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Olfaction plays an important role in social recognition in most mammals. Central arginine vasopressin (AVP) plays a role in this olfaction-based recognition. The high level of expression of AVP receptors in the accessory olfactory bulb (AOB) at the first relay of the vomeronasal system highlights the importance of AVP signaling at this stage. We therefore analyzed the effects of AVP on the synaptic plasticity of glutamatergic transmission from mitral cells to granule cells in AOB slices from male mice. To monitor the strength of the glutamatergic transmission, we measured the maximal initial slope of the lateral olfactory tract-evoked field potential, which represents the granule cell response to mitral cell activation. AVP paired with 100-Hz stimulation that only produced short-term potentiation enhanced the induction of long-term potentiation (LTP) in a dose-dependent manner. AVP-paired LTP was blocked by the selective AVP receptor 1a (AVPR1a) antagonist, d(CH 2 ) 5 [Tyr(Me) 2 ]AVP (Manning compound), but not by the AVPR1b antagonist SSR149415, and it was mimicked by the selective AVPR1a agonist [Phe 2 , Ile 3 , Orn 8 ]-vasopressin. We further examined the effect of AVP on the reciprocal transmission between mitral and granule cells by stimulating a mitral cell and recording the evoked inhibitory postsynaptic currents (IPSCs) from the same cell using conventional whole-cell patch-clamp techniques. AVP reduced the reciprocal IPSCs triggered by endogenous glutamate release from the excited mitral cell. These results suggest that AVP promotes the induction of LTP at the mitral-to-granule cell synapse via the activation of AVPR1a through an as-yet-to-be-determined mechanism in the AOB of male mice. [ABSTRACT FROM AUTHOR]

The throughput of information from the accessory olfactory bulb ( AOB) to downstream structures is controlled by reciprocal dendrodendritic inhibition of mitral cells by granule cells. Given the high expression levels of m Glu R2, a metabotropic glutamate receptor, in the AOB and the fact that the activation of m Glu R2 permits the formation of a specific olfactory memory, we reasoned that m Glu R2 might play an important role in regulating dendrodendritic inhibition. To test this hypothesis, we examined the effects of pharmacological and genetic manipulations of m Glu R2 on synaptic responses measured from mitral or granule cells in slice preparations from 23- to 36-day-old Balb/c mice. To evoke dendrodendritic inhibition, a depolarizing voltage step from -70 to 0 m V or a threshold current stimulus adjusted to elicit action potential(s) was applied to a mitral cell using either a nystatin-perforated or conventional whole-cell configuration. We found that an agonist for group II metabotropic glutamate receptors ( mGlu R2/ mGluR3), DCG- IV [(2 S,1′ R,2′ R,3′ R)-2-(2,3-dicarboxycyclopropyl)glycine], suppressed, whereas the m GluR2/m Glu R3 antagonist LY341495 [(αS)-α-amino-α-[(1S,2S)-2-carboxycyclopropyl]-9H-xanthine-9-propanoic acid] enhanced dendrodendritic inhibition. Genetic ablation of mGlu R2 markedly impaired the effects of DCG- IV and LY341495 on dendrodendritic inhibition. DCG- IV reduced both the frequency and the amplitude of spontaneous miniature excitatory postsynaptic currents recorded from granule cells. Additionally, DCG- IV inhibited high-voltage-activated calcium currents in both mitral and granule cells. These results suggest that m GluR2 reduces dendrodendritic inhibition by inhibiting synaptic transmission between mitral cells and granule cells in the AOB. [ABSTRACT FROM AUTHOR]

Snake vomeronasal receptor neurons in slice preparations were studied using the patch-clamp technique in the conventional and nystatin-perforated whole-cell configurations. The mean resting potential was approximately –70 mV; the average input resistance was 3 GΩ. Neurons required current injection of only 1–10 pA to display a variety of spiking patterns. Intracellular dialysis of 100 μM inositol 1,4,5-trisphosphate (IP[sub 3]) evoked an inward current in 38% of neurons, with an average peak amplitude of 16.4 ± 2.8 pA at a holding potential of –70mV. Application of 100 μM 3-deoxy-3-fluoro- d- myo-inositol 1,4,5-trisphosphate (F-IP[sub 3]), a derivative of IP[sub 3], also evoked an inward current in 4/8 (50%) neurons (32.6 ± 58 pA at –70 mV, n = 4). The reversal potentials of the induced components were estimated to be –14 ± 5 mV for IP[sub 3] and –17 ± 3 mV for F-IP[sub 3]. Bathing the neurons in 10 μM ruthenium red solution greatly reduced the IP[sub 3]-evoked inward current to 1.6 ± 1.1 pA at –70 mV ( n = 6). With Cs[sup +]-containing internal solution, neither the Ca[sup 2+]-ATPase inhibitor thapsigargin (1–50 μM) nor the Ca[sup 2+]-ionophore ionomycin (10 μM) evoked a significant current response, suggesting that IP[sub 3] can elicit current response in the neurons without mediation by intracellular Ca[sup 2+] stores. Intracellular application of 1 mM cAMP evoked no detectable current response. Extracellular application of chemoattractant for snakes evoked a very large inward current. The reversal potential of the chemoattractant-induced current was similar to that of the IP[sub 3]-induced current. The present results suggest that IP[sub 3] may act as a second messenger in the transduction of chemoattractants in the garter snake vomeronasal organ. [ABSTRACT FROM AUTHOR]

Background. We have observed changes in body reactions during cooking, which is one of the treatment modalities used in occupational therapy. The perception of food-related odors during cooking may have behavioral effects on human activities through the activation of appetitive motivation. Objectives. We investigated whether odor components contained in seasonings could facilitate the human motor system and the specificity of this effect. Methods. The subjects were 72 healthy adults, randomly assigned to a water exposure group, a phenylethyl alcohol (PEA, pleasant rose-like odor) exposure group, and a Japanese soy sauce (Koikuchi Shoyu) exposure group (n=24 each). The subjects' olfactory sense was stimulated by their sniffing of three different test tubes containing 5 ml of water, PEA, or Japanese soy sauce for 20 sec while they were seated. The modified Functional Reach Test (mFRT), which mimics a functional activity that is required in daily living and assesses a reliable measure of sitting balance, was performed prior to and immediately after the sniffing. Results. Sniffing the soy sauce increased the subjects' mFRT scores. This facilitation effect was odorant-specific and was absent when the subjects were presented with water or PEA. Conclusions. Cooking interventions are aimed at improving tool-handling skills such as using knives and chopsticks. The results indicate that treatment interventions using odors of seasonings would be effective for improving subjects' physical functions. [ABSTRACT FROM AUTHOR]

Tunicamycin (TM) induces endoplasmic reticulum (ER) stress and inhibits N-glycosylation in cells. ER stress is associated with neuronal death in neurodegenerative disorders, such as Parkinson’s disease and Alzheimer’s disease, and most patients complain of the impairment of olfactory recognition. Here we examined the effects of TM on aversive olfactory learning and the underlying synaptic plasticity in the main olfactory bulb (MOB). Behavioral experiments demonstrated that the intrabulbar infusion of TM disabled aversive olfactory learning without affecting short-term memory. Histological analyses revealed that TM infusion upregulated C/EBP homologous protein (CHOP), a marker of ER stress, in the mitral and granule cell layers of MOB. Electrophysiological data indicated that TM inhibited tetanus-induced long-term potentiation (LTP) at the dendrodendritic excitatory synapse from mitral to granule cells. A low dose of TM (250 nM) abolished the late phase of LTP, and a high dose (1 μM) inhibited the early and late phases of LTP. Further, high-dose, but not low-dose, TM reduced the paired-pulse facilitation ratio, suggesting that the inhibitory effects of TM on LTP are partially mediated through the presynaptic machinery. Thus, our results support the hypothesis that TM-induced ER stress impairs olfactory learning by inhibiting synaptic plasticity via presynaptic and postsynaptic mechanisms in MOB. [ABSTRACT FROM AUTHOR]

Abstract When female mice are mated, they form a memory to the pheromonal signal of their male partner. The neural changes underlying this memory occur in the accessory olfactory bulb, depend upon vaginocervical stimulation at mating and involve changes at the reciprocal synapses between mitral and granule cells. However, the action of vaginocervical stimulation on the reciprocal interactions between mitral and granule cells remains to be elucidated. We have examined the effects of vaginocervical stimulation on paired-pulse depression of amygdala-evoked field potentials recorded in the external plexiform layer of the accessory olfactory bulb (AOB) and the single-unit activity of mitral cells antidromically stimulated from the amygdala in urethane-anaesthetized female mice. Artificial vaginocervical stimulation reduced paired-pulse depression (considered to be due to feedback inhibition of the mitral cell dendrites from the granule cells via reciprocal dendrodendritic synapses) recorded in the AOB external plexiform layer. As would be expected from this result, vaginocervical stimulation also enhanced the spontaneous activity of a proportion of the mitral cells tested. These results suggest that vaginocervical stimulation reduces dendrodendritic feedback inhibition to mitral cells and enhances their activity. [ABSTRACT FROM AUTHOR]