by the substantia nigra on the diffusion of discharges toward spinal targets, while the nigrothalamic projection may transfer nigral influence on premotor neocortical epilepsy. Since there is probably an anatomical nigrohippocampal pathway arising from dopaminergic cells in the substantia nigra, we tested the effects of stimulating the substantia nigra pars compacta (SNpc) on focal hippocampal epilepsy induced by penicillin injection in the cat. The possibility of dopamine involvement was further tested by studying the effects of intraperitoneal injection of haloperidol, a dopamine receptor blocking agent on nigrohippocampal influences, while to verify the precise site of action, in other groups of cats, sulpiride and apomorphine (D-receptor antagonist and agonist, respectively) were locally administered in the dorsal hippocampus. Furthermore, modifications of hippocampal epileptiform EEG were studied in control conditions and following SNpc electrolytic lesions. Results showed a strong nigral suppressive effect on focal hippocampal epilepsy. Nigral stimulation induced a significant decrease in both frequency and amplitude of hippocampal spikes, which disappeared either about 10 min after i.p. injection of haloperidol 1 mg/kg or about 5 min after intrahippocampal administration of sulpiride, and did not return during a further hour or more of experimental observation. It should be emphasized that in the absence of nigral stimulation, both haloperidol and sulpiride did not modify hippocampal spike frequency. Apomorphine application to dorsal hippocampus induced a marked reduction of hippocampal epileptiform activity parallel to the effect observed during SNpc stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Cough and bronchoconstriction mediated by capsaicin-sensitive sensory neurons in the guinea-pig.

Neural pathways involved in cough and reflex bronchoconstriction and the effects of drugs on these airway reflexes have been studied in unanaesthetised guinea-pigs exposed to aerosols of citric acid (0.13-0.78 M), capsaicin (30 microM), nicotine (9.2 mM) and histamine (0.9 mM). The number of coughs was counted during the first 3 min of exposure and the time to onset of signs of dyspnea, as an indication of bronchoconstriction, was measured. Citric acid produced bronchoconstriction and dose-dependently increased the number of coughs. Capsaicin produced both cough and bronchoconstriction. Nicotine mainly produced cough and histamine bronchoconstriction. Pretreatment of adult guinea-pigs with capsaicin (50 mg kg-1 s.c.) produced a long-lasting (greater than or equal to 10 weeks) depletion of substance P- and calcitonin gene related peptide-like immunoreactivities in the sensory nerves of the larynx, tracheobronchial tree and lung. In capsaicin-treated animals, citric acid (0.39 M) and capsaicin (30 microM) caused neither cough nor bronchoconstriction. Nicotine (9.2 mM) and mechanical stimulation still produced cough, and histamine (0.9 mM) bronchoconstriction. It is concluded that in guinea-pigs both capsaicin-sensitive (probably C-fibre endings) and capsaicin-resistant (probably rapidly adapting stretch receptors) afferent neurons may be involved in cough and reflex bronchoconstriction.

Animals↗

PubMed1989

Electrophysiological connections between the hippocampus and entorhinal cortex in patients with complex partial seizures.

The electrophysiological properties of the neural pathways between the hippocampus and the entorhinal cortex were studied intraoperatively in 31 patients undergoing anterior temporal lobectomy for medically intractable complex partial seizures. The hippocampus, removed en bloc, was studied histologically and the pathology was correlated with the electrophysiological findings. In 29 of the patients, entorhinal stimulation evoked a characteristic positive-negative potential in the hippocampus. The entorhinal-evoked hippocampal response closely resembled, or was identical to, the spontaneously occurring hippocampal interictal spike discharge. In patients with Ammon's horn sclerosis in whom there was a major loss of neurons in the hippocampal subfields CA1, CA3, and CA4, the evoked responses were of simple morphology and long latency (mean 21.9 msec to the peak of the first potential). In patients with a ganglioglioma in whom the hippocampus was histologically normal, the evoked responses were of greater complexity and shorter latency (mean 11.8 msec). Stimulation at a single entorhinal site evoked similar waveforms at different hippocampal recording sites. Conversely, stimulation at different entorhinal sites evoked similar responses at a single hippocampal recording site. Stimulation of the hippocampus evoked a potential in the entorhinal cortex and, in some instances, in the amygdala, insula, and lateral temporal cortex. These connections may produce a positive feedback loop that favors seizure generation.

Amygdala↗

PubMed2004

Anatomical basis for a successful upper limb sympathectomy in the thoracoscopic era.

In this clinico-anatomical study, factors potentially responsible for unsuccessful upper limb sympathectomy (ULS) by the thoracoscopic route were evaluated. This study comprised two subsets: 1) in the clinical subset, 25 patients (n = 50 sides) underwent bilateral second thoracic ganglionectomy for palmar hyperhidrosis, and factors predisposing to unsuccessful ULS were identified; and 2) in the anatomical subset, the neural connections of the first and second intercostal spaces were bilaterally dissected in 22 adult cadavers (22 right, 21 left; n = 43 sides). Alternate neural pathways (ANP) were noted in 9 of 50 sides in the 25 clinical cases (18%). In three asthenic patients (5 sides), fascia overlying the longus colli muscle mimicked the sympathetic chain. The right superior intercostal vein (SIV) was located anterior to the second thoracic ganglion in 6 of 50 sides (12%) and predisposed to troublesome bleeding in 2 of 50 cases; the SIV was posterior to the ganglion in 19 of 50 sides (38%), posing no technical problem. On the left, the SIV was noted outside the field of dissection in all but one case. A successful outcome to sympathectomy was noted in all 25 patients. A spectrum of sympathetic contributions to the first thoracic ventral ramus for the first intercostal space was noted in 37 of 43 anatomical cases (86%). These were categorized according to the arrangements of the intrathoracic ramus between the second intercostal nerve and the first thoracic ventral ramus. The cervicothoracic ganglion (37/43 cases; 86%) and an independent inferior cervical ganglion (6/43 cases; 14%) were always located above the second rib. The second thoracic ganglion was consistently located in the second intercostal space. This study demonstrates that ANPs have little clinical significance when a second thoracic ganglionectomy is undertaken. Technical failures may be avoided if the surgeon is mindful of anatomical variations at surgery.

Adult↗

PubMed1988

Lateral hypothalamic area and paraventricular nucleus connections with subfornical organ neurons: an electrophysiological study in the rat.

The neural pathways from the lateral hypothalamic area (LHA) to the hypothalamic paraventricular nucleus (PVN) mediated by subfornical organ (SFO) neurons were examined in urethane-anesthetized male rats in order to determine the excitability of vasopressin (VP)-secreting neurons in the PVN. Microinjection of angiotensin II (AII) into the LHA excited the activity of nearly half (n = 8) of the SFO neurons (n = 18) activated antidromically by electrical stimulation of the PVN. Microinjection of AII into the LHA also caused excitation of approximately one-quarter (n = 11) of putative VP-secreting neurons (n = 45) in the PVN while the excitatory responses of the putative VP-secreting neurons were blocked or attenuated by pretreatment with the AII antagonist, saralasin (Sar), in the SFO. Electrical stimulation of the LHA, on the other hand, produced excitation (n = 17) or inhibition (n = 14) of the putative VP-secreting neurons (n = 52) in the PVN. About half of the excitatory responses to LHA stimulation were blocked or attenuated by pretreatment with Sar in the SFO, whereas the inhibitory responses were not affected. These results show some possible connections between the LHA and PVN, and suggest that AII-sensitive LHA neurons with efferent projections to the SFO may act to enhance the excitability of putative VP-secreting neurons in the PVN via an excitatory influence on the AII-sensitive SFO neurons.

Action Potentials↗

PubMed2005

Correction for direction-dependent distortions in diffusion tensor imaging using matched magnetic field maps.

Diffusion tensor imaging (DTI) has seen increased usage in clinical and basic science research in the past decade. By assessing the water diffusion anisotropy within biological tissues, e.g. brain, researchers can infer different fiber structures important for neural pathways. A typical DTI data set contains at least one base image and six diffusion-weighted images along non-collinear encoding directions. The resultant images can then be combined to derive the three principal axes of the diffusion tensor and their respective cross terms, which can in turn be used to compute fractional anisotropy (FA) maps, apparent diffusion coefficient (ADC) maps, and to construct axonal fibers. The above operations all assume that DTI images along different diffusion-weighting directions for the same brain register to each other without spatial distortions. This assumption is generally false, as the large diffusion-weighting gradients would usually induce eddy currents to generate diffusion-weighting direction-dependent field gradients, leading to mis-registration within the DTI data set. Traditional methods for correcting magnetic field-induced distortions do not usually take into account these direction-dependent eddy currents unique for DTI, and they are usually time-consuming because multiple phase images need to be acquired. In this report, we describe our theory and implementation of an efficient and effective method to correct for the main field and eddy current-induced direction-dependent distortions for DTI images under a unified framework to facilitate the daily practice of DTI acquisitions.

Anisotropy↗

PubMed1998

Neuronal cell bodies in paraventricular nucleus affect renal hemodynamics and excretion via the renal nerves.

Several lines of evidence support the existence of an oligosynaptic projection from the paraventricular nucleus of the hypothalamus (PVN) to the kidney in the rat. We sought to provide evidence that this neural pathway is capable of influencing renal function in rats. Bilateral microinjections of bicuculline (Bic; 1 nmol) into the PVN decreased glomerular filtration rate (59%), effective renal plasma flow (71%), urine flow (UV; 57%), and urinary sodium excretion (UNaV; 54%), accompanied by increased mean arterial pressure (17%) and heart rate (17%). These results were not obtained when Bic was injected outside the PVN or when vehicle (0.9% saline) was injected into the PVN. Bilateral renal denervation (5-7 days before the experiments) significantly reduced the renal vasoconstriction, attenuated the antidiuresis, and abolished the antinatriuresis evoked by PVN stimulation. On the other hand, both the antidiuresis and antinatriuresis evoked by PVN stimulation were undiminished after treatment with either of two vasopressin receptor antagonists ([beta-mercapto-beta,beta-cyclopentamethylenepropionyl1,O-Et-Tyr2, Val4,Arg8]vasopressin, a vasopressin V1 receptor antagonist, or [adamantaneacetyl1,O-Et-D-Tyr2,Val4,aminobutyryl6,Arg8, 9]-vasopressin, a V2 receptor antagonist). In renal-denervated rats treated with the same V2 receptor antagonist, PVN stimulation produced highly variable increases in both UV and UNaV, which overall were not statistically different than zero. We conclude that the activation of neurons in PVN evokes 1) renal vasoconstriction accompanied by antinatriuresis, both of which are attributable to the renal nerves, and 2) decreased water excretion, which is mediated by the renal nerves and vasopressin V2 receptors.

Animals↗

PubMed1994

Interaction between halothane and the nonadrenergic, noncholinergic inhibitory system in porcine trachealis muscle.

BACKGROUND: Volatile anesthetics significantly affect cholinergic neural transmission in the airways and relax airway smooth muscle. Activation of the nonadrenergic, noncholinergic inhibitory neural pathway, which is thought to be mediated by nitric oxide, relaxes human and procine airways. The purpose of the current study was to determine in the isolated porcine trachealis muscle whether relaxation of airway smooth muscle by halothane is mediated in part by activation of the nonadrenergic, noncholinergic inhibitory system. METHODS: Isometric tension was measured in porcine trachealis muscle suspended in tissue baths in the presence of propranalol (10(-6) M). After stimulation of postsynaptic nicotinic cholinergic receptors with 1,1-dimethyl-4-phenyl-piper-azinium iodide (10(-4) M) to prevent contractile responses to subsequent electrical field stimulation, carbachol (3 x 10(-7) M) was added to increase tone. Nonadrenergic, noncholinergic relaxation responses to electrical field stimulation were then measured in the presence of inhibitors of nitric oxide synthase or L-arginine (the substrate for nitric oxide synthase), in the presence and absence halothane. RESULTS: Electrical field stimulation produced frequency-dependent relaxations that were attenuated by inhibitors of nitric oxide synthase (NG-nitro-L-arginine methyl ester [L-NAME] or NG-monomethyl-L-arginine, 10(-4) M). Pretreatment with L-arginine (10(-4) M) prevented the effect of L-NAME. Halothane (0.5% or 1.0%) neither enhanced nor attenuated nonadrenergic, noncholinergic relaxations in the presence of L-NAME, D-NAME, L-arginine, or D-arginine. CONCLUSIONS: Halothane, at concentrations < or = 1.0%, does not relax porcine airway smooth muscle in vitro by activating the nonadrenergic, noncholinergic inhibitory system.

Adrenergic Antagonists↗

PubMed2006

Characteristic expression patterns of allatostatin-like peptide, FMRFamide-related peptide, orcokinin, tachykinin-related peptide, and SIFamide in the olfactory system of crayfish Procambarus clarkii.

The olfactory system plays important roles in various crustacean behaviors. Despite numerous studies on different aspects of the olfactory neural pathway, only the decapod-tachykinin-related peptide (decapod-TRP) has been identified as a neuromodulator in this processing to date. To establish the functions of other related neuropeptides, we initially performed cDNA cloning of FMRFamide-related peptide (FaRP) and allatostatin (AST)-like peptide from the crayfish Procambarus clarkii, followed by in situ hybridization (ISH) analysis of these peptides, along with decapod-TRP, orcokinin, and crustacean-SIFamide. Cloned FaRP cDNA encodes seven copies of C-terminal RN(F/Y)LRFamide-containing peptide, whereas AST-like peptide cDNA comprises 29 copies of AST-like peptide (-YXFGLamide) and three additional putative peptides. ISH analysis of the brain revealed specific expression of crustacean-SIFamide mRNA in most projection neurons (cell cluster 10), and predominant localization of other mRNAs to interneurons. The data suggest that the crustacean-SIFamide neuropeptide is involved in output of the deutocerebrum to the protocerebrum. Double-fluorescence ISH data further disclose that, in cluster 9, orcokinin is coexpressed in decapod-TRP-specific interneurons, whereas AST-like peptide-containing cells do not overlap with orcokinin-expressing cells. On the other hand, FaRP-expressing cells overlap with both orcokinin- and AST-like peptide-specific cells. In cluster 11, where signals for AST-like peptide are absent, a number of interneurons express both decapod-TRP and orcokinin, emphasizing a close relationship between these two factors with regard to olfactory processing, and possibly tactile and/or visual sensory systems. These characteristic expression patterns of neuropeptides support their distinct involvement in the modulation of olfactory processing.

Animals↗

PubMed2003

Dorsal horn neurons firing at high frequency, but not primary afferents, release opioid peptides that produce micro-opioid receptor internalization in the rat spinal cord.

To determine what neural pathways trigger opioid release in the dorsal horn, we stimulated the dorsal root, the dorsal horn, or the dorsolateral funiculus (DLF) in spinal cord slices while superfusing them with peptidase inhibitors to prevent opioid degradation. Internalization of mu-opioid receptors (MOR) and neurokinin 1 receptors (NK1R) was measured to assess opioid and neurokinin release, respectively. Dorsal root stimulation at low, high, or mixed frequencies produced abundant NK1R internalization but no MOR internalization, indicating that primary afferents do not release opioids. Moreover, capsaicin and NMDA also failed to produce MOR internalization. In contrast, dorsal horn stimulation elicited MOR internalization that increased with the frequency, being negligible at <10 Hz and maximal at 500 Hz. The internalization was abolished by the MOR antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP), in the presence of low Ca2+ and by the Na+ channel blocker lidocaine, confirming that it was caused by opioid release and neuronal firing. DLF stimulation in "oblique" slices (encompassing the DLF and the dorsal horn of T11-L4) produced MOR internalization, but only in areas near the stimulation site. Moreover, cutting oblique slices across the dorsal horn (but not across the DLF) eliminated MOR internalization in areas distal to the cut, indicating that it was produced by signals traveling in the dorsal horn and not via the DLF. These findings demonstrate that some dorsal horn neurons release opioids when they fire at high frequencies, perhaps by integrating signals from the rostral ventromedial medulla, primary afferents, and other areas of the spinal cord.

Anesthetics, Local↗

PubMed1996

A subset of estrogen receptor-containing neurons project to the median eminence in the ewe.

The neural pathways responsible for conveying the steroid feedback signals that ultimately affect reproductive neuroendocrine function remain largely undefined. One possibility involves a direct projection from estrogen receptor (ER)-containing neurons to the median eminence (ME), a site of neuroendocrine peptide release. To examine this possibility, 8 ewes received stereotaxic injections of the retrograde neuronal tract-tracing compound cholera toxin-beta subunit (CT beta) into the ME. Neurons sending projections to the ME and containing ER were identified using a dual-label immunoperoxidase method. Double-labeled cells were found in distinct regions: (1) the ER-rich arcuate nucleus (ARC) that contained the greatest number of double-labeled cells, and (2) the organum vasculosum of the lamina terminalis (OVLT) which contained a very consistent, but low, number of double-labeled cells. While a fairly large number of retrogradely-labeled ARC neurons containing ER were identified, the majority of ER-containing ARC neurons were unlabeled and thus send projections elsewhere. Other regions containing high concentrations of ER-positive cells such as the medial preoptic area (MPOA), anterior hypothalamic area, and ventrolateral portion of the ventromedial hypothalamic nucleus, were devoid of double-labeled cells. Similarly, regions rich in neuroendocrine neurons such as the periventricular hypothalamus and paraventricular and supraoptic hypothalamic nuclei contained no double-labeled cells. These results suggest that modulation of neuroendocrine secretory activity may occur directly at the level of the ME by ER-containing neurons located within restricted regions of the hypothalamus and forebrain. However, the relatively low proportion of ER-containing neurons projecting to the ME suggests that the influence of estradiol upon neuroendocrine function also may include target sites other than the ME.

Animals↗

PubMed2003

Multiple hypothalamic sites control the frequency of hippocampal theta rhythm.

Stimulation of a neural pathway originating in the brainstem reticular formation, with synapses in the medial hypothalamus, activates the hippocampal theta rhythm. The frequency of reticular-elicited theta is determined in the medial supramammillary nucleus (mSuM) completely in anaesthetised rats, but only partially when the animal is awake. We tested other medial hypothalamic sites for their capacity to control theta frequency in awake rats. Blockade of sodium channels (1 microl fast infusion of the local anaesthetic procaine, experiment 1) or increased inhibition by GABA (Chlordiazepoxide [CDP], experiment 2) was found to reduce or increase the frequency of reticular-elicited theta, depending on the precise site of injection, in the region of the dorsomedial hypothalamic nucleus (DMH) and the posterior hypothalamic nucleus (PH). A band of null sites for CDP was located in the region of the ventral border of PH and dorsal border of mSuM. Using 0.5 and 1 microl CDP, and slow infusions (experiment 3), it was found that effective PH sites were also separate from mSuM in the rostrocaudal direction. In experiment 4, the DMH/PH region was mapped with unilateral and bilateral slow infusions of 0.5 microl CDP. CDP significantly reduced frequency in medial (periventricular) and dorsal PH, but not DMH. Bilateral injections appeared to generally sum the usual effects of unilateral injection, producing effects of intermediate size. However, the absolute frequency change in any given site, or with any pair of sites, did not exceed 1 Hz, which is similar to what is seen with single injections in mSuM. Overall, it appears that at, any one time, theta frequency may be determined by a complex interplay between distinct but interacting modulatory regions in the medial hypothalamus.

Action Potentials↗

PubMed2003

Hypothalamus-brain stem circuitry responsible for vagal efferent signaling to the pancreas evoked by hypoglycemia in rat.

Circulating glucose levels significantly affect vagal neural activity, which is important in the regulation of pancreatic functions. Little is known about the mechanisms involved. This study investigates the neural pathways responsible for hypoglycemia-induced vagal efferent signaling to the pancreas and identifies the neurotransmitters involved. Vagal pancreatic efferent nerve activities were recorded in anesthetized rats. Insulin-induced hypoglycemia, a decrease of blood glucose levels from 114 +/- 5 to 74 +/- 6 mg dl(-1), stimulated an increase in pancreatic efferent nerve firing from a basal rate of 1.1 +/- 0.3 to 19 +/- 3 impulses 30 s(-1). In contrast, vagal primary afferent neuronal discharges recorded in the nodose ganglia were unaltered by systemic hypoglycemia. Vagal afferent rootlet section plus splanchnicotomy had no effect on hypoglycemia-induced vagal efferent firing, suggesting a central site of action. Decerebration reduced the increase in nerve firing stimulated by hypoglycemia from 21 +/- 4 to 9.6 +/- 2 impulses 30 s(-1). Chemical ablation of the lateral hypothalamic area, but not the arcuate nucleus, inhibited pancreatic nerve firing evoked by hypoglycemia. Microinjection of the orexin-A receptor antagonist SB-334867 into the dorsal motor nucleus of the vagus (DMV) inhibited pancreatic nerve firing evoked by insulin-induced hypoglycemia by 56%. In contrast, injection of orexin-A (20 pmol) into the DMV elicited a 30-fold increase in pancreatic nerve firing. We concluded that systemic hypoglycemia stimulates pancreatic efferent nerve firing through a central mechanism. Full expression of pancreatic nerve activities during hypoglycemia requires both the forebrain and the brain stem. In addition to activating neurons in the brain stem, central neuroglucopenia activates subpopulations of neurons in the lateral hypothalamic area that contain orexin. The released orexin acts on DMV neurons to stimulate pancreatic efferent nerve activities and thus regulate pancreatic functions.

Action Potentials↗