Increase In Spike Activity Research Articles

Interaction between serotonin and nitric oxide (NO) in the activation of the serotoninergic system in the common snail.

The effects of serotonin and NO donors on serotoninergic neurons (more than 60) in the brain of the common snail Helix lucorum were studied. Serotonin and NO donors induced depolarization in all neurons. and increased spike activity and activated the synchronous synaptic input, including train-like input. resulting in the onset of synchronous train activity in all these neurons. The excitatory effect of serotonin was significantly decreased by 5,7-dihydroxytryptamine (5.7-DOT) and monomethylarginine--a blocker of endogenous NO synthesis. Both these substances blocked the serotonin activation of the synchronous train input. 5.7-DOT also blocked the activation of this input by NO donors. but had no effect on their excitatory actions. The effects of 5,7-DOT developed quickly, were reversible, and were comparable to the effects of serotonin receptor antagonists. The data obtained here provide evidence that serotonin and NO have similar regulatory effects on the serotoninergic system in the snail brain. Not only do they excite serotoninergic neurons, but they also coordinate their functioning by activating common synaptic inputs. which are apparently also serotoninergic. It is suggested that NO has the role of a second messenger during serotoninergic excitation and functions as a co-transmitter for the presynaptic input.

Unravelling the neural circuitry for circadian regulation of sleep–wake cycles

A requirement for the fruitful analysis of a neurobiological process is the identification of neural circuits that are crucial for effecting the process. Circadian rhythms constitute one ubiquitous, but mechanistically complex, process that is important for regulating a variety of behavioral states, including sleep and waking. The circadian rhythmicity of sleep–wake cycles might be regulated by trans-synaptic signalling between neurons located in hypothalamic nuclei and in the noradrenergic locus coeruleus (LC). LC neurons fire briskly during waking, and they are less active during slow-wave sleep. However, it is not known whether the LC system is importantly involved in the circadian regulation of arousal. Circadian regulation of the sleep–wake cycle probably involves the suprachiasmatic nucleus (SCN) of the hypothalamus; lesions of the SCN eliminate the circadian rhythmicity of the sleep–wake cycle. This observation, and others, led to the hypothesis that connections between the SCN and brain structures that modulate arousal might underlie the circadian regulation of sleep–wake cycles. Direct demonstration of functional projections from the SCN to brain centers that regulate arousal, such as the LC, is vital for revealing how the SCN and LC regulate arousal.A study by Aston-Jones et al 1xA neural circuit for circadian regulation of arousal. Aston-Jones, G. et al. Nat. Neurosci. 2001; 4: 732–738Crossref | PubMed | Scopus (352)See all

Analysis of responses of Leidynema appendiculata to acetylcholine using electrophysiological techniques.

The electrophysiological responses of adult females of the insect-parasitic nematode Leidynema appendiculata, to 100 mM, 10 mM, and 1 mM acetylcholine were concentration dependent, with stimulation by 100 mM acetylcholine giving the largest increase in spike activity. By contrast, the delay in response was not concentration dependent. No increase in activity was obtained on stimulation with either 0.1 mM acetylcholine or phosphate-buffered saline. The lack of response to 0.1 mM acetylcholine was confirmed by sequential exposure of L. appendiculata to 0.1 mM acetylcholine and subsequently to 10 mM acetylcholine.

Electrophysiological analysis of responses of adult females of Brugia pahangi to some chemicals.

Electrophysiological techniques were used to obtain recordings of extracellular electrical activity from the anterior end of live adult females of Brugia pahangi. Stimulation with 100 mM, 10 mM and 1 mM acetylcholine resulted in an increase in spike activity which was concentration dependent, whereas stimulation with phosphate-buffered saline and 0.1 mM acetylcholine gave no increase in activity. The delay in response was not concentration dependent. The action of possible host cues was investigated. Stimulation with heat-inactivated foetal calf serum (IFCS) and 10 mM glutathione gave an increase in spike activity but exposure to 5 mg/dl haemoglobin elicited no response. The response to IFCS was found to be suppressed completely by pre-incubation for 30 min in ivermectin.

Single-unit recordings of arterial chemoreceptors from mouse petrosal ganglia in vitro.

A preparation was developed that allows for the recording of single-unit chemoreceptor activity from mouse carotid body in vitro. An anesthetized mouse was decapitated, and each carotid body was harvested, along with the sinus nerve, glossopharyngeal nerve, and petrosal ganglia. After exposure to collagenase/trypsin, the cleaned complex was transferred to a recording chamber where it was superfused with oxygenated saline. The ganglia was searched for evoked or spontaneous unit activity by using a glass suction electrode. Single-unit action potentials were 57 +/- 10 (SE) (n = 16) standard deviations above the recording noise, and spontaneous spikes were generated as a random process. Decreasing superfusate PO(2) to near 20 Torr caused an increase in spiking activity from 1. 3 +/- 0.4 to 14.1 +/- 1.9 Hz (n = 16). The use of mice for chemoreceptor studies may be advantageous because targeted gene deletions are well developed in the mouse model and may be useful in addressing unresolved questions regarding the mechanism of chemotransduction.

The effects of nitrite on the excitability of brain neurons in the common snail

Electrophysiological studies were performed on the effects of sodium nitrite (0.01-1 mM) on identified command neurons in the brain of the common snail. These studies showed that short periods of exposure to nitrite (from a few minutes up to 30 min) had little effect, producing a low level of depolarization and increases in neuron spike activity in only a few cases. Incubation of isolated brains with nitrite (1 mM) for periods ranging from 2 h to several days reduced excitation thresholds, significantly increased spike activity, increases responses to stimulation, and increases the levels of synaptic activity of the neurons studied. These effects increased with time and were stable, but were reversible on washing and were accompanied by depolarization and increased input resistance. The action of nitrite was imitated by known NO donors, and blockers of NO synthesis had the opposite effect. The possible mediation of the effects of nitrite by NO synthesis and the development of hypoxia is discussed.

Intraoperative localization of an epileptogenic focus with alfentanil and fentanyl.

We evaluated the effectiveness of alfentanil and fentanyl in stimulating epileptogenic activity during surgery for intractable temporal lobe epilepsy under general anesthesia. Ten patients received a standardized anesthetic induction with i.v. fentanyl 5 microg/kg, propofol 3-5 mg/kg, and atracurium 0.5 mg/kg. Maintenance was with isoflurane, 70% N2O/30% O2, and an atracurium infusion. After dural opening, droperidol 0.02 mg/kg was administered i.v.. Both inhaled anesthetics were discontinued and verified to be at 0 end-tidal concentration before the study. Baseline electrocorticography over the surface of the temporal lobe and depth electrode recordings in the amygdala and hippocampus were obtained, followed by 10 min of recording before and after the i.v. administration of both alfentanil 50 microg/kg and fentanyl 10 microg/kg. Any changes in cardiovascular variables were documented. The number of interictal epileptiform spikes at the most active site for each patient was tabulated before and after the administration of each drug. Both alfentanil and fentanyl induced an increase in spike activity in all patients. Alfentanil was more potent, increasing the median number of spikes per epoch from 18 to 58, compared with fentanyl (20 to 42 spikes) (P < 0.05). Alfentanil had a shorter duration of action (4.9+/-1.3 min) compared with fentanyl (8.5+/-2 min) (P < 0.009). In nine patients, the most active site was the hippocampus or amygdala. There was a decrease in mean blood pressure, but only after the administration of alfentanil (P < 0.05). Two patients had electrographic evidence of seizure activity. These opioids can be used to assist in the localization of the epileptogenic focus during surgery. Both alfentanil and fentanyl activate epileptiform activity in patients with temporal lobe epilepsy. These opioids can be used to assist in the localization of the epileptogenic focus during surgery.

Behavioral Responses to Aliphatic Aldehydes Can Be Predicted From Known Electrophysiological Responses of Mitral Cells in the Olfactory Bulb

For a better understanding of the encoding of odor quality in the olfactory system, it is critical to determine how electrophysiological responses to odorants are reflected in the behavioral responses to these odorants. In this article, we use a simple behavioral paradigm to show that the behavioral responses to similar odorants can be predicted from the electrophysiological responses of neurons in the olfactory bulb. Carbon chain length in aliphatic aldehydes has been used as a model for graded similarity among odorants. Recent electrophysiological experiments have shown that mitral cells in the rabbit olfactory bulb respond with similar response patterns to aliphatic aldehydes of similar chain length. On average, mitral cells responded with increased spiking activity to stimulation with two to three different aldehydes of neighboring chain length. We here show that the perception of these odorants can be predicted from the electrophysiological responses: rats that are conditioned to a given aldehyde generalize to aldehydes with one to two carbon differences in chain length from the conditioned aldehyde. When asked to discriminate between aldehydes of different chain lengths, rats learned to discriminate between any two odorants, but the rate of acquisition depended on the degree of similarity between the two odorants.

Spontaneous Calcium Oscillations in Embryonic Stem Cell-Derived Primitive Endodermal Cells

In vitrodifferentiation of mouse embryonic stem cells within three-dimensional cell aggregates called embryoid bodies parallels the development of postimplantation embryos at the egg cylinder stage, where visceral and parietal endoderm diverge from the primitive endoderm. We have investigated spontaneous [Ca2+]ioscillations by means of confocal laser-scanning microscopy in primitive endodermal cell layers of embryoid bodies during their differentiation to parietal and visceral endoderm. The frequency of [Ca2+]ioscillations increased from day 4 to day 19 of development, whereas their duration decreased from day 3 to days 16–17. Oscillations depended on both extracellular Ca2+and Ca2+release from intracellular stores as they were abolished in Ca2+-free solution and in the prescence of Ni2+and thapsigargin. Signal transduction operated via the phospholipase C (PLC)-mediated inositol 1,4,5-triphosphate (InsP3) pathway with a negative feedback loop via protein kinase C (PKC) as U73,122, a blocker of PLC; bisindolylmaleimide 1, staurosporine, and H-7, blockers of PKC; and 10 mM caffeine totally inhibited [Ca2+]ispiking. Thimerosal, which hypersensitizes the InsP3receptor, as well as vasopressin and bradykinin, which act via the InsP3pathway, increased the frequency of [Ca2+]ispikes. In the prescence of brefeldin A (50 μM) or monensin (20 μM), which both inhibit endo/exocytotic vesicle pathways, an immediate transient increase in spiking activity was followed by a decline within 1 to 2 h. In the presence of brefeldin A or thapsigargin or in the absence of extracellular Ca2+, endocytotic vesicles were absent, suggesting that oscillating [Ca2+]itransients are involved in the exo/endocytotic vesicle shuttle.

Are oxygen dependent K + channels essential for carotid body chemo-transduction?

The mechanism by which the carotid body senses hypoxia and causes an increase in spiking activity on the sinus nerve is not well resolved. Most experimental attention is focused on the glomus cell, a secretory cell which is apposed to the afferent nerve endings and which is the presumed site of oxygen sensing. It is proposed that hypoxia causes glomus cell depolarization by inhibiting an oxygen-sensitive K + current. This leads to depolarization, activation of voltage-gated calcium influx and enhanced secretion of an excitatory transmitter. At present, 4 candidate oxygen-sensitive K + currents have been identified based on patch-clamp studies of isolated glomus cells. Recent experiments using intact carotid bodies have been undertaken to identify which current is most likely to mediate the hypoxia response. Three of the four currents are sensitive to K + channel blocking agents (TEA, 4-AP and charybdotoxin), yet all these agents failed to mimic hypoxia, neither stimulating chemoreceptor nerve activity nor enhancing catecholamine secretion. Thus, the fourth current, a leak current which is insensitive to these agents is the most likely candidate for mediating glomus cell depolarization, but the drug-sensitivity of this current is not yet known which precludes a direct test of this speculation.

Electrophysiological Responses of Male Potato Cyst Nematodes, Globodera rostochiensis and G. pallida, to Some Chemicals

Electrophysiological techniques and behavioral bioassays were used to evaluate the responses of males of the potato cyst nematodesGlobodera rostochiensis and G. pallidato various chemicals. Exposure of all males of both species to acetylcholine elicited strong electrophysiological responses and positive movement towards the source. By contrast, neither glycine nor citric acid induced any marked electrophysiological responses and only males of G. pallida showed significant behavioral responses, moving toward glycine and away from citric acid. The electrophysiological and behavioral responses to GABA and α-aminobutyric acid were complementary, with G. rostochiensis showing significant response only to the latter and G. pallida responding significantly only to the former. The electrophysiological response of individuals of both species to L- and D-tryptophan varied from no response to a strong response with a significant mean increase in spike activity of G. rostochiensis to D-tryptophan and of G. pallida to L-tryptophan; behavioral bioassays showed L-tryptophan was a deterrent for G. pallida. Males of both species responded significantly in both electrophysiological and behavioral assays to L-glutamic acid but not to D-glutamic acid.

Endotoxin induces biphasic alterations in small intestinal myoelectric activity in fasted newborn piglets.

Previous studies have shown that i.v. endotoxin infusion causes gastrointestinal dysfunction and intestinal injury in piglets. The aim of this study was to investigate the effects of endotoxin on intestinal myoelectric activity in newborn swine and to correlate this with gastrointestinal and hemodynamic events. Three pairs of electrodes were implanted in the jejunal wall of piglets, and after recovery, intestinal myoelectric activity was continuously recorded in the conscious, fasted condition. The intestinal myoelectric activity on the control day showed regular, repeating migrating myoelectric complex (MMC) cycles, each of which was composed of the classic phases I, II, and III. Mean cycle duration was 67.0 +/- 18.7 min (+/- SD), and phase III comprised 9.1 +/- 2.2% of each cycle. On the next day, infusion of 30 micrograms/kg endotoxin caused an initial, prolonged quiescent period and delayed the appearance of the first postendotoxin phase III complex. After the quiescent period, there was a period of irregular spiking activity followed by several shortened MMC cycles (47.9 +/- 22.7 min, p < 0.01 versus control) with a prolongation of the percentage of time spent in phase III (15.4 +/- 11.3%, p < 0.01). Endotoxin thus produced biphasic alterations in intestinal myoelectric activity characterized by an initial quiescence followed by increased gastrointestinal smooth muscle activity. Animals developed diarrhea, hypotension, and tachycardia about 1 h after endotoxin infusion in temporal association with increased spiking activity and MMC cycling. These studies are the first to show this biphasic response to endotoxin.

Activation of cells of cochlear nucleus by electrical stimulation of lateral hypothalamus.

Effects of electrical stimulation of the lateral hypothalamus (HS) were examined in 67 cells of the dorsal or ventral cochlear nucleus. Both short latency activity in the 10-20 ms post-stimulus period and late activity in the > 20 ms post-stimulus period were elicited in response to HS. A greater percentage of units exhibited the short latency response in dorsal (89%) than ventral (68%) cochlear nucleus. It was not previously recognized that stimulation of the hypothalamus could elicit increases in spike activity in this auditory relay nucleus. The hypothalamus is known to play a role in visceral-emotional functions, including feeding, fleeing, fighting and reproductive behavior. These results suggest a means by which neural activities supporting these functions could influence acoustic relay transmissions.

Contribution of Astroglia to Functionally Activated Energy Metabolism

Studies of local glucose utilization in neural tissues in vivo with the autoradiographic [14C]deoxyglucose method have demonstrated that energy metabolism increases almost linearly with the degree of functional activation, i.e. spike frequency, in the terminal projection zones of activated pathways. The increased metabolism is found in neuropil and is minimal or undetectable in neuronal cell bodies. Electrical stimulation, increased extracellular [K+] ([K+]o), or opening of Na+ channels with veratridine stimulates metabolism in neutral tissues, and this increase is blocked by ouabain, a specific inhibitor of Na+,K(+)-ATPase. Activation of this enzyme to restore ionic gradients across cellular membranes appears to mediate the function-related increase in energy metabolism. The metabolic activation is, therefore, not directly related to the functional activity itself but to processes operating to recover from that activity. The limited spatial resolution of the [14C]DG method precludes identification of cellular elements in neuropil participating in the metabolic activation, e.g. axonal terminals, dendrites, or astrocytic processes enveloping the synapses. We have, therefore, attempted to stimulate in vitro conditions to be expected from functional activation and increased spike activity in vivo, e.g. increased extracellular [K+], intracellular [Na+], or extracellular neurotransmitter levels, and examined their effects on glucose metabolism in neurons and astroglia in culture. Increased [K+]o stimulated [14C]DG phosphorylation in neuronal and mixed neuronal-astroglial cultures, but not in astroglial cultures assayed in bicarbonate buffer; it did occasionally stimulate metabolism in astroglia when assayed in HEPES or phosphate buffers, but these effects were variable and inconsistent. Veratridine (75 microM) stimulated [14C]DG phosphorylation in neurons and astroglia; these stimulations were blocked by 1 mM ouabain or 10 microM tetrodotoxin (TTX), which blocks voltage-dependent Na+ channels. The Na+ ionophore monensin (10 microM) doubled the rate of metabolism, a stimulation that was only partially blocked by ouabain and unaffected by TTX. L-Glutamate (500 microM) stimulated [14C]DG phosphorylation in astroglia, but this stimulation was probably secondary to Na+ uptake into the cells via a sodium/glutamate co-transporter because it was not blocked by inhibitors of NMDA or non-NMDA receptors but was absent in Na(+)-free medium. These results indicate that astroglia contribute to the increased energy metabolism in neuropil during functional activation by mechanisms that promote Na+ entry into the cells.

Effect of various doses of erythromycin on colonic myoelectrical activity in IBS patients

Abstract Erythromycin mimics the effects of motilin but its action on colonic motility is still controversial. The aim of this study was to evaluate the effect of intravenous infusions of various doses of erythromycin on colonic motility in patients with irritable bowel syndrome (IBS).At 09.00 hours, day 1 (D1), an intraluminal probe was introduced up to the right colon in 24 IBS patients with myoelectrical activity recorded for 48 h. Patients were randomised in three groups of eight, receiving either erythromycin 1.5, 3 or 7 mg kg−1. All were investigated as follows: at 09.00 hours, D2, fasted patients were infused with erythromycin in 30 min; at 09.00 hours, D3, glycerol 10 ml was injected intraluminally. Colonic activity was measured 30 min before the infusion started, during and 30 min after it, separately in the left and right colons, and expressed in time occupied during the recording period.Basal activity was similar in both parts of the colon. During and after erythromycin 1.5 and 3 mg kg−1, colonic activity remained unchanged. Erythromycin 7 mg kg−1 induced a moderate increase in spiking activity (long spike bursts or LSBs + 33%; migrating LSBs or MLSBs + 41%) in the right colon, no change being statistically significant; activities in the left colon were similar to basal level.During the first 30 min following glycerol injection, mean short spike burst or SSB activity did not change, mean LSB activity increased by seven fold (P = 0.014) and MLSB activity by ten fold (P = 0.023).Erythromycin at doses from 1.5 to 7 mg kg−1 failed to stimulate colonic motility in IBS patients. By contrast, response to glycerol was strong, suggesting normal colonic responsiveness. Erythromycin stimulatory effects could be limited to the upper gut at least in IBS patients.

Induction of c-fos expression in hypothalamic magnocellular neurons requires synaptic activation and not simply increased spike activity

Magnocellular neurons of the hypothalamic supraoptic nucleus have been shown to express the immediate-early gene c-fos in a number of experimental and physiological circumstances. In each case the induction of the immediate-early gene followed the increase in the spike activity of the cells. Since an increase in the intracellular concentration of calcium following influx through voltage-sensitive calcium channels is a known stimulus for c-fos expression and since the action potentials of these neurons have a large calcium component, we hypothesized that c-fos induction in these neurons could be attributed to calcium influx during spike activity. In the present experiments we use extracellular recording and immunocytochemistry for Fos, the protein product of c-fos, to demonstrate the activation of the cells following intracerebroventricular administration of the muscarinic agonist, carbachol. Fos expression following carbachol injection was then compared with that induced by a similar number of antidromically evoked action potentials. Antidromic activation, unlike the activation induced by carbachol, did not lead to the induction of Fos. We conclude that Fos induction in these neurons requires receptor activation rather than spike activity.

Prostaglandin E2 (PGE2)‐evolted chloride secretion in guinea‐pig colon is mediated by nerve‐dependent and nerve‐independent mechanisms

Abstract Conventional flux chamber and intracellular recording methods were used to investigate the effect of prostaglandin E2 on ion transport and on electrical behaviour of submucosal neurones in guinea‐pig colon. In flux chamber experiments, prostaglandin E2 evoked a dose‐dependent increase in short‐circuit current. The response was reduced by serosal addition of bumetanide, tetrodotoxin or atropine, but not hexamethonium or piroxicam. This indicates that the response to prostaglandin E2 was mediated in part by activation of chloride secretion via submucosal neurons. Application of prostaglandin E2 to submucosal neurones evoked a depolarization of the membrane potential associated with an enhanced spike discharge which was frequently triggered by fEPSPs. The depolarizing response to prostaglandin E2 was not affected by tetrodotoxin, indicative of a direct effect of prostaglandin E2 on the impaled neurones. However, the increased spike activity was synaptically driven suggesting an additional activation of other cells. Prostaglandin E2 had no excitatory or inhibitory effect on cholinergic fast excitatory postsynaptic potentials. The study suggests that prostaglandin E2 may function as a neuromodulator to evoke nerve‐mediated chloride secretion through activation of submucosal neurones. The results further indicate that prostaglandin E2 may influence mucosal function by altering electrical behaviour of submucosal neurones leading to spread of excitation throughout the plexus.

FMRFamide and GABA Produce Functionally Opposite Effects on Prey-Capture Reactions in the Pteropod Mollusk Clione limacina.

The effects of FMRFamide and gamma-aminobutyric acid (GABA) on prey-capture reactions in Clione and on cerebral A and B neurons, which control opposite movements of prey capture appendages, have been studied. FMRFamide hyperpolarized A neurons and depolarized and increased spike activity in B neurons. FMRFamide thus had a reciprocal effect on A and B neurons, triggering buccal cone withdrawal. In addition, FMRFamide inhibited swimming, acceleration of which is a component of feeding arousal. Many neurons throughout the central nervous system showed FMRFamide immunoreactivity. Dense networks of immunoreactive fibers were localized in the head wall, buccal mass and in buccal cones, adjacent to striated longitudinal muscle cells. In wings, immunoreactive processes were found mainly in association with smooth retractor muscles. GABA depolarized and activated A neurons but hyperpolarized and inhibited B neurons. The overall effect of GABA thus resulted in extrusion of buccal cones. Both direct GABA responses and inhibitory postsynaptic potentials (IPSPs) induced in B neurons by A neuron activity were chloride-mediated. However, picrotoxin and bicuculline did not block IPSPs or direct GABA responses in B cells.

Brain factors control the activity of prothoracic gland nerves in the cockroach Periplaneta americana

Neurotropic factors of the brain with stimulating effects on the discharging pattern of the prothoracic gland nerve in the cockroach Periplaneta americana were investigated. Homogenates of brains from 13- to 15- and from 20-day-old last-instar larvae as well as of corpora cardiaca from 15- to 16-day-old larvae stimulated spike activity of the prothoracic gland nerve in in situ and in vitro experiments. The neurotropic effect was dose dependent in a range of 0.75 to three brain equivalents and was mainly due to an increase of the small type of action potentials. The increase of spike activity in preparations without the suboesophageal ganglion differed from those with this ganglion by a factor of 10 3. Therefore, the effect of brain homogenates on spike activity in the prothoracic gland nerve is possibly dependent on the control of the prothoracic ganglion by the suboesophageal ganglion. The neurotropic brain factors were inactivated by pronase treatment and methanolic extraction. Gelfiltration on Sephadex G 100 resulted in two active fractions ranging near the upper and the lower exclusion limit.

The responses of peripheral and central mechanosensory lateral line units of weakly electric fish to moving objects

Mechanosensory lateral line afferents of weakly electric fish (Eigenmannia) responded to an object which moved parallel to the long axis of the fish with phases of increased spike activity separated by phases of below spontaneous activity. Responses increased with object speed but finally may show saturation. At increasingly greater distances the responses decayed as a power function of distance. For different object velocities the exponents (mean±SD) describing this response falloff were -0.71±0.4 (20 cm/s object velocity) and-1.9±1.25 (10 cm/s). Opposite directions of object movement may cause an inversion of the main features of the response histograms. In terms of peak spike rate or total number of spikes elicited, however, primary lateral line afferents were not directionally sensitive. Central (midbrain) lateral line units of weakly electric fish (Apteronotus) showed a jittery response if an object moved by. In midbrain mechanosensory lateral line, ampullary, and tuberous units the response to a rostral-tocaudal object movement may be different from that elicited by a caudal-to-rostral object motion. Central units of Apteronotus may receive input from two or more sensory modalities. Units may be lateral line-tuberous or lateral line-ampullary. Multimodal lateral line units were OR units, i.e., the units were reliably driven by a unimodal stimulus of either modality. The receptive fields of central units demonstrate a weak somatotopic organization of lateral line input: anterior body areas project to rostral midbrain, posterior body areas project to caudal midbrain.