Administration of amyloid-β oligomer to the buccal ganglia may reduce food intake and cholinergic synaptic responses within the feeding neural circuit in Aplysia kurodai.

Anorexia is a behavioral change caused by functional brain disorders in patients with Alzheimer's disease (AD). Amyloid-β (1-42) oligomers (o-Aβ) are possible causative agents of AD that impair signaling via synaptic dysfunction. In this study, we used Aplysia kurodai to study functional disorders of the brain through o-Aβ.

An age-related decline in the cholinergic synaptic response may cause the firing pattern in the jaw-closing motor neurons, which resembles the aversive taste response in the feeding behavior of old Aplysia kurodai.

Anorexia due to aging is recognized as a syndrome of animal feeding behavior. Age-related functional disorders of the brain often cause behavioral changes. We used Aplysia kurodai to study this neural mechanism, following our previous study on food preference behaviors.

Effects of aging on the food intake in the feeding behavior of Aplysia kurodai.

In wild Aplysia, the birthdate of animals can typically not be determined. Therefore, we sought a reliable index of old age by taking into consideration the distinguished Japanese seasons. Large amounts of eggs and dead bodies were present on the coast during and after the second half of May (MayS).

Activity changes in jaw motor neurons induced by egg-laying hormone contribute to the feeding suppression during egg-laying behavior in Aplysia kurodai.

Egg-laying behavior in Aplysia is accompanied by behavioral changes such as feeding suppression. We investigated the effects of the egg-laying hormone (ELH) on food intake, the activity patterns of jaw muscles, and the activity of buccal neurons (multi-action neuron [MA1] and jaw-closing motor neuron [JC2]), which are elements of the feeding neural circuits controlling jaw movements in Aplysia kurodai. Injection of ELH into the body cavity inhibited the intake of seaweed.

Nerve growth factor increases electrical activity of neural cells derived from murine bone marrow stromal cells.

Objective: Nerve growth factor (NGF) triggers long-term neuronal excitability. We examined its effect on murine bone marrow stromal cells (BMSC)-derived neurons.

Methods: With an optimal differentiation protocol, BMSCs were differentiated into neurons in culture.

Effective amino acid composition of seaweeds inducing food preference behaviors in Aplysia kurodai.

Aplysia kurodai feeds on Ulva but rejects Gelidium and Pachydictyon with distinct patterned jaw movements. We previously demonstrated that these movements are induced by taste alone. Thus some chemicals may contribute to induction of these responses.

Functional transplant of photoactivated adenylyl cyclase (PAC) into Aplysia sensory neurons.

In neural mechanisms of animal learning, intracellular cAMP has been known to play an important role. In the present experiments we attempted functional transplant of a photoactivated adenylyl cyclase (PAC) isolated from Euglena into Aplysia neurons, and explored whether PAC can produce cAMP in the neurons by light stimulation. Serotonergic modulation of mechanoafferent sensory neurons in Aplysia pleural ganglia has been reported to increase intracellular cAMP level and promotes synaptic transmission to motor neurons by increasing spike width of sensory neurons.

A CPG component LE generates depolarization of buccal neurons by producing constant plateau potentials during feeding responses of Aplysia kurodai.

In the buccal ganglia of Aplysia kurodai we have identified neurons (here termed LE neurons, or LE) producing plateau potentials lasting several seconds by application of short depolarizing currents. Results obtained from experiments using various bath solutions suggest that generation of these plateau potentials may be an endogenous property of LE. Application of various intensities or lengths of depolarizing currents induced in LE almost constant plateau potentials with fixed duration and depolarizing size.

Responses of cerebral GABA-containing CBM neuron to taste stimulation with seaweed extracts in Aplysia kurodai.

Aplysia kurodai distributed along Japan feeds well on Ulva pertusa but rejects Gelidium amansii with distinctive patterned movements of the jaws and radula. On the ventral side of the cerebral M cluster, four cell bodies of higher order neurons that send axons to the buccal ganglia are distributed (CBM neurons). We have previously shown that the dopaminergic CBM1 modulates basic feeding circuits in the buccal ganglia for rejection by firing at higher frequency after application of the aversive taste of seaweed such as Gelidium amansii.

Modulation of a feeding neural circuit by microinjection of K+ channel expression genes into a single identified neuron in Aplysia kurodai.

In Aplysia buccal ganglion expression genes for voltage-dependent K(+) channels (AKv1.1a) were injected into one of four electrically coupled multi-action (MA) neurons that directly inhibit jaw-closing (JC) motor neurons and may cooperatively generate their firing pattern during the feeding response. Following the DNA injection, the firing threshold increased and the spike frequency at the same current decreased in the current-induced excitation of the MA neuron; indicating a decrease in excitability of the MA neuron.

Search for cerebral G cluster neurons responding to taste stimulation with seaweed in Aplysia kurodai by the use of calcium imaging.

The calcium imaging method can detect the spike activities of many neurons simultaneously. In the present experiments, this method was used to search for unique neurons contributing to feeding behavior in the cerebral ganglia of Aplysia kurodai. We mainly explored the neurons whose cell bodies were located in the G cluster and the neuropile region posterior to this cluster on the ventral surface of the cerebral ganglia.

Cerebral CBM1 neuron contributes to synaptic modulation appearing during rejection of seaweed in Aplysia kurodai.

The Japanese species Aplysia kurodai feeds well on Ulva but rejects Gelidium with distinctive rhythmic patterned movements of the jaws and radula. We have previously shown that the patterned jaw movements during the rejection of Gelidium might be caused by long-lasting suppression of the monosynaptic transmission from the multiaction MA neurons to the jaw-closing (JC) motor neurons in the buccal ganglia and that the modulation might be directly produced by some cerebral neurons. In the present paper, we have identified a pair of catecholaminergic neurons (CBM1) in bilateral cerebral M clusters.