Brain-machine interfaces typically rely on electrophysiological signals to interpret and transmit neurological information. In biological systems, however, neurotransmitters are chemical-based inter-neuron messengers. This mismatch can potentially lead to incorrect interpretation of transmitted neuron information. Here we report a chemically mediated artificial neuron that can receive and release the neurotransmitter dopamine. The artificial neuron detects dopamine using a carbon-based electrochemical sensor and then processes the sensory signals using a memristor with synaptic plasticity, before stimulating dopamine release through a heat-responsive hydrogel. The system responds to dopamine exocytosis from rat pheochromocytoma cells and also releases dopamine to activate pheochromocytoma cells, forming a chemical communication loop similar to interneurons. To illustrate the potential of the approach, we show that the artificial neuron can trigger the controllable movement of a mouse leg and a robotic hand.Brain-machine interfaces (BMIs) can bridge the gap between humans and machines through the interpretation and transmission of neurological information. This is a critical process in neuron rehabilitation, cyborg construction and ultimately consciousness detection and control. [1][2][3] Current state-of-the-art BMI technologies rely on the translation of electrophysiological signals, 4-6 such as surface (ex-vivo) or intracellular (in-vivo) bioelectrical potentials. [7][8][9] However, in biological neuronnetworks a large portion of intelligent information -including memory and emotion

The pubertal process is characterized by an activation of physiological events within the hypothalamic-adenohypophyseal–gonadal axis which culminate in reproductive competence. Excessive weight gain and adiposity during the juvenile period is associated with accelerated onset of puberty in females. The mechanisms and pathways by which excess energy balance advances puberty are unclear, but appear to involve an early escape from estradiol negative feedback and early initiation of high-frequency episodic gonadotropin-releasing hormone (GnRH) secretion. Hypothalamic neurons, particularly neuropeptide Y and proopiomelanocortin neurons are likely important components of the pathway sensing and transmitting metabolic information to the control of GnRH secretion. Kisspeptin neurons may also have a role as effector neurons integrating metabolic and gonadal steroid feedback effects on GnRH secretion at the time of puberty. Recent studies indicate that leptin-responsive neurons within the ventral premammillary nucleus play a critical role in pubertal progression and challenge the relevance of kisspeptin neurons in this process. Nevertheless, the nutritional control of puberty is likely to involve an integration of major sensor and effector pathways that interact with modulatory circuitries for a fine control of GnRH neuron function. In this review, observations made in ruminant species are emphasized for a comparative perspective.

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